Federal Registers - Table of Contents Federal Registers - Table of Contents
• Publication Date: 02/28/2006
• Publication Type: Final Rules
• Fed Register #: 71:10099-10385
• Standard Number: 1910; 1915; 1917; 1918; 1926
• Title: Occupational Exposure to Hexavalent Chromium

[Federal Register: February 28, 2006 (Volume 71, Number 39)]
[Rules and Regulations]               
[Page 10099-10385]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr28fe06-25]                         
 
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Part II

Department of Labor

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Occupational Safety and Health Administration

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29 CFR Parts 1910, 1915, et al.

Occupational Exposure to Hexavalent Chromium; Final Rule

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DEPARTMENT OF LABOR

Occupational Safety and Health Administration

29 CFR Parts 1910, 1915, 1917, 1918, and 1926

[Docket No. H054A]
RIN 1218-AB45

 
Occupational Exposure to Hexavalent Chromium

AGENCY: Occupational Safety and Health Administration (OSHA), 
Department of Labor.

ACTION: Final rule.

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SUMMARY: The Occupational Safety and Health Administration (OSHA) is 
amending the existing standard which limits occupational exposure to 
hexavalent chromium (Cr(VI)). OSHA has determined based upon the best 
evidence currently available that at the current permissible exposure 
limit (PEL) for Cr(VI), workers face a significant risk to material 
impairment of their health. The evidence in the record for this 
rulemaking indicates that workers exposed to Cr(VI) are at an increased 
risk of developing lung cancer. The record also indicates that 
occupational exposure to Cr(VI) may result in asthma, and damage to the 
nasal epithelia and skin.
    The final rule establishes an 8-hour time-weighted average (TWA) 
exposure limit of 5 micrograms of Cr(VI) per cubic meter of air (5 
[mu]g/m\3\). This is a considerable reduction from the previous PEL of 
1 milligram per 10 cubic meters of air (1 mg/10 m\3\, or 100 [mu]g/
m\3\) reported as CrO3, which is equivalent to a limit of 52 
[mu]g/m\3\ as Cr(VI). The final rule also contains ancillary provisions 
for worker protection such as requirements for exposure determination, 
preferred exposure control methods, including a compliance alternative 
for a small sector for which the new PEL is infeasible, respiratory 
protection, protective clothing and equipment, hygiene areas and 
practices, medical surveillance, recordkeeping, and start-up dates that 
include four years for the implementation of engineering controls to 
meet the PEL.
    The final standard separately regulates general industry, 
construction, and shipyards in order to tailor requirements to the 
unique circumstances found in each of these sectors.
    The PEL established by this rule reduces the significant risk posed 
to workers by occupational exposure to Cr(VI) to the maximum extent 
that is technologically and economically feasible.

DATES: This final rule becomes effective on May 30, 2006. Start-up 
dates for specific provisions are set in Sec.  1910.1026(n) for general 
industry; Sec.  1915.1026(l) for shipyards; and Sec.  1926.1126(l) for 
construction. However, affected parties do not have to comply with the 
information collection requirements in the final rule until the 
Department of Labor publishes in the Federal Register the control 
numbers assigned by the Office of Management and Budget (OMB). 
Publication of the control numbers notifies the public that OMB has 
approved these information collection requirements under the Paperwork 
Reduction Act of 1995.

ADDRESSES: In compliance with 28 U.S.C. 2112(a), the Agency designates 
the Associate Solicitor for Occupational Safety and Health, Office of 
the Solicitor, Room S-4004, U.S. Department of Labor, 200 Constitution 
Avenue, NW., Washington, DC 20210, as the recipient of petitions for 
review of these standards.

FOR FURTHER INFORMATION CONTACT: Mr. Kevin Ropp, Director, OSHA Office 
of Communications, Room N-3647, U.S. Department of Labor, 200 
Constitution Avenue, NW., Washington, DC 20210; telephone (202) 693-
1999.

SUPPLEMENTARY INFORMATION: The following table of contents lays out the 
structure of the preamble to the final standards. This preamble 
contains a detailed description of OSHA's legal obligations, the 
analyses and rationale supporting the Agency's determination, including 
a summary of and response to comments and data submitted during the 
rulemaking.

I. General
II. Pertinent Legal Authority
III. Events Leading to the Final Standard
IV. Chemical Properties and Industrial Uses
V. Health Effects
    A. Absorption, Distribution, Metabolic Reduction and Elimination
    1. Deposition and Clearance of Inhaled Cr(VI) From the 
Respiratory Tract
    2. Absorption of Inhaled Cr(VI) Into the Bloodstream
    3. Dermal Absorption of Cr(VI)
    4. Absorption of Cr(VI) by the Oral Route
    5. Distribution of Cr(VI) in the Body
    6. Metabolic Reduction of Cr(VI)
    7. Elimination of Cr(VI) From the Body
    8. Physiologically-Based Pharmacokinetic Modeling
    9. Summary
    B. Carcinogenic Effects
    1. Evidence From Chromate Production Workers
    2. Evidence From Chromate Pigment Production Workers
    3. Evidence From Workers in Chromium Plating
    4. Evidence From Stainless Steel Welders
    5. Evidence From Ferrochromium Workers
    6. Evidence From Workers in Other Industry Sectors
    7. Evidence From Experimental Animal Studies
    8. Mechanistic Considerations
    C. Non-Cancer Respiratory Effects
    1. Nasal Irritation, Nasal Tissue Ulcerations and Nasal Septum 
Perforations
    2. Occupational Asthma
    3. Bronchitis
    4. Summary
    D. Dermal Effects
    E. Other Health Effects
VI. Quantitative Risk Assessment
    A. Introduction
    B. Study Selection
    1. Gibb Cohort
    2. Luippold Cohort
    3. Mancuso Cohort
    4. Hayes Cohort
    5. Gerin Cohort
    6. Alexander Cohort
    7. Studies Selected for the Quantitative Risk Assessment
    C. Quantitative Risk Assessments Based on the Gibb Cohort
    1. Environ Risk Assessments
    2. National Institute for Occupational Safety and Health (NIOSH) 
Risk Assessment
    3. Exponent Risk Assessment
    4. Summary of Risk Assessments Based on the Gibb Cohort
    D. Quantitative Risk Assessments Based on the Luippold Cohort
    E. Quantitative Risk Assessments Based on the Mancuso, Hayes, 
Gerin, and Alexander Cohorts
    1. Mancuso Cohort
    2. Hayes Cohort
    3. Gerin Cohort
    4. Alexander Cohort
    F. Summary of Risk Estimates Based on Gibb, Luippold, and 
Additional Cohorts
    G. Issues and Uncertainties
    1. Uncertainty With Regard to Worker Exposure to Cr(VI)
    2. Model Uncertainty, Exposure Threshold, and Dose Rate Effects
    3. Influence of Smoking, Race, and the Healthy Worker Survivor 
Effect
    4. Suitability of Risk Estimates for Cr(VI) Exposures in Other 
Industries
    H. Conclusions
VII. Significance of Risk
    A. Material Impairment of Health
    1. Lung Cancer
    2. Non-Cancer Impairments
    B. Risk Assessment
    1. Lung Cancer Risk Based on the Gibb Cohort
    2. Lung Cancer Risk Based on the Luippold Cohort
    3. Risk of Non-Cancer Impairments
    C. Significance of Risk and Risk Reduction
VIII. Summary of the Final Economic Analysis and Regulatory 
Flexibility Analysis
IX. OMB Review Under the Paperwork Reduction Act of 1995
X. Federalism
XI. State Plans
XII. Unfunded Mandates
XIII. Protecting Children from Environmental Health and Safety Risks
XIV. Environmental Impacts
XV. Summary and Explanation of the Standards
    (a) Scope
    (b) Definitions
    (c) Permissible Exposure Limit (PEL)
    (d) Exposure Determination
    (e) Regulated Areas
    (f) Methods of Compliance
    (g) Respiratory Protection
    (h) Protective Work Clothing and Equipment
    (i) Hygiene Areas and Practices
    (j) Housekeeping
    (k) Medical Surveillance
    (l) Communication of Chromium (VI) Hazards to Employees
    (m) Recordkeeping
    (n) Dates
XVI. Authority and Signature
XVII. Final Standards

I. General

    This final rule establishes a permissible exposure limit (PEL) of 5 
micrograms of Cr(VI) per cubic meter of air (5 [mu]g/m\3\) as an 8-hour 
time-weighted average for all Cr(VI) compounds. After consideration of 
all comments and evidence submitted during this rulemaking, OSHA has 
made a final determination that a PEL of 5 [mu]g/m\3\ is necessary to 
reduce the significant health risks posed by occupational exposures to 
Cr(VI); it is the lowest level that is technologically and economically 
feasible for industries impacted by this rule. A full explanation of 
OSHA's rationale for establishing this PEL is presented in the 
following preamble sections: V (Health Effects), VI (Quantitative Risk 
Assessment), VII (Significance of Risk), VIII (Summary of the Final 
Economic Analysis and Regulatory Flexibility Analysis), and XV (Summary 
and Explanation of the Standard, paragraph (c), Permissible Exposure 
Limit).
    OSHA is establishing three separate standards covering occupational 
exposures to Cr(VI) for: general industry (29 CFR 1910.1026); shipyards 
(29 CFR 1915.1026), and construction (29 CFR 1926.1126). In addition to 
the PEL, these three standards include ancillary provisions for 
exposure determination, methods of compliance, respiratory protection, 
protective work clothing and equipment, hygiene areas and practices, 
medical surveillance, communication of Cr(VI) hazards to employees, 
recordkeeping, and compliance dates. The general industry standard has 
additional provisions for regulated areas and housekeeping. The Summary 
and Explanation section of this preamble (Section XV, paragraphs (d) 
through (n)) includes a full discussion of the basis for including 
these provisions in the final standards.
    Several major changes were made to the October 4, 2004 proposed 
rule as a result of OSHA's analysis of comments and data received 
during the comment periods and public hearings. The major changes are 
summarized below and are fully discussed in the Summary and Explanation 
section of this preamble (Section XV)
    Scope. As proposed, the standards apply to occupational exposures 
to Cr(VI) in all forms and compounds with limited exceptions. OSHA has 
made a final determination to exclude from coverage of these final 
standards exposures that occur in the application of pesticides 
containing Cr(VI) (e.g., the treatment of wood with preservatives). 
These exposures are already covered by the Environmental Protection 
Agency. OSHA is also excluding exposures to portland cement and 
exposures in work settings where the employer has objective data 
demonstrating that a material containing chromium or a specific 
process, operation, or activity involving chromium cannot release 
dusts, fumes, or mists of Cr(VI) in concentrations at or above 0.5 
[mu]g/m\3\ under any expected conditions of use. OSHA believes that the 
weight of evidence in this rulemaking demonstrates that the primary 
risk in these two exposure scenarios can be effectively addressed 
through existing OSHA standards for personal protective equipment, 
hygiene, hazard communication and the PELs for portland cement or 
particulates not otherwise regulated (PNOR).
    Permissible Exposure Limit. OSHA proposed a PEL of 1 [mu]g/m\3\ but 
has now determined that a PEL 5 [mu]g/m\3\ is the lowest level that is 
technologically and economically feasible.
    Exposure Determination. OSHA did not include a provision for 
exposure determination in the proposed shipyard and construction 
standards, reasoning that the obligation to meet the proposed PEL would 
implicitly necessitate performance-based monitoring by the employer to 
ensure compliance with the PEL. However, OSHA was convinced by 
arguments presented during the rulemaking that an explicit requirement 
for exposure determination is necessary to ensure that employee 
exposures are adequately characterized. Therefore OSHA has included a 
provision for exposure determination for general industry, shipyards 
and construction in the final rule. In order to provide additional 
flexibility in characterizing employee exposures, OSHA is allowing 
employers to choose between a scheduled monitoring option and a 
performance-based option for making exposure determinations.
    Methods of Compliance. Under the proposed rule employers were to 
use engineering and work practice controls to achieve the proposed PEL 
unless the employer could demonstrate such controls are not feasible. 
In the final rule, OSHA has retained this exception but has added a 
provision that only requires employers to use engineering and work 
practice controls to reduce or maintain employee exposures to 25 [mu]g/
m\3\ when painting aircraft or large aircraft parts in the aerospace 
industry to the extent such controls are feasible. The employer must 
then supplement those engineering controls with respiratory protection 
to achieve the PEL. As discussed more fully in the Summary of the Final 
Economic Analysis and Regulatory Flexibility Analysis (Section VIII) 
and the Summary and Explanation (Section XV) OSHA has determined that 
this is the lowest level achievable through the use of engineering and 
work practice controls alone for these limited operations.
    Housekeeping. In the proposed rule, cleaning methods such as 
shoveling, sweeping, and brushing were prohibited unless they were the 
only effective means available to clean surfaces contaminated with 
Cr(VI). The final standard has modified this prohibition to make clear 
only dry shoveling, sweeping and brushing are prohibited so that 
effective wet shoveling, sweeping, and brushing would be allowed. OSHA 
is also adding a provision that allows the use of compressed air to 
remove Cr(VI) when no alternative method is feasible.
    Medical Surveillance. As proposed and continued in these final 
standards, medical surveillance is required to be provided to employees 
experiencing signs or symptoms of the adverse health effects associated 
with Cr(VI) exposure or exposed in an emergency. In addition, for 
general industry, employees exposed above the PEL for 30 or more days a 
year were to be provided medical surveillance. In the final standard, 
OSHA has changed the trigger for medical surveillance to exposure above 
the action level (instead of the PEL) for 30 days a year to take into 
account the existing risks at the new PEL. This provision has also been 
extended to the standards for shipyards and construction since those 
employers now will be required to perform an exposure determination and 
thus will be able to determine which employees are exposed above the 
action level 30 or more days a year.
    Communication of Hazards. In the proposed standard, OSHA specified 
the sign for the demarcation of regulated areas in general industry and 
the label for contaminated work clothing or equipment and Cr(VI) 
contaminated waste and debris. The proposed standard also listed the 
various elements to be covered for employee training. In order to 
simplify requirements under this section of the final standard and 
reduce confusion between this standard and the Hazard Communication 
Standard, OSHA has removed the requirement for special signs and labels 
and the specification of employee training elements. Instead, the final 
standard requires that signs, labels and training be in accordance with 
the Hazard Communication Standard (29 CFR 1910.1200). The only 
additional training elements required in the final rule are those 
related specifically to the contents of the final Cr(VI) standards. 
While the final standards have removed language in the communication of 
hazards provisions to make them more consistent with OSHA's existing 
Hazard Communication Standard, the employers obligation to mark 
regulated areas (where regulated areas are required), to label Cr(VI) 
contaminated clothing and wastes, and to train on the hazards of Cr(VI) 
have not changed.
    Recordkeeping. In the proposed standards for shipyards and 
construction there were no recordkeeping requirements for exposure 
records since there was not a requirement for exposure determination. 
The final standard now requires exposure determination for shipyards 
and construction and therefore, OSHA has also added provisions for 
exposure records to be maintained in these final standards. In keeping 
with its intent to be consistent with the Hazard Communication 
Standard, OSHA has removed the requirement for training records in the 
final standards.
    Dates. In the proposed standard, the effective date of the standard 
was 60 days after the publication date; the start-up date for all 
provisions except engineering controls was 90 days after the effective 
date; and the start-up date for engineering controls was two years 
after the effective date. OSHA believes that it is appropriate to allow 
additional time for employers, particularly small employers, to meet 
the requirements of the final rule. The effective and start-up dates 
have been extended as follows: the effective date for the final rule is 
changed to 90 days after the publication date; the start-up date for 
all provisions except engineering controls is changed to 180 days after 
the effective date for employers with 20 or more employees; the start-
up date for all provisions except engineering controls is changed to 
one year after the effective date for employers with 19 or fewer 
employees; and the start-up date for engineering controls is changed to 
four years after the effective date for all employers.

II. Pertinent Legal Authority

    The purpose of the Occupational Safety and Health Act, 29 U.S.C. 
651 et seq. ("the Act") is to,

* * * assure so far as possible every working man and woman in the 
nation safe and healthful working conditions and to preserve our 
human resources. 29 U.S.C. 651(b).

    To achieve this goal Congress authorized the Secretary of Labor 
(the Secretary) to promulgate and enforce occupational safety and 
health standards. 29 U.S.C. 654(b) (requiring employers to comply with 
OSHA standards), 655(a) (authorizing summary adoption of existing 
consensus and federal standards within two years of the Act's 
enactment), and 655(b) (authorizing promulgation, modification or 
revocation of standards pursuant to notice and comment).
    The Act provides that in promulgating health standards dealing with 
toxic materials or harmful physical agents, such as this standard 
regulating occupational exposure to Cr(VI), the Secretary,

* * * shall set the standard which most adequately assures, to the 
extent feasible, on the basis of the best available evidence that no 
employee will suffer material impairment of health or functional 
capacity even if such employee has regular exposure to the hazard 
dealt with by such standard for the period of his working life. 29 
U.S.C. Sec.  655(b)(5).

    The Supreme Court has held that before the Secretary can promulgate 
any permanent health or safety standard, she must make a threshold 
finding that significant risk is present and that such risk can be 
eliminated or lessened by a change in practices. Industrial Union 
Dept., AFL-CIO v. American Petroleum Institute, 448 U.S. 607, 641-42 
(1980) (plurality opinion) ("The Benzene case"). The Court further 
observed that what constitutes "significant risk" is "not a 
mathematical straitjacket" and must be "based largely on policy 
considerations." The Benzene case, 448 U.S. at 655. The Court gave the 
example that if,

* * * the odds are one in a billion that a person will die from 
cancer * * * the risk clearly could not be considered significant. 
On the other hand, if the odds are one in one thousand that regular 
inhalation of gasoline vapors that are 2% benzene will be fatal, a 
reasonable person might well consider the risk significant. * * * 
Id.

    OSHA standards must be both technologically and economically 
feasible. United Steelworkers v. Marshall, 647 F.2d 1189, 1264 (D.C. 
Cir. 1980) ("The Lead I case"). The Supreme Court has defined 
feasibility as "capable of being done." American Textile Mfrs. Inst. 
v. Donovan, 425 U.S. 490, 509 (1981) ("The Cotton dust case"). The 
courts have further clarified that a standard is technologically 
feasible if OSHA proves a reasonable possibility,

* * * within the limits of the best available evidence * * * that 
the typical firm will be able to develop and install engineering and 
work practice controls that can meet the PEL in most of its 
operations. See The Lead I case, 647 F.2d at 1272.

    With respect to economic feasibility, the courts have held that a 
standard is feasible if it does not threaten massive dislocation to or 
imperil the existence of the industry. See The Lead case, 647 F.2d at 
1265. A court must examine the cost of compliance with an OSHA standard 
"in relation to the financial health and profitability of the industry 
and the likely effect of such costs on unit consumer prices." Id.

    [The] practical question is whether the standard threatens the 
competitive stability of an industry, * * * or whether any intra-
industry or inter-industry discrimination in the standard might 
wreck such stability or lead to undue concentration. Id. (citing 
Industrial Union Dept., AFL-CIO v. Hodgson, 499 F.2d 467 (D.C. Cir. 
1974)).

    The courts have further observed that granting companies reasonable 
time to comply with new PEL's may enhance economic feasibility. Id. 
While a standard must be economically feasible, the Supreme Court has 
held that a cost-benefit analysis of health standards is not required 
by the Act because a feasibility analysis is. The Cotton dust case, 453 
U.S. at 509. Finally, unlike safety standards, health standards must 
eliminate risk or reduce it to the maximum extent that is 
technologically and economically feasible. See International Union, 
United Automobile, Aerospace & Agricultural Implement Workers of 
America, UAW v. OSHA, 938 F.2d 1310, 1313 (D.C. Cir. 1991); Control of 
Hazardous Energy Sources (Lockout/Tagout), Final rule; supplemental 
statement of reasons, (58 FR 16612, March 30, 1993).

III. Events Leading to the Final Standard

    OSHA's previous standards for workplace exposure to Cr(VI) were 
adopted in 1971, pursuant to section 6(a) of the Act, from a 1943 
American National Standards Institute (ANSI) recommendation originally 
tissues (36 FR at 10466, 5/29/71; Ex. 20-3). OSHA's general industry 
standard set a permissible exposure limit (PEL) of 1 mg chromium 
trioxide per 10 m\3\ air in the workplace (1 mg/10 m\3\ 
CrO3) as a ceiling concentration, which corresponds to a 
concentration of 52 [mu]g/m\3\ Cr(VI). A separate rule promulgated for 
the construction industry set an eight-hour time-weighted-average PEL 
of 1 mg/10 m3 CrO3, also equivalent to 52 [mu]g/
m\3\ Cr(VI), adopted from the American Conference of Governmental 
Industrial Hygienists (ACGIH) 1970 Threshold Limit Value (TLV) (36 FR 
at 7340, 4/17/71).
    Following the ANSI standard of 1943, other occupational and public 
health organizations evaluated Cr(VI) as a workplace and environmental 
hazard and formulated recommendations to control exposure. The ACGIH 
first recommended control of workplace exposures to chromium in 1946, 
recommending a time-weighted average Maximum Allowable Concentration 
(later called a Threshold Limit Value) of 100 [mu]g/m\3\ for chromic 
acid and chromates as Cr2O3 (Ex. 5-37), and later 
classified certain Cr(VI) compounds as class A1 (confirmed human) 
carcinogens in 1974. In 1975, the NIOSH Criteria for a Recommended 
Standard recommended that occupational exposure to Cr(VI) compounds 
should be limited to a 10-hour TWA of 1 [mu]g/m\3\, except for some 
forms of Cr(VI) then believed to be noncarcinogenic (Ex. 3-92). The 
National Toxicology Program's First Annual Report on Carcinogens 
identified calcium chromate, chromium chromate, strontium chromate, and 
zinc chromate as carcinogens in 1980 (Ex. 35-157).
    During the 1980s, regulatory and standards organizations came to 
recognize Cr(VI) compounds in general as carcinogens. The Environmental 
Protection Agency (EPA) Health Assessment Document of 1984 stated that,

* * * using the IARC [International Agency for Research on Cancer] 
classification scheme, the level of evidence available for the 
combined animal and human data would place hexavalent chromium (Cr 
VI) compounds into Group 1, meaning that there is decisive evidence 
for the carcinogenicity of those compounds in humans (Ex. 19-1, p. 
7-107).

    In 1988 IARC evaluated the available evidence regarding Cr(VI) 
carcinogenicity, concluding in 1990 that

* * * [t]here is sufficient evidence in humans for the 
carcinogenicity of chromium[VI] compounds as encountered in the 
chromate production, chromate pigment production and chromium 
plating industries, [and] sufficient evidence in experimental 
animals for the carcinogenicity of calcium chromate, zinc chromates, 
strontium chromate and lead chromates (Ex. 18-3, p. 213).

    In September 1988, NIOSH advised OSHA to consider all Cr(VI) 
compounds as potential occupational carcinogens (Ex. 31-22-22). ACGIH 
now classifies water-insoluble and water-soluble Cr(IV) compounds as 
class A1 carcinogens (Ex. 35-207). Current ACGIH standards include 
specific 8-hour time-weighted average TLVs for calcium chromate (1 
[mu]g/m3), lead chromate (12 [mu]g/m3), strontium 
chromate (0.5 [mu]g/m3), and zinc chromates (10 [mu]g/
m3), and generic TLVs for water soluble (50 [mu]g/
m3) and insoluble (10 [mu]g/m3) forms of 
hexavalent chromium not otherwise classified, all measured as chromium 
(Ex. 35-207).
    In July 1993, OSHA was petitioned for an emergency temporary 
standard to reduce occupational exposures to Cr(VI) compounds (Ex. 1). 
The Oil, Chemical, and Atomic Workers International Union (OCAW) and 
Public Citizen's Health Research Group (Public Citizen), citing 
evidence that occupational exposure to Cr(VI) increases workers' risk 
of lung cancer, petitioned OSHA to promulgate an emergency temporary 
standard to lower the PEL for Cr(VI) compounds to 0.5 [mu]g/
m3 as an eight-hour time-weighted average (TWA). Upon review 
of the petition, OSHA agreed that there was evidence of increased 
cancer risk from exposure to Cr(VI) at the existing PEL, but found that 
the available data did not show the "grave danger" required to 
support an emergency temporary standard (Ex. 1-C). The Agency therefore 
denied the request for an emergency temporary standard, but initiated 
Section 6(b)(5) rulemaking and began performing preliminary analyses 
relevant to the rule.
    In 1997, Public Citizen petitioned the United States Court of 
Appeals for the Third Circuit to compel OSHA to complete rulemaking 
lowering the standard for occupational exposure to Cr(VI). The Court 
denied Public Citizen's request, concluding that there was no 
unreasonable delay and dismissed the suit. Oil, Chemical and Atomic 
Workers Union and Public Citizen Health Research Group v. OSHA, 145 
F.3d 120 (3rd Cir. 1998). Afterwards, the Agency continued its data 
collection and analytic efforts on Cr(VI) (Ex. 35-208, p. 3). In 2002, 
Public Citizen again petitioned the Court to compel OSHA to commence 
rulemaking to lower the Cr(VI) standard (Ex. 31-24-1). Meanwhile on 
August 22, 2002, OSHA published a Request for Information on Cr(VI) to 
solicit additional information on key issues related to controlling 
exposures to Cr(VI) (FR 67 at 54389), and on December 4, 2002 announced 
its intent to proceed with developing a proposed standard (Ex. 35-306). 
On December 24, 2002, the Court granted Public Citizen's petition, and 
ordered the Agency to proceed expeditiously with a Cr(VI) standard. See 
Public Citizen Health Research Group v. Chao, 314 F.3d 143 (3rd Cir. 
2002)). In a subsequent order, the Court established a compressed 
schedule for completion of the rulemaking, with deadlines of October 4, 
2004 for publication of a proposed standard and January 18, 2006 for 
publication of a final standard (Ex. 35-304).
    In 2003, as required by the Small Business Regulatory Enforcement 
Act (SBREFA), OSHA initiated SBREFA proceedings, seeking the advice of 
small business representatives on the proposed rule. The SBREFA panel, 
including representatives from OSHA, the Small Business Administration 
(SBA), and the Office of Management and Budget (OMB), was convened on 
December 23, 2003. The panel conferred with representatives from small 
entities in chemical, alloy, and pigment manufacturing, electroplating, 
welding, aerospace, concrete, shipbuilding, masonry, and construction 
on March 16-17, 2004, and delivered its final report to OSHA on April 
20, 2004. The Panel's report, including comments from the small entity 
representatives (SERS) and recommendations to OSHA for the proposed 
rule, is available in the Cr(VI) rulemaking docket (Ex. 34). The SBREFA 
Panel made recommendations on a variety of subjects. The most important 
recommendations with respect to alternatives that OSHA should consider 
included: A higher PEL than the PEL of 1; excluding cement from the 
scope of the standard; the use of SECALs for some industries; different 
PELS for different Hexavalent chromium compounds; a multi-year phase-in 
to the standards; and further consideration to approaches suited to the 
special conditions of the maritime and construction industries. OSHA 
has adapted many of these recommendations: The PEL is now 5; cement has 
been excluded from the scope of the standard; a compliance alternative, 
similar to a SECAL, has been used in aerospace industry; the standard 
allows four years to phase in engineering controls; and a new 
performance based monitoring approach for all industries, among other 
changes, all of which should make it easier for all
industries with changing work place conditions to meet the standard in 
a cost effective way. A full discussion of all of the recommendations, 
and OSHA's responses to them, is provided in Section VIII of this 
Preamble.
    In addition to undertaking SBREFA proceedings, in early 2004, OSHA 
provided the Advisory Committee on Construction Safety and Health 
(ACCSH) and the Maritime Advisory Committee on Occupational Safety and 
Health (MACOSH) with copies of the draft proposed rule for review. OSHA 
representatives met with ACCSH in February 2004 and May 2004 to discuss 
the rulemaking and receive their comments and recommendations. On 
February 13, 2004, ACCSH recommended that portland cement should be 
included within the scope of the proposed standard (Ex. 35-307, pp. 
288-293) and that identical PELs should be set for construction, 
maritime, and general industry (Ex. 35-307, pp. 293-297). On May 18, 
2004, ACCSH recommended that the construction industry should be 
included in the current rulemaking, and affirmed its earlier 
recommendation regarding portland cement. OSHA representatives met with 
MACOSH in March 2004. On March 3, 2004, MACOSH collected and forwarded 
additional exposure monitoring data to OSHA to help the Agency better 
evaluate exposures to Cr(VI) in shipyards (Ex. 35-309, p. 208). MACOSH 
also recommended a separate Cr(VI) standard for the maritime industry, 
arguing that maritime involves different exposures and requires 
different means of exposure control than general industry and 
construction (Ex. 35-309, p. 227).
    In accordance with the Court's rulemaking schedule, OSHA published 
the proposed standard for hexavalent chromium on October 4, 2004 (69 FR 
at 59306). The proposal included a notice of public hearing in 
Washington, DC (69 FR at 59306, 59445-59446). The notice also invited 
interested persons to submit comments on the proposal until January 3, 
2005. In the proposal, OSHA solicited public input on 65 issues 
regarding the human health risks of Cr(VI) exposure, the impact of the 
proposed rule on Cr(VI) users, and other issues of particular interest 
to the Agency (69 FR at 59306-59312).
    OSHA convened the public hearing on February 1, 2005, with 
Administrative Law Judges John M. Vittone and Thomas M. Burke 
presiding. At the conclusion of the hearing on February 15, 2005, Judge 
Burke set a deadline of March 21, 2005, for the submission of post 
hearing comments, additional information and data relevant to the 
rulemaking, and a deadline of April 20, 2005, for the submission of 
additional written comments, arguments, summations, and briefs. A wide 
range of employees, employers, union representatives, trade 
associations, government agencies and other interested parties 
participated in the public hearing or contributed written comments. 
Issues raised in their comments and testimony are addressed in the 
relevant sections of this preamble (e.g., comments on the risk 
assessment are discussed in section VI; comments on the benefits 
analysis in section VIII). On December 22, 2005, OSHA filed a motion 
with the U.S. Court of Appeals for the Third Circuit requesting an 
extension of the court-mandated deadline for the publication of the 
final rule by six weeks, to February 28, 2006 (Ex. 48-13). The Court 
granted the request on January 17, 2006 (Ex. 48-15).
    As mandated by the Act, the final standard on occupational exposure 
to hexavalent chromium is based on careful consideration of the entire 
record of this proceeding, including materials discussed or relied upon 
in the proposal, the record of the hearing, and all written comments 
and exhibits received.
    OSHA has developed separate final standards for general industry, 
shipyards, and the construction industry. The Agency has concluded that 
excess exposure to Cr(VI) in any form poses a significant risk of 
material impairment to the health of workers, by causing or 
contributing to adverse health effects including lung cancer, non-
cancer respiratory effects, and dermal effects. OSHA determined that 
the TWA PEL should not be set above 5 [mu]g/m3 based on the 
evidence in the record and its own quantitative risk assessment. The 
TWA PEL of 5 [mu]g/m3 reduces the significant risk posed to 
workers by occupational exposure to Cr(VI) to the maximum extent that 
is technologically and economically feasible. (See discussion of the 
PEL in Section XV below.)

IV. Chemical Properties and Industrial Uses

    Chromium is a metal that exists in several oxidation or valence 
states, ranging from chromium (-II) to chromium (+VI). The elemental 
valence state, chromium (0), does not occur in nature. Chromium 
compounds are very stable in the trivalent state and occur naturally in 
this state in ores such as ferrochromite, or chromite ore 
(FeCr2O4). The hexavalent, Cr(VI) or chromate, is 
the second most stable state. It rarely occurs naturally; most Cr(VI) 
compounds are man made.
    Chromium compounds in higher valence states are able to undergo 
"reduction" to lower valence states; chromium compounds in lower 
valence states are able to undergo "oxidation" to higher valence 
states. Thus, Cr(VI) compounds can be reduced to Cr(III) in the 
presence of oxidizable organic matter. Chromium can also be reduced in 
the presence of inorganic chemicals such as iron.
    Chromium does exist in less stable oxidation (valence) states such 
as Cr(II), Cr(IV), and Cr(V). Anhydrous Cr(II) salts are relatively 
stable, but the divalent state (II, or chromous) is generally 
relatively unstable and is readily oxidized to the trivalent (III or 
chromic) state. Compounds in valence states such as (IV) and (V) 
usually require special handling procedures as a result of their 
instability. Cr(IV) oxide (CrO2) is used in magnetic 
recording and storage devices, but very few other Cr(IV) compounds have 
industrial use. Evidence exists that both Cr(IV) and Cr(V) are formed 
as transient intermediates in the reduction of Cr(VI) to Cr(III) in the 
body.
    Chromium (III) is also an essential nutrient that plays a role in 
glucose, fat, and protein metabolism by causing the action of insulin 
to be more effective. Chromium picolinate, a trivalent form of chromium 
combined with picolinic acid, is used as a dietary supplement, because 
it is claimed to speed metabolism.
    Elemental chromium and the chromium compounds in their different 
valence states have various physical and chemical properties, including 
differing solubilities. Most chromium species are solid. Elemental 
chromium is a steel gray solid, with high melting and boiling points 
(1857 [deg]C and 2672 [deg]C, respectively), and is insoluble in water 
and common organic solvents. Chromium (III) chloride is a violet or 
purple solid, with high melting and sublimation points (1150 [deg]C and 
1300 [deg]C, respectively), and is slightly soluble in hot water and 
insoluble in common organic solvents. Ferrochromite is a brown-black 
solid; chromium (III) oxide is a green solid; and chromium (III) 
sulfate is a violet or red solid, insoluble in water and slightly 
soluble in ethanol. Chromium (III) picolinate is a ruby red crystal 
soluble in water (1 part per million at 25 [deg]C). Chromium (IV) oxide 
is a brown-black solid that decomposes at 300 [deg]C and is insoluble 
in water.
    Cr(VI) compounds have mostly lemon yellow to orange to dark red 
hues. They are typically crystalline, granular, or powdery although one 
compound (chromyl chloride) exists in liquid form. For example, chromyl 
chloride is a dark red liquid that decomposes into chromate ion and 
hydrochloric acid in water. Chromic acids are dark red crystals that are 
very soluble in water. Other examples of soluble chromates are sodium 
chromate (yellow crystals) and sodium dichromate (reddish to bright orange 
crystals). Lead chromate oxide is typically a red crystalline powder. Zinc 
chromate is typically seen as lemon yellow crystals which decompose in 
hot water and are soluble in acids and liquid ammonia. Other chromates 
such as barium, calcium, lead, strontium, and zinc chromates vary in 
color from light yellow to greenish yellow to orange-yellow and exist 
in solid form as crystals or powder.
    The Color Pigments Manufacturers Association (CPMA) provided 
additional information on lead chromate and some other chromates used 
in their pigments (Ex. 38-205, pp. 12-13). CPMA describes two main lead 
chromate color groups: the chrome yellow pigments and the orange to red 
varieties known as molybdate orange pigments. The chrome yellow 
pigments are solid solution crystal compositions of lead chromate and 
lead sulfate. Molybdate orange pigments are solid solution crystal 
compositions of lead chromate, lead sulfate, and lead molybdate (Ex. 
38-205, p. 12). CPMA also describes a basic lead chromate called 
"chrome orange," and a lead chromate precipitated "onto a core" of 
silica (Ex. 38-205, p. 13).
    OSHA re-examined available information on solubility values in 
light of comments from the CPMA and Dominion Color Corporation (DCC) on 
qualitative solubility designations and CPMA's claim of low 
bioavailability of lead chromate due to its extremely low solubility 
(Exs. 38-201-1, p. 4; 38-205, p. 95). There was not always agreement or 
consistency with the qualitative assignments of solubilities. 
Quantitative values for the same compound also differ depending on the 
source of information.
    The Table IV-1 is the result of OSHA's re-examination of 
quantitative water solubility values and qualitative designations. 
Qualitative designations as well as quantitative values are listed as 
they were provided by the source. As can be seen by the Table IV-1, 
qualitative descriptions vary by the descriptive terminology chosen by 
the source.
BILLING CODE 4510-26-P

Click here to view table IV-1

BILLING CODE 4510-26-C
    OSHA has made some generalizations to describe the water 
solubilities of chromates in subsequent sections of this Federal 
Register notice. OSHA has divided Cr(VI) compounds and mixtures into 
three categories based on solubility values. Compounds and mixtures 
with water solubilities less than 0.01 g/l are referred to as water 
insoluble. Compounds and mixtures between 0.01 g/l and 500 g/l are 
referred to as slightly soluble. Compounds and mixtures with water 
solubility values of 500 g/l or greater are referred to as highly 
water soluble. It should be noted that these boundaries for insoluble, 
slightly soluble, and highly soluble are arbitrary designations for the 
sake of further description elsewhere in this document. Quantitative 
values take precedence over qualitative designations. For example, zinc 
chromates would be slightly soluble where their solubility values exceed 0.01 g/l.
    Some major users of chromium are the metallurgical, refractory, and 
chemical industries. Chromium is used by the metallurgical industry to 
produce stainless steel, alloy steel, and nonferrous alloys. Chromium 
is alloyed with other metals and plated on metal and plastic substrates 
to improve corrosion resistance and provide protective coatings for 
automotive and equipment accessories. Welders use stainless steel 
welding rods when joining metal parts.
    Cr(VI) compounds are widely used in the chemical industry in 
pigments, metal plating, and chemical synthesis as ingredients and 
catalysts. Chromates are used as high quality pigments for textile 
dyes, paints, inks, glass, and plastics. Cr(VI) can be produced during 
welding operations even if the chromium was originally present in 
another valence state. While Cr(VI) is not intentionally added to 
portland cement, it is often present as an impurity.
    Occupational exposures to Cr(VI) can occur from inhalation of mists 
(e.g., chrome plating, painting), dusts (e.g., inorganic pigments), or 
fumes (e.g., stainless steel welding), and from dermal contact (e.g., 
cement workers).
    There are about thirty major industries and processes where Cr(VI) 
is used. These include producers of chromates and related chemicals 
from chromite ore, electroplating, welding, painting, chromate pigment 
production and use, steel mills, and iron and steel foundries. A 
detailed discussion of the uses of Cr(VI) in industry is found in 
Section VIII of this preamble.

V. Health Effects

    This section summarizes key studies of adverse health effects 
resulting from exposure to hexavalent chromium (Cr(VI)) in humans and 
experimental animals, as well as information on the fate of Cr(VI) in 
the body and laboratory research that relates to its toxic mode of 
action. The primary health impairments from workplace exposure to 
Cr(VI) are lung cancer, asthma, and damage to the nasal epithelia and 
skin. While this chapter on health effects does not describe all of the 
many studies that have been conducted on Cr(VI) toxicity, it includes a 
selection of those that are relevant to the rulemaking and 
representative of the scientific literature on Cr(VI) health effects.

A. Absorption, Distribution, Metabolic Reduction and Elimination

    Although chromium can exist in a number of different valence 
states, Cr(VI) is the form considered to be the greatest health risk. 
Cr(VI) enters the body by inhalation, ingestion, or absorption through 
the skin. For occupational exposure, the airways and skin are the 
primary routes of uptake. The following discussion summarizes key 
aspects of Cr(VI) uptake, distribution, metabolism, and elimination.

1. Deposition and Clearance of Inhaled Cr(VI) From the Respiratory 
Tract

    Various anatomical, physical and physiological factors determine 
both the fractional and regional deposition of inhaled particulate 
matter. Due to the airflow patterns in the lung, more particles tend to 
deposit at certain preferred regions in the lung. It is therefore 
possible to have a buildup of chromium at certain sites in the 
bronchial tree that could create areas of very high chromium 
concentration. A high degree of correspondence between the efficiency 
of particle deposition and the frequency of bronchial tumors at sites 
in the upper bronchial tree was reported in research by Schlesinger and 
Lippman that compared the distribution of cancer sites in published 
reports of primary bronchogenic tumors with experimentally determined 
particle deposition patterns (Ex. 35-102).
    Large inhaled particles (>5 [mu]m) are efficiently removed from the 
air-stream in the extrathoracic region (Ex. 35-175). Particles greater 
than 2.5 [mu]m are generally deposited in the tracheobronchial regions, 
whereas particles less than 2.5 [mu]m are generally deposited in the 
pulmonary region. Some larger particles (>2.5 [mu]m) can reach the 
pulmonary region. The mucociliary escalator predominantly clears 
particles that deposit in the extrathoracic and the tracheobronchial 
region of the lung. Individuals exposed to high particulate levels of 
Cr(VI) may also have altered respiratory mucociliary clearance. 
Particulates that reach the alveoli can be absorbed into the 
bloodstream or cleared by phagocytosis.
2. Absorption of Inhaled Cr(VI) Into the Bloodstream
    The absorption of inhaled chromium compounds depends on a number of 
factors, including physical and chemical properties of the particles 
(oxidation state, size, solubility) and the activity of alveolar 
macrophages (Ex. 35-41). The hexavalent chromate anions 
(CrO4)2- enter cells via facilitated diffusion 
through non-specific anion channels (similar to phosphate and sulfate 
anions). As demonstrated in research by Suzuki et al., a portion of 
water soluble Cr(VI) is rapidly transported to the bloodstream in rats 
(Ex. 35-97). Rats were exposed to 7.3-15.9 mg Cr(VI)/m\3\ as potassium 
dichromate for 2-6 hours. Following exposure to Cr(VI), the ratio of 
blood chromium/lung chromium was 1.440.30 at 0.5 hours, 
0.810.10 at 18 hours, 0.850.20 at 48 hours, and 
0.960.22 at 168 hours after exposure.
    Once the Cr(VI) particles reach the alveoli, absorption into the 
bloodstream is greatly dependent on solubility. More soluble chromates 
are absorbed faster than water insoluble chromates, while insoluble 
chromates are poorly absorbed and therefore have longer resident time 
in the lungs. This effect has been demonstrated in research by Bragt 
and van Dura on the kinetics of three Cr(VI) compounds: highly soluble 
sodium chromate, slightly soluble zinc chromate and water insoluble 
lead chromate (Ex. 35-56). They instilled \51\chromium-labeled 
compounds (0.38 mg Cr(VI)/kg as sodium chromate, 0.36 mg Cr(VI)/kg as 
zinc chromate, or 0.21 mg Cr(VI)/kg as lead chromate) intratracheally 
in rats. Peak blood levels of \51\chromium were reached after 30 
minutes for sodium chromate (0.35 [mu]g chromium/ml), and after 24 
hours for zinc chromate (0.60 [mu]g chromium/ml) and lead chromate 
(0.007 [mu]g chromium/ml). At 30 minutes after administration, the 
lungs contained 36, 25, and 81% of the respective dose of the sodium, 
zinc, and lead chromate. On day six, >80% of the dose of all three 
compounds had been cleared from the lungs, during which time the 
disappearance from lungs followed linear first-order kinetics. The 
residual amount left in the lungs on day 50 or 51 was 3.0, 3.9, and 
13.9%, respectively. From these results authors concluded that zinc 
chromate, which is less soluble than sodium chromate, is more slowly 
absorbed from the lungs. Lead chromate was more poorly and slowly 
absorbed, as indicated by very low levels in blood and greater 
retention in the lungs. The authors also noted that the kinetics of 
sodium and zinc chromates were very similar. Zinc chromate, which is 
less soluble than sodium chromate, was slowly absorbed from the lung, 
but the maximal blood levels were higher than those resulting from an 
equivalent dose of sodium chromate. The authors believe that this was 
probably the result of hemorrhages macroscopically visible in the lungs 
of zinc chromate-treated rats 24 hours following intratracheal administration. 
Boeing Corporation commented that this study does not show that the highly water 
soluble sodium chromate is cleared more rapidly or retained in the lung for 
shorter periods than the less soluble zinc chromate (Ex. 38-106-2, p. 
18-19). This comment is addressed in the Carcinogenic Effects 
Conclusion Section V.B.9 dealing with the carcinogenicity of slightly 
soluble Cr(VI) compounds.
    Studies by Langard et al. and Adachi et al. provide further 
evidence of absorption of chromates from the lungs (Exs. 35-93; 189). 
In Langard et al., rats exposed to 2.1 mg Cr(VI)/m\3\ as zinc chromate 
for 6 hours/day achieved steady state concentrations in the blood after 
4 days of exposure (Ex. 35-93). Adachi et al. studied rats that were 
subject to a single inhalation exposure to chromic acid mist generated 
from electroplating at a concentration of 3.18 mg Cr(VI)/m\3\ for 30 
minutes which was then rapidly absorbed from the lungs (Ex. 189). The 
amount of chromium in the lungs of these rats declined from 13.0 mg 
immediately after exposure to 1.1 mg after 4 weeks, with an overall 
half-life of five days.
    Several other studies have reported absorption of chromium from the 
lungs after intratracheal instillation (Exs. 7-9; 9-81; Visek et al. 
1953 as cited in Ex. 35-41). These studies indicated that 53-85% of 
Cr(VI) compounds (particle size < 5 [mu]m) were cleared from the lungs 
by absorption into the bloodstream or by mucociliary clearance in the 
pharynx; the rest remained in the lungs. Absorption of Cr(VI) from the 
respiratory tract of workers has been shown in several studies that 
identified chromium in the urine, serum and red blood cells following 
occupational exposure (Exs. 5-12; 35-294; 35-84).
    Evidence indicates that even chromates encapsulated in a paint 
matrix may be released in the lungs (Ex. 31-15, p. 2). In a study of 
chromates in aircraft spray paint, LaPuma et al. measured the mass of 
Cr(VI) released from particles into water originating from three types 
of paint particles: solvent-borne epoxy (25% strontium chromate 
(SrCrO4)), water-borne epoxy (30% SrCrO4) and 
polyurethane (20% SrCrO4) (Ex. 31-2-1). The mean fraction of 
Cr(VI) released into the water after one and 24 hours for each primer 
averaged: 70% and 85% (solvent epoxy), 74% and 84% (water epoxy), and 
94% and 95% (polyurethane). Correlations between particle size and the 
fraction of Cr(VI) released indicated that smaller particles (< 5 [mu]m) 
release a larger fraction of Cr(VI) versus larger particles (>5 [mu]m). 
This study demonstrates that the paint matrix only modestly hinders 
Cr(VI) release into a fluid, especially with smaller particles. Larger 
particles, which contain the majority of Cr(VI) due to their size, 
appear to release proportionally less Cr(VI) (as a percent of total 
Cr(VI)) than smaller particles. Some commenters suggested that the 
above research shows that the slightly soluble Cr(VI) from aircraft 
spray paint is less likely to reach and be absorbed in the 
bronchoalveolar region of the lung than a highly soluble Cr(VI) form, 
such as chromic acid aerosol (Exs. 38-106-2; 39-43, 44-33). This issue 
is further discussed in the Carcinogenic Effects Conclusion Section 
V.B.9.a and in the Quantitative Risk Assessment Section VI.G.4.a.
    A number of questions remain unanswered regarding encapsulated 
Cr(VI) and bioavailability from the lung. There is a lack of detailed 
information on the efficiency of encapsulation and whether all of the 
chromate molecules are encapsulated. The stability of the encapsulated 
product in physiological and environmental conditions over time has not 
been demonstrated. Finally, the fate of inhaled encapsulated Cr(VI) in 
the respiratory tract and the extent of distribution in systemic 
tissues has not been thoroughly studied.
3. Dermal Absorption of Cr(VI)
    Both human and animal studies demonstrate that Cr(VI) compounds are 
absorbed after dermal exposure. Dermal absorption depends on the 
oxidation state of chromium, the vehicle and the integrity of the skin. 
Cr(VI) readily traverses the epidermis to the dermis (Exs. 9-49; 309). 
The histological distribution of Cr(VI) within intact human skin was 
studied by Liden and Lundberg (Ex. 35-80). They applied test solutions 
of potassium dichromate in petrolatum or in water as occluded circular 
patches of filter paper to the skin. Results with potassium dichromate 
in water revealed that Cr(VI) penetrated beyond the dermis and 
penetration reached steady state with resorption by the lymph and blood 
vessels by 5 hours. About 10 times more chromium penetrated when 
potassium dichromate was applied in petrolatum than when applied in 
water, indicating that organic solvents facilitate the absorption of 
Cr(VI) from the skin. Research by Baranowska-Dutkiewicz also 
demonstrated that the absorption rates of sodium chromate solutions 
from the occluded forearm skin of volunteers increase with increasing 
concentration (Ex. 35-75). The rates were 1.1 [mu]g Cr(VI)/cm\2\/hour 
for a 0.01 molar solution, 6.4 [mu]g Cr(VI)/cm\2\/hour for a 0.1 molar 
solution, and 10 [mu]g Cr(VI)/cm\2\/hour for a 0.2 molar solution.
    Additional studies have demonstrated that the absorption of Cr(VI) 
compounds can take place through the dermal route. Using volunteers, 
Mali found that potassium dichromate penetrates the intact epidermis 
(Exs. 9-49; 35-41). Wahlberg and Skog demonstrated the presence of 
chromium in the blood, spleen, bone marrow, lymph glands, urine and 
kidneys of guinea pigs dermally exposed to \51\chromium labeled Cr(VI) 
compounds (Ex. 35-81).
4. Absorption of Cr(VI) by the Oral Route
    Inhaled Cr(VI) can enter the digestive tract as a result of 
mucocilliary clearance and swallowing. Studies indicate Cr(VI) is 
absorbed from the gastrointestinal tract. For example, in a study by 
Donaldson and Barreras, the six-day fecal and 24-hour urinary excretion 
patterns of radioactivity in groups of six volunteers given Cr(VI) as 
sodium chromate labeled with \51\chromium indicated that at least 2.1% 
of the Cr(VI) was absorbed. After intraduodenal administration at least 
10% of the Cr(VI) compound was absorbed. These studies also 
demonstrated that Cr(VI) compounds are reduced to Cr(III) compounds in 
the stomach, thereby accounting for the relatively poor 
gastrointestinal absorption of orally administered Cr(VI) compounds 
(Exs. 35-96; 35-41). In the gastrointestinal tract, Cr(VI) can be 
reduced to Cr(III) by gastric juices, which is then poorly absorbed 
(Underwood, 1971 as cited in Ex. 19-1; Ex. 35-85).
    In a study conducted by Clapp et al., treatment of rats by gavage 
with an unencapsulated lead chromate pigment or with a silica-
encapsulated lead chromate pigment resulted in no measurable blood 
levels of chromium (measured as Cr(III), detection limit = 10 [mu]g/L) 
after two or four weeks of treatment or after a two-week recovery 
period. However, kidney levels of chromium (measured as Cr(III)) were 
significantly higher in the rats that received the unencapsulated 
pigment when compared to the rats that received the encapsulated 
pigment, indicating that silica encapsulation may reduce the 
gastrointestinal bioavailability of chromium from lead chromate 
pigments (Ex. 11-5). This study does not address the bioavailability of 
encapsulated chromate pigments from the lung where residence time could 
be different.
5. Distribution of Cr(VI) in the Body
    Once in the bloodstream, Cr(VI) is taken up into erythrocytes, 
where it is reduced to lower oxidation states and forms chromium 
protein complexes during reduction (Ex. 35-41). Once complexed with 
protein, chromium cannot leave the cell and chromium ions are unable to 
repenetrate the membrane and move back into the plasma (Exs. 7-6; 7-7; 
19-1; 35-41; 35-52). Once inside the blood cell, the intracellular 
Cr(VI) reduction to Cr(III) depletes Cr(VI) concentration in the red 
blood cell (Ex. 35-89). This serves to enhance diffusion of Cr(VI) from 
the plasma into the erythrocyte resulting in very low plasma levels of 
Cr(VI). It is also believed that the rate of uptake of Cr(VI) by red 
blood cells may not exceed the rate at which they reduce Cr(VI) to 
Cr(III) (Ex. 35-99). The higher tissue levels of chromium after 
administration of Cr(VI) than after administration of Cr(III) reflect 
the greater tendency of Cr(VI) to traverse plasma membranes and bind to 
intracellular proteins in the various tissues, which may explain the 
greater degree of toxicity associated with Cr(VI) (MacKenzie et al. 
1958 as cited in 35-52; Maruyama 1982 as cited in 35-41; Ex. 35-71).
    Examination of autopsy tissues from chromate workers who were 
occupationally exposed to Cr(VI) showed that the highest chromium 
levels were in the lungs. The liver, bladder, and bone also had 
chromium levels above background. Mancuso examined tissues from three 
individuals with lung cancer who were exposed to chromium in the 
workplace (Ex. 124). One was employed for 15 years as a welder, the 
second and third worked for 10.2 years and 31.8 years, respectively, in 
ore milling and preparations and boiler operations. The cumulative 
chromium exposures for the three workers were estimated to be 3.45, 
4.59, and 11.38 mg/m\3\-years, respectively. Tissues from the first 
worker were analyzed 3.5 years after last exposure, the second worker 
18 years after last exposure, and the third worker 0.6 years after last 
exposure. All tissues from the three workers had elevated levels of 
chromium, with the possible exception of neural tissues. Levels were 
orders of magnitude higher in the lungs when compared to other tissues. 
Similar results were also reported in autopsy studies of people who may 
have been exposed to chromium in the workplace as well as chrome 
platers and chromate refining workers (Exs. 35-92; 21-1; 35-74; 35-88).
    Animal studies have shown similar distribution patterns after 
inhalation exposure. For example, a study by Baetjer et al. 
investigated the distribution of Cr(VI) in guinea pigs after 
intratracheal instillation of slightly soluble potassium dichromate 
(Ex. 7-8). At 24 hours after instillation, 11% of the original dose of 
chromium from potassium dichromate remained in the lungs, 8% in the 
erythrocytes, 1% in plasma, 3% in the kidney, and 4% in the liver. The 
muscle, skin, and adrenal glands contained only a trace. All tissue 
concentrations of chromium declined to low or nondetectable levels in 
140 days, with the exception of the lungs and spleen.
6. Metabolic Reduction of Cr(VI)
    Cr(VI) is reduced to Cr(III) in the lungs by a variety of reducing 
agents. This serves to limit uptake into lung cells and absorption into 
the bloodstream. Cr(V) and Cr(IV) are transient intermediates in this 
process. The genotoxic effects produced by the Cr(VI) are related to 
the reduction process and are further discussed in the section V.B.8 on 
Mechanistic Considerations.
    In vivo and in vitro experiments in rats indicated that, in the 
lungs, Cr(VI) can be reduced to Cr(III) by ascorbate and glutathione. A 
study by Suzuki and Fukuda showed that the reduction of Cr(VI) by 
glutathione is slower than the reduction by ascorbate (Ex. 35-65). 
Other studies have reported the reduction of Cr(VI) to Cr(III) by 
epithelial lining fluid (ELF) obtained from the lungs of 15 individuals 
by bronchial lavage. The average overall reduction capacity was 0.6 
[mu]g Cr(VI)/mg of ELF protein. In addition, cell extracts made from 
pulmonary alveolar macrophages derived from five healthy male 
volunteers were able to reduce an average of 4.8 [mu]g Cr(VI)/10\6\ 
cells or 14.4 [mu]g Cr(VI)/mg protein (Ex. 35-83). Postmitochondrial 
(S12) preparations of human lung cells (peripheral lung parenchyma and 
bronchial preparations) were also able to reduce Cr(VI) to Cr(III) (De 
Flora et al. 1984 as cited in Ex. 35-41).
7. Elimination of Cr(VI) From the Body
    Excretion of chromium from Cr(VI) compounds is predominantly in the 
urine, although there is some biliary excretion into the feces. In both 
urine and feces, the chromium is present as low molecular weight 
Cr(III) complexes. Absorbed chromium is excreted from the body in a 
rapid phase representing clearance from the blood and at least two 
slower phases representing clearance from tissues. Urinary excretion 
accounts for over 50% of eliminated chromium (Ex. 35-41). Although 
chromium is excreted in urine and feces, the intestine plays only a 
minor part in chromium elimination, representing only about 5% of 
elimination from the blood (Ex. 19-1). Normal urinary levels of 
chromium in humans have been reported to range from 0.24-1.8 [mu]g/L 
with a median level of 0.4 [mu]g/L (Ex. 35-79). Humans exposed to 0.01-
0.1 mg Cr(VI)/m\3\ as potassium dichromate (8-hour time-weighted 
average) had urinary excretion levels from 0.0247 to 0.037 mg Cr(III)/
L. Workers exposed mainly to Cr(VI) compounds had higher urinary 
chromium levels than workers exposed primarily to Cr(III) compounds. An 
analysis of the urine did not detect Cr(VI), indicating that Cr(VI) was 
rapidly reduced before excretion (Exs. 35-294; 5-48).
    A half-life of 15-41 hours has been estimated for chromium in urine 
for four welders using a linear one-compartment kinetic model (Exs. 35-
73; 5-52; 5-53). Limited work on modeling the absorption and deposition 
of chromium indicates that adipose and muscle tissue retain chromium at 
a moderate level for about two weeks, while the liver and spleen store 
chromium for up to 12 months. The estimated half-life for whole body 
chromium retention is 22 days for Cr(VI) (Ex. 19-1). The half-life of 
chromium in the human lung is 616 days, which is similar to the half-
life in rats (Ex. 7-5).
    Elimination of chromium was shown to be very slow in rats exposed 
to 2.1 mg Cr(VI)/m\3\ as zinc chromate six hours/day for four days. 
Urinary levels of chromium remained almost constant for four days after 
exposure and then decreased (Ex. 35-93). After intratracheal 
administration of sodium dichromate to rats, peak urinary chromium 
concentrations were observed at six hours, after which the urinary 
concentrations declined rapidly (Ex. 35-94). The more prolonged 
elimination of the moderately soluble zinc chromate as compared to the 
more soluble sodium dichromate is consistent with the influence of 
Cr(VI) solubility on absorption from the respiratory tract discussed 
earlier.
    Information regarding the excretion of chromium in humans after 
dermal exposure to chromium or its compounds is limited. Fourteen days 
after application of a salve containing water soluble potassium 
chromate, which resulted in skin necrosis and sloughing at the 
application site, chromium was found at 8 mg/L in the urine and 0.61 
mg/100 g in the feces of one individual (Brieger 1920 as cited in Ex. 
19-1). A slight increase over background levels of urinary chromium was 
observed in four subjects submersed in a tub of chlorinated water containing 
22 mg Cr(VI)/L as potassium dichromate for three hours (Ex. 31-22-6). For 
three of the four subjects, the increase in urinary chromium excretion 
was less than 1 [mu]g/day over the five-day collection period. Chromium 
was detected in the urine of guinea pigs after radiolabeled sodium 
chromate solution was applied to the skin (Ex. 35-81).
8. Physiologically-Based Pharmacokinetic Modeling
    Physiologically-based pharmacokinetic (PBPK) models have been 
developed that simulate absorption, distribution, metabolism, and 
excretion of Cr(VI) and Cr(III) compounds in humans (Ex. 35-95) and 
rats (Exs. 35-86; 35-70). The original model (Ex. 35-86) evolved from a 
similar model for lead, and contained compartments for the lung, GI 
tract, skin, blood, liver, kidney, bone, well-perfused tissues, and 
slowly perfused tissues. The model was refined to include two lung 
subcompartments for chromium, one of which allowed inhaled chromium to 
enter the blood and GI tract and the other only allowed chromium to 
enter the GI tract (Ex. 35-70). Reduction of Cr(VI) to Cr(III) was 
considered to occur in every tissue compartment except bone.
    The model was developed from several data sets in which rats were 
dosed with Cr(VI) or Cr(III) intravenously, orally or by intratracheal 
instillation, because different distribution and excretion patterns 
occur depending on the route of administration. In most cases, the 
model parameters (e.g., tissue partitioning, absorption, reduction 
rates) were estimated by fitting model simulations to experimental 
data. The optimized rat model was validated against the 1978 Langard 
inhalation study (Ex. 35-93). Chromium blood levels were overpredicted 
during the four-day inhalation exposure period, but blood levels during 
the post-exposure period were well predicted by the model. The model-
predicted levels of liver chromium were high, but other tissue levels 
were closely estimated.
    A human PBPK model recently developed by O'Flaherty et al. is able 
to predict tissue levels from ingestion of Cr(VI) (Ex. 35-95). The 
model incorporates differential oral absorption of Cr(VI) and Cr(III), 
rapid reduction of Cr(VI) to Cr(III) in major body fluids and tissues, 
and concentration-dependent urinary clearance. The model does not 
include a physiologic lung compartment, but can be used to estimate an 
upper limit on pulmonary absorption of inhaled chromium. The model was 
calibrated against blood and urine chromium concentration data from a 
group of controlled studies in which adult human volunteers drank 
solutions of soluble Cr(III) or Cr(VI).
    PBPK models are increasingly used in risk assessments, primarily to 
predict the concentration of a potentially toxic chemical that will be 
delivered to any given target tissue following various combinations of 
route, dose level, and test species. Further development of the 
respiratory tract portion of the model, specific Cr(VI) rate data on 
extracellular reduction and uptake into lung cells, and more precise 
understanding of critical pathways inside target cells would improve 
the model value for risk assessment purposes.
9. Summary
    Based on the studies presented above, evidence exists in the 
literature that shows Cr(VI) can be systemically absorbed by the 
respiratory tract. The absorption of inhaled chromium compounds depends 
on a number of factors, including physical and chemical properties of 
the particles (oxidation state, size, and solubility), the reduction 
capacity of the ELF and alveolar macrophages and clearance by the 
mucocliary escalator and phagocytosis. Highly water soluble Cr(VI) 
compounds (e.g. sodium chromate) enter the bloodstream more readily 
than highly insoluble Cr(VI) compounds (e.g. lead chromate). However, 
insoluble compounds may have longer residence time in lung. Absorption 
of Cr(VI) can also take place after oral and dermal exposure, 
particularly if the exposures are high.
    The chromate (CrO4) 2- enters cells via 
facilitated diffusion through non-specific anion channels (similar to 
phosphate and sulfate anions). Following absorption of Cr(VI) compounds 
from various exposure routes, chromium is taken up by the blood cells 
and is widely distributed in tissues as Cr(VI). Inside blood cells and 
tissues, Cr(VI) is rapidly reduced to lower oxidation states and bound 
to macromolecules which may result in genotoxic or cytotoxic effects. 
However, in the blood a substantial proportion of Cr(VI) is taken up 
into erythrocytes, where it is reduced to Cr(III) and becomes bound to 
hemoglobin and other proteins.
    Inhaled Cr(VI) is reduced to Cr(III) in vivo by a variety of 
reducing agents. Ascorbate and glutathione in the ELF and macrophages 
have been shown to reduce Cr(VI) to Cr(III) in the lungs. After oral 
exposure, gastric juices are also responsible for reducing Cr(VI) to 
Cr(III). This serves to limit the amount of Cr(VI) systemically 
absorbed.
    Absorbed chromium is excreted from the body in a rapid phase 
representing clearance from the blood and at least two slower phases 
representing clearance from tissues. Urinary excretion is the primary 
route of elimination, accounting for over 50% of eliminated chromium. 
Although chromium is excreted in urine and feces, the intestine plays 
only a minor part in chromium elimination representing only about 5% of 
elimination from the blood.

B. Carcinogenic Effects

    There has been extensive study on the potential for Cr(VI) to cause 
carcinogenic effects, particularly cancer of the lung. OSHA reviewed 
epidemiologic data from several industry sectors including chromate 
production, chromate pigment production, chromium plating, stainless 
steel welding, and ferrochromium production. Supporting evidence from 
animal studies and mechanistic considerations are also evaluated in 
this section.
1. Evidence from Chromate Production Workers
    The epidemiologic literature of workers in the chromate production 
industry represents the earliest and best-documented relationship 
between exposure to chromium and lung cancer. The earliest study of 
chromate production workers in the United States was reported by Machle 
and Gregorius in 1948 (Ex. 7-2). In the United States, two chromate 
production plants, one in Baltimore, MD, and one in Painesville, OH, 
have been the subject of multiple studies. Both plants were included in 
the 1948 Machle and Gregorius study and again in the study conducted by 
the Public Health Service and published in 1953 (Ex. 7-3). Both of 
these studies reported the results in aggregate. The Baltimore chromate 
production plant was studied by Hayes et al. (Ex. 7-14) and more 
recently by Gibb et al. (Ex. 31-22-11). The chromate production plant 
in Painesville, OH, has been followed since the 1950s by Mancuso with 
his most recent follow-up published in 1997. The most recent study of 
the Painesville plant was published by Luippold et al. (Ex. 31-18-4). 
The studies by Gibb and Luippold present historical exposure data for 
the time periods covered by their respective studies. The Gibb exposure 
data are especially interesting since the industrial hygiene data were 
collected on a routine basis and not for compliance purposes. These 
routine air measurements may be more representative of those typically 
encountered by the exposed workers. In Great Britain, three plants have been 
studied repeatedly, with reports published between 1952 and 1991. Other 
studies of cohorts in the United States, Germany, Italy and Japan are 
also reported. The elevated lung cancer mortality reported in the great 
majority of these cohorts and the significant upward trends with 
duration of employment and cumulative exposure provide some of the 
strongest evidence that Cr(VI) is carcinogenic to workers. A summary of 
selected human epidemiologic studies in chromate production workers is 
presented in Table V-1.

BILLING CODE 4510-26-P

Click here to view table V-1

BILLING CODE 4510-26-C
    The basic hexavalent chromate production process involves milling 
and mixing trivalent chromite ore with soda ash, sometimes in the 
presence of lime (Exs. 7-103; 35-61). The mixture is 'roasted' at a 
high temperature, which oxidizes much of the chromite to hexavalent 
sodium chromate. Depending on the lime content used in the process, the 
roast also contains other chromate species, especially calcium
chromate under high lime conditions. The highly water-soluble sodium 
chromate is water-extracted from the water-insoluble trivalent chromite 
and the less water-soluble chromates (e.g., calcium chromate) in the 
'leaching' process. The sodium chromate leachate is reacted with 
sulfuric acid and sodium bisulfate to form sodium dichromate. The 
sodium dichromate is prepared and packaged as a crystalline powder to 
be sold as final product or sometimes used as the starting material to 
make other chromates such as chromic acid and potassium dichromate.

a. Cohort Studies of the Baltimore Facility. The Hayes et al. study of 
the Baltimore, Maryland chromate production plant was designed to 
determine whether changes in the industrial process at one chromium 
chemical production facility were associated with a decreased risk of 
cancer, particularly cancer of the respiratory system (Ex. 7-14). Four 
thousand two hundred and seventeen (4,217) employees were identified as 
newly employed between January 1, 1945 and December 31, 1974. Excluded 
from this initial enumeration were employees who: (1) were working as 
of 1945, but had been hired prior to 1945 and (2) had been hired since 
1945 but who had previously been employed at the plant. Excluded from 
the final cohort were those employed less than 90 days; women; those 
with unknown length of employment; those with no work history; and 
those of unknown age. The final cohort included 2,101 employees (1,803 
hourly and 298 salaried).
    Hayes divided the production process into three departments: (1) 
The mill and roast or "dry end" department which consists of 
grinding, roasting and leaching processes; (2) the bichromate 
department which consists of the acidification and crystallization 
processes; and (3) the special products department which produces 
secondary products including chromic acid. The bichromate and special 
products departments are referred to as the "wet end".
    The construction of a new mill and roast and bichromate plant that 
opened during 1950 and 1951 and a new chromic acid and special products 
plant that opened in 1960 were cited by Hayes as "notable production 
changes" (Ex. 7-14). The new facilities were designed to "obtain 
improvements in process technique and in environmental control of 
exposure to chromium bearing dusts * * *" (Ex. 7-14).
    Plant-related work and health histories were abstracted for each 
employee from plant records. Each job on the employee's work history 
was characterized according to whether the job exposure occurred in (1) 
a newly constructed facility, (2) an old facility, or (3) could not be 
classified as having occurred in the new or the old facility. Those who 
ever worked in an old facility or whose work location(s) could not be 
distinguished based upon job title were considered as having a high or 
questionable exposure. Only those who worked exclusively in the new 
facility were defined for study purposes as "low exposure". Data on 
cigarette smoking were abstracted from plant records, but were not 
utilized in any analyses since the investigators thought them "not to 
be of sufficient quality to allow analysis."
    One thousand one hundred and sixty nine (1,169) cohort members were 
identified as alive, 494 not individually identified as alive and 438 
as deceased. Death certificates could not be located for 35 reported 
decedents. Deaths were coded to the 8th revision of the International 
Classification of Diseases.
    Mortality analysis was limited to the 1,803 hourly employees 
calculating the standardized mortality ratios (SMRs) for specific 
causes of death. The SMR is a ratio of the number of deaths observed in 
the study population to the number that would be expected if that study 
population had the same specific mortality rate as a standard reference 
population (e.g., age-, gender-, calendar year adjusted U.S. 
population). The SMR is typically multiplied by 100, so a SMR greater 
than 100 represents an elevated mortality in the study cohort relative 
to the reference group. In the Hayes study, the expected number of 
deaths was based upon Baltimore, Maryland male mortality rates 
standardized for age, race and time period. For those where race was 
unknown, the expected numbers were derived from mortality rates for 
whites. Cancer of the trachea, bronchus and lung accounted for 69% of 
the 86 cancer deaths identified and was statistically significantly 
elevated (O=59; E=29.16; SMR=202; 95% CI: 155-263).
    Analysis of lung cancer deaths among hourly workers by year of 
initial employment (1945-1949; 1950-1959 and 1960-1974), exposure 
category (low exposure or questionable/high exposure) and duration of 
employment (short term defined as 90 days-2 years; long term defined as 
3 years +) was also conducted. For those workers characterized as 
having questionable/high exposure, the SMRs were significantly elevated 
for the 1945-1949 and the 1950-1959 hire periods and for both short- 
and long-term workers (not statistically significant for the short-term 
workers initially hired 1945-1949). For those characterized as low 
exposure, there was an elevated SMR for the long-term workers hired 
between 1950 and 1959, but based only on three deaths (not 
statistically significant). No lung cancer cases were observed for 
workers hired 1960-1974.
    Case-control analyses of (1) a history of ever having been employed 
in selected jobs or combinations of jobs or (2) a history of specified 
morbid conditions and combinations of conditions reported on plant 
medical records were conducted. Cases were defined as decedents (both 
hourly and salaried were included in the analyses) whose underlying or 
contributing cause of death was lung cancer. Controls were defined as 
deaths from causes other than malignant or benign tumors. Cases and 
controls were matched on race (white/non-white), year of initial 
employment (+/-3 years), age at time of initial employment (+/-5 years) 
and total duration of employment (90 days-2 years; 3-4 years and 5 
years +). An odds ratio (OR) was determined where the ratio is the odds 
of employment in a job involving Cr(VI) exposure for the cases relative 
to the controls.
    Based upon matched pairs, analysis by job position showed 
significantly elevated odds ratios for special products (OR=2.6) and 
bichromate and special products (OR=3.3). The relative risk for 
bichromate alone was also elevated (OR=2.1, not statistically 
significant).
    The possible association of lung cancer and three health conditions 
(skin ulcers, nasal perforation and dermatitis) as recorded in the 
plant medical records was also assessed. Of the three medical 
conditions, only the odds ratio for dermatitis was statistically 
significant (OR=3.0). When various combinations of the three conditions 
were examined, the odds ratio for having all three conditions was 
statistically significantly elevated (OR=6.0).
    Braver et al. used data from the Hayes study discussed above and 
the results of 555 air samples taken during the period 1945-1950 by the 
Baltimore City Health Department, the U.S. Public Health Service, and 
the companies that owned the plant, in an attempt to examine the 
relationship between exposure to Cr(VI) and the occurrence of lung 
cancer (Ex. 7-17). According to the authors, methods for determining 
the air concentrations of Cr(VI) have changed since the industrial 
hygiene data were collected at the Baltimore plant between 1945 and 
1959. The authors asked the National Institute for Occupational Safety 
and Health (NIOSH) and the Occupational Safety and Health
Administration (OSHA) to review the available documents on the methods 
of collecting air samples, stability of Cr(VI) in the sampling media 
after collection and the methods of analyzing Cr(VI) that were used to 
collect the samples during that period.
    Air samples were collected by both midget impingers and high volume 
samplers. According to the NIOSH/OSHA review, high volume samplers 
could have led to a "significant" loss of Cr(VI) due to the reduction 
of Cr(VI) to Cr(III) by glass or cellulose ester filters, acid 
extraction of the chromate from the filter, or improper storage of 
samples. The midget impinger was "less subject" to loss of Cr(VI) 
according to the panel since neither filters nor acid extraction from 
filters was employed. However, if iron was present or if the samples 
were stored for too long, conversion from Cr(VI) to Cr(III) may have 
occurred. The midget impinger can only detect water soluble Cr(VI). The 
authors noted that, according to a 1949 industrial hygiene survey by 
the U.S. Public Health Service, very little water insoluble Cr(VI) was 
found at the Baltimore plant. One NIOSH/OSHA panel member characterized 
midget impinger results as "reproducible" and "accuracy * * * fairly 
solid unless substantial reducing agents (e.g., iron) are present" 
(Ex. 7-17, p. 370). Based upon the panel's recommendations, the authors 
used the midget impinger results to develop their exposure estimates 
even though the panel concluded that the midget impinger methods "tend 
toward underestimation" of Cr(VI).
    The authors also cite other factors related to the industrial 
hygiene data that could have potentially influenced the accuracy of 
their exposure estimates (either overestimating or underestimating the 
exposure). These include: Measurements may have been taken primarily in 
"problem" areas of the plant; the plants may have been cleaned or 
certain processes shut down prior to industrial hygiene monitoring by 
outside groups; respirator use; and periodic high exposures (due to 
infrequent maintenance operations or failure of exposure control 
equipment) which were not measured and therefore not reflected in the 
available data.
    The authors estimated exposure indices for cohorts rather than for 
specific individuals using hire period (1945-1949 or 1950-1959) and 
duration of exposure, defined as short (at least 90 days but less than 
three years) and long (three years or more). The usual exposure to 
Cr(VI) for both the short- and long-term workers hired 1945-1949 was 
calculated as the average of the mean annual air concentration for 
1945-1947 and 1949 (data were missing for 1948). This was estimated to 
be 413 [mu]g/m3. The usual exposure to Cr(VI) was estimated 
to be 218 [mu]g/m3 for the short and long employees hired 
between 1950 and 1959 based on air measurements in the older facility 
in the early 1950s.
    Cumulative exposure was calculated as the usual exposure level 
times average duration. Short-term workers, regardless of length of 
employment, were assumed to have received 1.6 years of exposure 
regardless of hire period. For long-term workers, the average length of 
exposure was 12.3 years. Those hired 1945-1949 were assigned five years 
at an exposure of 413 [mu]g/m3 and 7.3 years at an exposure 
of 218 [mu]g/m3. For the long-term workers hired between 
1950 and 1959, the average length of exposure was estimated to be 13.4 
years. The authors estimated that the cumulative exposures at which 
"significant increases in lung cancer mortality" were observed in the 
Hayes study were 0.35, 0.67, 2.93 and 3.65 mg/m3--years. The 
association seen by the authors appears more likely to be the result of 
duration of employment rather than the magnitude of exposure since the 
variation in the latter was small.
    Gibb et al. relied upon the Hayes study to investigate mortality in 
a second cohort of the Baltimore plant (Ex. 31-22-11). The Hayes cohort 
was composed of 1,803 hourly and 298 salaried workers newly employed 
between January 1, 1945 and December 31, 1974. Gibb excluded 734 
workers who began work prior to August 1, 1950 and included 990 workers 
employed after August 1, 1950 who worked less than 90 days, resulting 
in a cohort of 2,357 males followed for the period August 1, 1950 
through December 31, 1992. Fifty-one percent (1,205) of the cohort was 
white; 36% (848) nonwhite. Race was unknown for 13% (304) of the 
cohort. The plant closed in 1985.
    Deaths were coded according to the 8th revision of the 
International Classification of Diseases. Person years of observation 
were calculated from the beginning of employment until death or 
December 31, 1992, whichever came earlier. Smoking data (yes/no) were 
available for 2,137 (93.3%) of the cohort from company records.
    Between 1950 and 1985, approximately 70,000 measurements of 
airborne Cr(VI) were collected utilizing several different sampling 
methods. The program of routine air sampling for Cr(VI) was initiated 
to "characterize 'typical/usual exposures' of workers" (Ex. 31-22-11, 
p. 117). Area samples were collected during the earlier time periods, 
while both area and personal samples were collected starting in 1977. 
Exposure estimates were derived from the area sampling systems and were 
adjusted to "an equivalent personal exposure estimate using job-
specific ratios of the mean area and personal sampling exposure 
estimates for the period 1978-1985 * * *" (Ex. 31-22-11, p. 117). 
According to the author, comparison of the area and personal samples 
showed "no significant differences" for about two-thirds of the job 
titles. For several job titles with a "significant point source of 
contamination" the area sampling methods "significantly 
underestimated" personal exposure estimates and were adjusted "by the 
ratio of the two" (Ex. 31-22-11, p. 118).
    A job exposure matrix (JEM) was constructed, where air sampling 
data were available, containing annual average exposure for each job 
title. Data could not be located for the periods 1950-1956 and 1960-
1961. Exposures were modeled for the missing data using the ratio of 
the measured exposure for a job title to the average of all measured 
job titles in the same department. For the time periods where 
"extensive" data were missing, a simple straight line interpolation 
between years with known exposures was employed.
    To estimate airborne Cr(III) concentrations, 72 composite dust 
samples were collected at or near the fixed site air monitoring 
stations about three years after the facility closed. The dust samples 
were analyzed for Cr(VI) content using ion chromatography. Cr(III) 
content was determined through inductively coupled plasma spectroscopic 
analysis of the residue. The Cr(III):Cr(VI) ratio was calculated for 
each area corresponding to the air sampling zones and the measured 
Cr(VI) air concentration adjusted based on this ratio. Worker exposures 
were calculated for each job title and weighted by the fraction of time 
spent in each air-monitoring zone. The Cr(III):Cr(VI) ratio was derived 
in this manner for each job title based on the distribution of time 
spent in exposure zones in 1978. Cr(VI) exposures in the JEM were 
multiplied by this ratio to estimate Cr(III) exposures.
    Information on smoking was collected at the time of hire for 
approximately 90% of the cohort. Of the 122 lung cancer cases, 116 were 
smokers and four were non smokers at the time of hire. Smoking status 
was unknown for two lung cancer cases. As discussed below, these data 
were used by the study authors to adjust for smoking in their 
proportional hazards regression models used to determine whether lung 
cancer mortality in the worker cohort increased with increasing cumulative
Cr(VI) exposure.
    A total of 855 observed deaths (472 white; 323 nonwhite and 60 race 
unknown) were reported. SMRs were calculated using U.S. rates for 
overall mortality. Maryland rates (the state in which the plant was 
located) were used to analyze lung cancer mortality in order to better 
account for regional differences in disease fatality. SMRs were not 
adjusted for smoking. In the public hearing, Dr. Gibb explained that it 
was more appropriate to adjust for smoking in the proportional hazards 
models than in the SMRs, because the analyst must make more assumptions 
to adjust the SMRs for smoking than to adjust the regression model (Tr. 
124).
    A statistically significant lung cancer SMR, based on the national 
rate, was found for whites (O=71; SMR=186; 95% CI: 145-234); nonwhites 
(O=47; SMR=188; 95% CI: 138-251) and the total cohort (O=122; SMR=180; 
95% CI: 149-214). The ratio of observed to expected lung cancer deaths 
(O/E) for the entire cohort stratified by race and cumulative exposure 
quartile were computed. Cumulative exposure was lagged five years (only 
exposure occurring five years before a given age was counted). The cut 
point for the quartiles divided the cohort into four equal groups based 
upon their cumulative exposure at the end of their working history (0-
0.00149 mgCrO\3\/m3-yr; 0.0015-0.0089 mgCrO3/m\3\-yr; 0.009-
0.0769 mgCrO3/m\3\-yr; and 0.077-5.25 mgCrO3/
m\3\-yr). For whites, the relative risk of lung cancer was 
significantly elevated for the second through fourth exposure quartiles 
with O/E values of 0.8, 2.1, 2.1 and 1.7 for the four quartiles, 
respectively. For nonwhites, the O/E values by exposure quartiles were 
1.1, 0.9, 1.2 and 2.9, respectively. Only the highest exposure quartile 
was significantly elevated. For the total cohort, a significant 
exposure-response trend was observed such that lung cancer mortality 
increased with increasing cumulative Cr(VI) exposure.
    Proportional hazards models were used to assess the relationship 
between chromium exposure and the risk of lung cancer. The lowest 
exposure quartile was used as the reference group. The median exposure 
in each quartile was used as the measure of cumulative Cr(VI) exposure. 
When smoking status was included in the model, relative lung cancer 
risks of 1.83, 2.48 and 3.32 for the second, third and fourth exposure 
quartiles respectively were estimated. Smoking, Cr(III) exposure, and 
work duration were also significant predictors of lung cancer risk in 
the model.
    The analysis attempted to separate the effects into two 
multivariate proportionate hazards models (one model incorporated the 
log of cumulative Cr(VI) exposure, the log of cumulative Cr(III) 
exposure and smoking; the second incorporated the log of cumulative 
Cr(VI), work duration and smoking). In either regression model, lung 
cancer mortality remained significantly associated (p <  .05) with 
cumulative Cr(VI) exposure even after controlling for the combination 
of smoking and Cr(III) exposure or the combination of smoking and work 
duration. On the other hand, lung cancer mortality was not 
significantly associated with cumulative Cr(III) or work duration in 
the multivariate analysis indicating lung cancer risk was more strongly 
correlated with cumulative Cr(VI) exposure than the other variables.
    Exponent, as part of a larger submission from the Chrome Coalition, 
submitted comments on the Gibb paper prior to the publication of the 
proposed rule. These comments asked that OSHA review methodological 
issues believed by Exponent to impact upon the usefulness of the Gibb 
data in a risk assessment analysis. While Exponent states that the Gibb 
study offers data that "are substantially better for cancer risk than 
the Mancuso study * * * they believe that further scrutiny of some of 
the methods and analytical procedures is necessary (Ex. 31-18-15-1, p. 
5).
    The issues raised by Exponent and the Chrome Coalition (Ex. 31-18-
14) concerning the Gibb paper are: selection of the appropriate 
reference population for compilation of expected numbers for use in the 
SMR analysis; inclusion of short term workers (<  1 year); expansion of 
the number of exposure groupings to evaluate dose response trends; 
analyzing dose response by peak JEM exposure levels; analyzing dose-
response at exposures above and below the current PEL and calculating 
smoking-adjusted SMRs for use in dose-response assessments. Exponent 
obtained the original data from the Gibb study. The data were 
reanalyzed to address the issues cited above. Exponent's findings are 
presented in Exhibit 31-18-15-1 and are discussed below.
    Exponent suggested that Gibb's use of U.S. and Maryland mortality 
rates for developing expectations for the SMR analysis was 
inappropriate. It suggested that Baltimore city mortality rates would 
have been the appropriate standard to select since those mortality 
rates would more accurately reflect the mortality experience of those 
who worked at the plant. Exponent reran the SMR analysis to compare the 
SMR values reported by Gibb (U.S. mortality rates for SMR analysis) 
with the results of an SMR analysis using Maryland mortality rates and 
Baltimore mortality rates. Gibb reported a lung cancer SMR of 1.86 (95% 
CI: 1.45-2.34) for white males based upon 71 lung cancer deaths using 
U.S. mortality rates. Reanalysis of the data produced a lung cancer SMR 
of 1.85 (95% CI: 1.44-2.33) for white males based on U.S. mortality 
rates, roughly the same value obtained by Gibb. When Maryland and 
Baltimore rates are used, the SMR drops to 1.70 and 1.25 respectively.
    Exponent suggested conducting sensitivity analysis that excludes 
short-term workers (defined as those with one year of employment) since 
the epidemiologic literature suggests that the mortality of short-term 
workers is different than long-term workers. Short-term workers in the 
Gibb study comprise 65% of the cohort and 54% of the lung cancers. The 
Coalition also suggested that data pertaining to short-term employees' 
information are of "questionable usefulness for assessing the 
increased cancer risk from chronic occupational exposure to Cr(VI)" 
(Ex. 31-18-15-1, p. 5).
    Lung cancer SMRs were calculated for those who worked for less than 
one year and for those who worked one year or more. Exponent defined 
short-term workers as those who worked less than one year "because it 
is consistent with the inclusion criteria used by others studying 
chromate chemical production worker cohorts" (Ex. 31-18-15-1, p. 12). 
Exponent also suggested that Gibb's breakdown of exposure by quartile 
was not the most "appropriate" way of assessing dose-response since 
cumulative Cr(VI) exposures remained near zero until the 50th to 60th 
percentile, "so there was no real distinction between the first two 
quartiles * * * (Ex. 31-18-15-1, p. 24). They also suggested that 
combining "all workers together at the 75th quartile * * * does not 
properly account for the heterogeneity of exposure in this group" (Ex. 
31-18-15-1, p. 24). The Exponent reanalysis used six cumulative 
exposure levels of Cr(VI) compared with the four cumulative exposure 
levels of Cr(VI) in the Gibb analysis. The lower levels of exposure 
were combined and "more homogeneous" categories were developed for 
the higher exposure levels.
    Using these re-groupings and excluding workers with less than one 
year of employment, Exponent reported that the highest SMRs are seen in 
the highest exposure group (1.5-< 5.25 mg CrO3/m\3\-years) for both white 
and nonwhite, based on either the Maryland or the Baltimore mortality rates.
The authors did not find "that the inclusion of short-term workers had a 
significant impact on the results, especially if Baltimore rates are used 
in the SMR calculations' (Ex. 31-18-15-1, p. 28).
    Analysis of length of employment and "peak" (i.e., highest 
recorded mean annual) exposure level to Cr(VI) was conducted. Exponent 
reported that approximately 50% of the cohort had "only very low" 
peak exposure levels (<7.2 [mu]g CrO3/m\3\ or approximately 
3.6 [mu]g/m\3\ of Cr(VI)). The majority of the short-term workers had 
peak exposures of <100 [mu]g CrO3/m\3\. There were five peak 
Cr(VI) exposure levels (<7.2 [mu]g CrO3/m\3\; 7.2-<19.3 
[mu]g CrO3/m\3\; 19.3-<48.0 [mu]g CrO3/m\3\; 
48.0-<105 [mu]g CrO3/m\3\; 105-<182 [mu]g CrO3/
m\3\; and 182-<806 [mu]g CrO3/m\3\) included in the 
analyses. Overall, the lung cancer SMRs for the entire cohort grouped 
according to the six peak exposure categories were slightly higher 
using Maryland reference rates compared to Baltimore reference rates.
    The Exponent analysis of workers who were ever exposed above the 
current PEL versus those never exposed above the current PEL produced 
slightly higher SMRs for those ever exposed, with the SMRs higher using 
the Maryland standard rather than the Baltimore standard. The only 
statistically significant result was for all lung cancer deaths 
combined.
    Assessment was made of the potential impact of smoking on the lung 
cancer SMRs since Gibb did not adjust the SMRs for smoking. Exponent 
stated that the smoking-adjusted SMRs are more appropriate for use in 
the risk assessment than the unadjusted SMRs. It should be noted that 
smoking adjusted SMRs could not be calculated using Baltimore reference 
rates. As noted by the authors, the smoking adjusted SMRs produced 
using Maryland reference rates are, by exposure, "reasonably 
consistent with the Baltimore-referenced SMRs" (Ex. 31-18-15-1, p. 
41).
    Gibb et al. included workers regardless of duration of employment, 
and the cohort was heavily weighted by those individuals who worked 
less than 90 days. In an attempt to clarify this issue, Exponent 
produced analyses of short-term workers, particularly with respect to 
exposures. Exponent redefined short-term workers as those who worked 
less than one year, to be consistent with the definition used in other 
studies of chromate producers. OSHA finds this reanalysis excluding 
short-term workers to be useful. It suggests that including cohort 
workers employed less than one year did not substantively alter the 
conclusions of Gibb et al. with regard to the association between 
Cr(VI) exposure and lung cancer mortality. It should be noted that in 
the Hayes study of the Baltimore plant, the cohort is defined as anyone 
who worked 90 days or more.
    Hayes et al. used Baltimore mortality rates while Gibb et al. used 
U.S. mortality rates to calculate expectations for overall SMRs. To 
calculate expectations for the analysis of lung cancer mortality and 
exposure, Gibb et al. used Maryland state mortality rates. The SMR 
analyses provided by Exponent using both Maryland and Baltimore rates 
are useful. The data showed that using Baltimore rates raised the 
expected number of lung cancer deaths and, thus, lowered the SMRs. 
However, there remained a statistically significant increase in lung 
cancer risk among the exposed workers and a significant upward trend 
with cumulative Cr(VI) exposure. The comparison group should be as 
similar as possible with respect to all other factors that may be 
related to the disease except the determinant under study. Since the 
largest portion of the cohort (45%) died in the city of Baltimore, and 
even those whose deaths occurred outside of Baltimore (16%) most likely 
lived in proximity to the city, the use of Baltimore mortality rates as 
an external reference population is preferable.
    Gibb's selection of the cut points for the exposure quartiles was 
accomplished by dividing the workers in the cohort into four equal 
groups based on their cumulative exposure at the end of their working 
history. Using the same method but excluding the short-term workers 
would have resulted in slightly different cumulative exposure 
quartiles. Exponent expressed a preference for a six-tiered exposure 
grouping. The impact of using different exposure groupings is further 
discussed in section VI.C of the quantitative risk assessment.
    The exposure matrix of Gibb et al. utilizes an unusually high-
quality set of industrial hygiene data. Over 70,000 samples taken to 
characterize the "typical/usual" working environment is more 
extensive industrial hygiene data then is commonly available for most 
exposure assessments. However, there are several unresolved issues 
regarding the exposure assessment, including the impact of the 
different industrial hygiene sampling techniques used over the sampling 
time frame, how the use of different sampling techniques was taken into 
account in developing the exposure assessment and the use of area vs. 
personal samples.
    Exponent and the Chrome Coalition also suggested that the SMRs 
should have been adjusted for smoking. According to Exponent, smoking 
adjusted SMRs based upon the Maryland mortality rates produced SMRs 
similar to the SMRs obtained using Baltimore mortality rates (Ex. 31-
18-15-1). The accuracy of the smoking data is questionable since it 
represents information obtained at the time of hire. Hayes abstracted 
the smoking data from the plant medical records, but "found it not to 
be of sufficient quality to allow analysis." One advantage to using 
the Baltimore mortality data may be to better control for the potential 
confounding of smoking.
    The Gibb study is one of the better cohort mortality studies of 
workers in the chromium production industry. The quality of the 
available industrial hygiene data and its characterization as 
"typical/usual" makes the Gibb study particularly useful for risk 
assessment.

b. Cohort Studies of the Painesville Facility. The Ohio Department of 
Health conducted epidemiological and environmental studies at a plant 
in Painesville that manufactured sodium bichromate from chromite ore. 
Mancuso and Hueper (Ex. 7-12) reported an excess of respiratory cancer 
among chromate workers when compared to the county in which the plant 
was located. Among the 33 deaths in males who had worked at the plant 
for a minimum of one year, 18.2% were from respiratory cancer. In 
contrast, the expected frequency of respiratory cancer among males in 
the county in which the plant was located was 1.2%. Although the 
authors did not include a formal statistical comparison, the lung 
cancer mortality rate among the exposed workers would be significantly 
greater than the county rate.
    Mancuso (Ex. 7-11) updated his 1951 study of 332 chromate 
production workers employed during the period 1931-1937. Age adjusted 
mortality rates were calculated by the direct method using the 
distribution of person years by age group for the total chromate 
population as the standard. Vital status follow-up through 1974 found 
173 deaths. Of the 66 cancer deaths, 41 (62.1%) were lung cancers. A 
cluster of lung cancer deaths was observed in workers with 27-36 years 
since first employment.
    Mancuso used industrial hygiene data collected in 1949 to calculate 
weighted average exposures to water-soluble (presumed to be Cr(VI)), 
insoluble (presumed to be principally Cr(III)) and
total chromium (Ex. 7-98). The age-adjusted lung cancer death rate 
increased from 144.6 (based upon two deaths) to 649.6 (based upon 14 
deaths) per 100,000 in five exposure categories ranging from a low of 
0.25-0.49 to a high of 4.0+ mg/m\3\-years for the insoluble Cr(III) 
exposures. For exposure to soluble Cr(VI), the age adjusted lung cancer 
rates ranged from 80.2 (based upon three deaths) to 998.7 (based upon 
12 deaths) in five exposure categories ranging from < 0.25 to 2.0+ mg/
m\3\-years. For total chromium, the age-adjusted death rates ranged 
from 225.7 (based upon three deaths) to 741.5 (based upon 16 deaths) 
for exposures ranging from 0.50-0.99 mg/m\3\-years to 6.0+ mg/m\3\-
years.
    Age-adjusted lung cancer death rates also were calculated by 
classifying workers by the levels of insoluble Cr(III) and total 
chromium exposure. From the data presented, it appears that for a fixed 
level of insoluble Cr(III), the lung cancer risk appears to increase as 
the total chromium increases (Ex. 7-11).
    Mancuso (Ex. 23) updated the 1975 study. As of December 31, 1993, 
283 (85%) cohort members had died and 49 could not be found. Of the 102 
cancer deaths, 66 were lung cancers. The age-adjusted lung cancer death 
rate per 100,000 ranged from 187.9 (based upon four deaths) to 1,254.1 
(based upon 15 deaths) for insoluble Cr(III) exposure categories 
ranging from 0.25-0.49 to 4.00-5.00 mg/m\3\ years. For the highest 
exposure to insoluble Cr(III) (6.00+ mg/m\3\ years) the age-adjusted 
lung cancer death rate per 100,000 fell slightly to 1,045.5 based upon 
seven deaths.
    The age-adjusted lung cancer death rate per 100,000 ranged from 
99.7 (based upon five deaths) to 2,848.3 (based upon two deaths) for 
soluble Cr(VI) exposure categories ranging from < 0.25 to 4.00+ mg/m\3\ 
years. For total chromium, the age-adjusted lung cancer death rate per 
100,000 ranged from 64.7 (based upon two deaths) to 1,106.7 (based upon 
21 deaths) for exposure categories ranging from < 0.50 to 6.00+ mg/m\3\ 
years.
    To investigate whether the increase in the lung cancer death rate 
was due to one form of chromium compound (presumed insoluble Cr(III) or 
soluble Cr(VI)), age-adjusted lung cancer mortality rates were 
calculated by classifying workers by the levels of exposure to 
insoluble Cr(III) and total chromium. For a fixed level of insoluble 
Cr(III), the lung cancer rate appears to increase as the total chromium 
increases for each of the six total chromium exposure categories, 
except for the 1.00-1.99 mg/m\3\-years category. For the fixed exposure 
categories for total chromium, increasing exposures to levels of 
insoluble Cr(III) showed an increased age-adjusted death rate from lung 
cancer in three of the six total chromium exposure categories.
    For a fixed level of soluble Cr(VI), the lung cancer death rate 
increased as total chromium categories of exposure increased for three 
of the six gradients of soluble Cr(VI). For the fixed exposure 
categories of total chromium, the increasing exposure to specific 
levels of soluble Cr(VI) led to an increase in two of the six total 
chromium exposure categories. Mancuso concluded that the relationship 
of lung cancer is not confined solely to either soluble or insoluble 
chromium. Unfortunately, it is difficult to attribute these findings 
specifically to Cr(III) [as insoluble chromium] and Cr(VI) [as soluble 
chromium] since it is likely that some slightly soluble and insoluble 
Cr(VI) as well as Cr(III) contributed to the insoluble chromium 
measurement.
    Luippold et al. conducted a retrospective cohort study of 493 
former employees of the chromate production plant in Painesville, Ohio 
(Ex. 31-18-4). This Painesville cohort does not overlap with the 
Mancuso cohort and is defined as employees hired beginning in 1940 who 
worked for a minimum of one year at Painesville and did not work at any 
other facility owned by the same company that used or produced Cr(VI). 
An exception to the last criterion was the inclusion of workers who 
subsequently were employed at a company plant in North Carolina (number 
not provided). Four cohort members were identified as female. The 
cohort was followed for the period January 1, 1941 through December 31, 
1997. Thirty-two percent of the cohort worked for 10 or more years.
    Information on potential confounders was limited. Smoking status 
(yes/no) was available for only 35% of the cohort from surveys 
administered between 1960 and 1965 or from employee medical files. For 
those employees where smoking data were available, 78% were smokers 
(responded yes on at least one survey or were identified as smokers 
from the medical file). Information on race also was limited, the death 
certificate being the primary source of information.
    Results of the vital status follow-up were: 303 deaths; 132 
presumed alive and 47 vital status unknown. Deaths were coded to the 
9th revision of the International Classification of Diseases. Cause of 
death could not be located for two decedents. For five decedents the 
cause of death was only available from data collected by Mancuso and 
was recoded from the 7th to the 9th revision of the ICD. There were no 
lung cancer deaths among the five recoded deaths.
    SMRs were calculated based upon two reference populations: The U.S. 
(white males) and the state of Ohio (white males). Lung cancer SMRs 
stratified by year of hire, duration of exposure, time since first 
employment and cumulative exposure group also were calculated.
    Proctor et al. analyzed airborne Cr(VI) levels throughout the 
facility for the years 1943 to 1971 (the plant closed April 1972) from 
800 area air sampling measurements from 21 industrial hygiene surveys 
(Ex. 35-61). A job exposure matrix (JEM) was constructed for 22 
exposure areas for each month of plant operation. Gaps in the matrix 
were completed by computing the arithmetic mean concentration from area 
sampling data, averaged by exposure area over three time periods (1940-
1949; 1950-1959 and 1960-1971) which coincided with process changes at 
the plant (Ex. 31-18-1)
    The production of water-soluble sodium chromate was the primary 
operation at the Painesville plant. It involved a high lime roasting 
process that produced a water insoluble Cr(VI) residue (calcium 
chromate) as byproduct that was transported in open conveyors and 
likely contributed to worker exposure until the conveyors were covered 
during plant renovations in 1949. The average airborne soluble Cr(VI) 
from industrial hygiene surveys in 1943 and 1948 was 0.72 mg/m\3\ with 
considerable variability among departments. During these surveys, the 
authors believe the reported levels may have underestimated total 
Cr(VI) exposure by 20 percent or less for some workers due to the 
presence of insoluble Cr(VI) dust.
    Reductions in Cr(VI) levels over time coincided with improvements 
in the chromate production process. Industrial hygiene surveys over the 
period from 1957 to 1964 revealed average Cr(VI) levels of 270 [mu]g/
m\3\. Another series of plant renovations in the early 1960s lowered 
average Cr(VI) levels to 39 [mu]g/m\3\ over the period from 1965 to 
1972. The highest Cr(VI) concentrations generally occurred in the 
shipping, lime and ash, and filtering operations while the locker 
rooms, laboratory, maintenance shop and outdoor raw liquor storage 
areas had the lowest Cr(VI) levels.
    The average cumulative Cr(VI) exposure (mg/m\3\-yrs) for the cohort 
was 1.58 mg/m\3\-yrs and ranged from 0.006 to 27.8 mg/m\3\-yrs. For 
those who died from lung cancer, the average Cr(VI) exposure was 3.28 
mg/m\3\-yrs and ranged from 0.06 to 27.8 mg/m\3\-yrs.
According to the authors, 60% of the cohort accumulated an estimated 
Cr(VI) exposure of 1.00 mg/m\3\-yrs or less.
    Sixty-three per cent of the study cohort was reported as deceased 
at the end of the follow-up period (December 31, 1997). There was a 
statistically significant increase for the all causes of death category 
based on both the national and Ohio state standard mortality rates 
(national: O=303; E=225.6; SMR=134; 95% CI: 120-150; state: O=303; 
E=235; SMR=129; 95% CI: 115-144). Fifty-three of the 90 cancer deaths 
were cancers of the respiratory system with 51 coded as lung cancer. 
The SMR for lung cancer is statistically significant using both 
reference populations (national O= 51; E=19; SMR 268; 95% CI: 200-352; 
state O=51; E=21.2; SMR 241; 95% CI: 180-317).
    SMRs also were calculated by year of hire, duration of employment, 
time since first employment and cumulative Cr(VI) exposure, mg/m\3\-
years. The highest lung cancer SMRs were for those hired during the 
earliest time periods. For the period 1940-1949, the lung cancer SMR 
was 326 (O=30; E=9.2; 95% CI: 220-465); for 1950-1959, the lung cancer 
SMR was 275 (O=15; E=5.5; 95% CI: 154-454). For the period 1960-1971, 
the lung cancer SMR was just under 100 based upon six deaths with 6.5 
expected.
    Lung cancer SMRs based upon duration of employment (years) 
increased as duration of employment increased. For those with one to 
four years of employment, the lung cancer SMR was 137 based upon nine 
deaths (E=6.6; 95% CI: 62-260); for five to nine years of employment, 
the lung cancer SMR was 160 (O=8; E=5.0; 95% CI: 69-314). For those 
with 10-19 years of employment, the lung cancer SMR was 169 (O=7; 
E=4.1; 95% CI: 68-349), and for those with 20 or more years of 
employment, the lung cancer SMR was 497 (O=27; E=5.4; 95% CI: 328-723).
    Analyses of cumulative Cr(VI) exposure found the lung cancer SMR 
(based upon the Ohio standard) in the highest exposure group (2.70-
27.80 mg/m\3\-yrs) was 463 (O=20; E=4.3; 95% CI: 183-398). In the 1.05-
2.69 mg/m\3\-yrs cumulative exposure group, the lung cancer SMR was 365 
based upon 16 deaths (E=4.4; 95% CI: 208-592). For the cumulative 
exposure groups 0.49-1.04, 0.20-0.48 and 0.00-0.19, the lung cancer 
SMRs were 91 (O=4; E=4.4; 95% CI: 25-234; 184 (O=8; E=4.4; 95% CI: 79-
362) and 67 (O=3; E=4.5; 95% CI: 14-196). A test for trend showed a 
strong relationship between lung cancer mortality and cumulative Cr(VI) 
exposure (p=0.00002). The authors claim that the SMRs are also 
consistent with a threshold effect since there was no statistically 
significant trend for excess lung cancer mortality with cumulative 
Cr(VI) exposures less than about 1 mg/m\3\-yrs. The issue of whether 
the cumulative Cr(VI) exposure-lung cancer response is best represented 
by a threshold effect is discussed further in preamble section VI on 
the quantitative risk assessment.
    The Painesville cohort is small (482 employees). Excluded from the 
cohort were six employees who worked at other chromate plants after 
Painesville closed. However, exceptions were made for employees who 
subsequently worked at the company's North Carolina plant (number not 
provided) because exposure data were available from the North Carolina 
plant. Subsequent exposure to Cr(VI) by other terminated employees is 
unknown and not taken into account by the investigators. Therefore, the 
extent of the bias introduced is unknown.
    The 10% lost to follow-up (47 employees) in a cohort of this size 
is striking. Four of the forty-seven had "substantial" follow-up that 
ended in 1997 just before the end date of the study. For the remaining 
43, most were lost in the 1950s and 1960s (most is not defined). Since 
person-years are truncated at the time individuals are lost to follow 
up, the potential implication of lost person years could impact the 
width of the confidence intervals.
    The authors used U.S. and Ohio mortality rates for the standards to 
compute the expectations for the SMRs, stating that the use of Ohio 
rates minimizes bias that could occur from regional differences in 
mortality. It is unclear why county rates were not used to address the 
differences in regional mortality.
c. Other Cohort Studies. The first study of cancer of the respiratory 
system in the U.S. chromate producing industry was reported by Machle 
and Gregorius (Ex. 7-2). The study involved a total of 11,000 person-
years of observation between 1933 and 1947. There were 193 deaths; 42 
were due to cancer of the respiratory system. The proportion of 
respiratory cancer deaths among chromate workers was compared with 
proportions of respiratory cancer deaths among Metropolitan Life 
Insurance industrial policyholders. A non-significant excess 
respiratory cancer among chromate production workers was found. No 
attempt was made to control for confounding factors (e.g., age). While 
some exposure data are presented, the authors state that one cannot 
associate tumor rates with tasks (and hence specific exposures) because 
of "shifting of personnel" and the lack of work history records.
    Baetjer reported the results of a case-control study based upon 
records of two Baltimore hospitals (Ex. 7-7). A history of working with 
chromates was determined from these hospital records and the proportion 
of lung cancer cases determined to have been exposed to chromates was 
compared with the proportion of controls exposed. Of the lung cancer 
cases, 3.4% had worked in a chromate manufacturing plant, while none of 
the controls had such a history recorded in the medical record. The 
results were statistically significant and Baetjer concluded that the 
data confirmed the conclusions reached by Machle and Gregorius that 
"the number of deaths due to cancer of the lung and bronchi is greater 
in the chromate-producing industry than would normally be expected" 
(Ex. 7-7, p. 516).
    As a part of a larger study carried out by the U.S. Public Health 
Service, the morbidity and mortality of male workers in seven U.S. 
chromate manufacturing plants during the period 1940-1950 was reported 
(Exs. 7-1; 7-3). Nearly 29 times as many deaths from respiratory cancer 
(excluding larynx) were found among workers in the chromate industry 
when compared to mortality rates for the total U.S. for the period 
1940-1948. The lung cancer risk was higher at the younger ages (a 40-
fold risk at ages 15-45; a 30-fold risk at ages 45-54 and a 20-fold 
risk at ages 55-74). Analysis of respiratory cancer deaths (excluding 
larynx) by race showed an observed to expected ratio of 14.29 for white 
males and 80 for nonwhite males.
    Taylor conducted a mortality study in a cohort of 1,212 chromate 
workers followed over a 24 year (1937-1960) period (Ex. 7-5). The 
workers were from three chromate plants that included approximately 70% 
of the total population of U.S. chromate workers in 1937. In addition, 
the plants had been in continuous operation for the study period 
(January 1, 1937 to December 31, 1960). The cohort was followed 
utilizing records of Old Age and Survivors Disability Insurance 
(OASDI). Results were reported both in terms of SMRs and conditional 
probabilities of survival to various ages comparing the mortality 
experience of chromate workers to the U.S. civilian male population. No 
measures of chromate exposure were reported although results are 
provided in terms of duration of employment. Taylor concluded that not 
only was there an excess in mortality from respiratory cancer, but from 
other causes as well, especially as duration of employment increased.
    In a reanalysis of Taylor's data, Enterline excluded those workers 
born prior to 1889 and analyzed the data by follow-up period using U.S. 
rates (Ex. 7-4). The SMR for respiratory cancer for all time periods 
showed a nine-fold excess (O=69 deaths; E=7.3). Respiratory cancer 
deaths comprised 28% of all deaths. Two of the respiratory cancer 
deaths were malignant neoplasms of the maxillary sinuses, a number 
according to Enterline, "greatly in excess of that expected based on 
the experience of the U.S. male population." Also slightly elevated 
were cancers of the digestive organs (O=16; E=10.4) and non-malignant 
respiratory disease (O=13; E=8.9).
    Pastides et al. conducted a cohort study of workers at a North 
Carolina chromium chemical production facility (Ex. 7-93). Opened in 
1971, this facility is the largest chromium chemical production 
facility in the United States. A low-lime process was used since the 
plant began operation. Three hundred and ninety eight workers employed 
for a minimum of one year between September 4, 1971 and December 31, 
1989 comprised the study cohort. A self-administered employee 
questionnaire was used to collect data concerning medical history, 
smoking, plant work history, previous employment and exposure to other 
potential chemical hazards. Personal air monitoring results for Cr(VI) 
were available from company records for the period February 1974 
through April 1989 for 352 of the 398 cohort members. A job matrix 
utilizing exposure area and calendar year was devised. The exposure 
means from the matrix were linked to each employee's work history to 
produce the individual exposure estimates by multiplying the mean 
Cr(VI) value from the matrix by the duration (time) in a particular 
exposure area (job). Annual values were summed to estimate total 
cumulative exposure.
    Personal air monitoring indicated that TWA Cr(VI) air 
concentrations were generally very low. Roughly half the samples were 
less than 1 [mu]g/m3, about 75 percent were below 3 [mu]g/
m3, and 96 percent were below 25 [mu]g/m3. The 
average worker's age was 42 years and mean duration of employment was 
9.5 years. Two thirds of the workers had accumulated less than 0.01 
[mu]g/m3-yr cumulative Cr(VI) exposure. SMRs were computed 
using National, State (not reported) and county mortality rates (eight 
adjoining North Carolina counties, including the county in which the 
plant is located). Two of the 17 recorded deaths in the cohort were 
from lung cancers. The SMRs for lung cancer were 127 (95% CI: 22-398) 
and 97 (95% CI: 17-306) based on U.S. and North Carolina county 
mortality rates, respectively. The North Carolina cohort is still 
relatively young and not enough time has elapsed to reach any 
conclusions regarding lung cancer risk and Cr(VI) exposure.
    In 2005, Luippold et al. published a study of mortality among two 
cohorts of chromate production workers with low exposures (Ex. 47-24-
2). Luippold et al. studied a total of 617 workers with at least one 
year of employment, including 430 at the North Carolina plant studied 
by Pastides et al. (1994) ("Plant 1") and 187 hired after the 1980 
institution of exposure-reducing process and work practice changes at a 
second U.S. plant ("Plant 2"). A high-lime process was never used at 
Plant 1, and workers drawn from Plant 2 were hired after the 
institution of a low lime process, so that exposures to calcium 
chromate in both cohorts were likely minimal. Personal air-monitoring 
measures available from 1974 to 1988 for the first plant and from 1981 
to 1998 for the second plant indicated that exposure levels at both 
plants were low, with overall geometric mean concentrations below 1.5 
[mu]g/m3 and area-specific average personal air sampling 
values not exceeding 10 [mu]g/m3 for most years (Ex. 47-24-
2, p. 383).
    Workers were followed through 1998. By the end of follow-up, which 
lasted an average of 20.1 years for workers at Plant 1 and 10.1 years 
at Plant 2, 27 cohort members (4%) were deceased. There was a 41% 
deficit in all-cause mortality when compared to all-cause mortality 
from age-specific state reference rates, suggesting a strong healthy 
worker effect. Lung cancer was 16% lower than expected based on three 
observed vs. 3.59 expected cases, also using age-specific state 
reference rates (Ex. 47-24-2, p. 383). The authors stated that "[t]he 
absence of an elevated lung cancer risk may be a favorable reflection 
of the postchange environment", but cautioned that longer follow-up 
allowing an appropriate latency for the entire cohort would be required 
to confirm this conclusion (Ex. 47-24-2, p. 381). OSHA received several 
written testimony regarding this cohort during the post-hearing comment 
period. These are discussed in section VI.B.7 on the quantitative risk 
assessment.
    A study of four chromate producing facilities in New Jersey was 
reported by Rosenman (Ex. 35-104). A total of 3,408 individuals were 
identified from the four facilities over different time periods (plant 
A from 1951-1954; plant B from 1951-1971; plant C from 1937-1964 and 
plant D 1937-1954). No Cr(VI) exposure data was collected for this 
study. Proportionate mortality ratios (PMRs) and proportionate cancer 
mortality ratios (PCMRs), adjusted by race, age, and calendar year, 
were calculated for the three companies (plants A and B are owned by 
one company). Unlike SMRs, PMRs are not based on the expected mortality 
rates in a standardized population but, instead, merely represent the 
proportional distribution of deaths in the cohort relative to the 
general U.S. population. Analyses were done evaluating duration of work 
and latency from first employment.
    Significantly elevated PMRs were seen for lung cancer among white 
males (170 deaths, PMR=1.95; 95% CI: 1.67-2.27) and black males (54 
deaths, PMR=1.88; 95% CI: 1.41-2.45). PMRs were also significantly 
elevated (regardless of race) for those who worked 1-10, 11-20 and >20 
years and consistently higher for white and black workers 11-20 years 
and >20 years since first hire. The results were less consistent for 
those with 10 or fewer years since first hire.
    Bidstrup and Case reported the mortality experience of 723 workers 
at three chromate producing factories in Great Britain (Ex. 7-20). Lung 
cancer mortality was 3.6 times that expected (O=12; E=3.3) for England 
and Wales. Alderson et al. conducted a follow-up of workers from the 
three plants in the U.K. (Bolton, Rutherglen and Eaglescliffe) 
originally studied by Bidstrup (Ex. 7-22). Until the late 1950s, all 
three plants operated a "high-lime" process. This process potentially 
produced significant quantities of calcium chromate as a by-product as 
well as the intended sodium dichromate. Process changes occurred during 
the 1940s and 1950s. The major change, according to the author, was the 
introduction of the "no-lime" process, which eliminated unwanted 
production of calcium chromate. The no-lime process was introduced at 
Eaglescliffe 1957-1959 and by 1961 all production at the plant was by 
this process. Rutherglen operated a low-lime process from 1957/1959 
until it closed in 1967. Bolton never changed to the low lime process. 
The plant closed in 1966. Subjects were eligible for entry into the 
study if they had received an X-ray examination at work and had been 
employed for a minimum of one year between 1948 and 1977. Of the 3,898 
workers enumerated at the three plants, 2,715 met the cohort entrance 
criteria, (alive: 1,999; deceased: 602; emigrated: 35; and lost to 
follow-up: 79). Those lost to follow-up were not included in the 
analyses. Eaglescliffe contributed the greatest number of subjects to 
the study (1,418). Rutherglen contributed the largest number of total 
deaths (369, or 61%). Lung cancer comprised the majority of cancer deaths
and was statistically significantly elevated for the entire cohort 
(O=116; E=47.96; SMR= 240; p < 0.001). Two deaths from nasal cancer were
observed, both from Rutherglen.
    SMRs were computed for Eaglescliffe by duration of employment, 
which was defined based upon plant process updates (those who only 
worked before the plant modification, those who worked both before and 
after the modifications, or those who worked only after the 
modifications were completed). Of the 179 deaths at the Eaglescliffe 
plant, 40 are in the pre-change group; 129 in the pre-/post-change and 
10 in the post-change. A total of 36 lung cancer deaths occurred at the 
plant, in the pre-change group O=7; E=2.3; SMR=303; in the pre-/post-
change group O=27; E=13; SMR=2.03 and in the post-change group O=2; 
E=1.07; SMR=187.
    In an attempt to address several potential confounders, regression 
analysis examined the contributions of various risk factors to lung 
cancer. Duration of employment, duration of follow-up and working 
before or after plant modification appear to be greater risk factors 
for lung cancer, while age at entry or estimated degree of chromate 
exposure had less influence.
    Davies updated the work of Alderson, et al. concerning lung cancer 
in the U.K. chromate producing industry (Ex. 7-99). The study cohort 
included payroll employees who worked a minimum of one year during the 
period January 1, 1950 and June 30, 1976 at any of the three facilities 
(Bolton, Eaglescliffe or Rutherglen). Contract employees were excluded 
unless they later joined the workforce, in which case their contract 
work was taken into account.
    Based upon the date of hire, the workers were assigned to one of 
three groups. The first, or "early" group, consists of workers hired 
prior to January 1945 who are considered long term workers, but do not 
comprise a cohort since those who left or died prior to 1950 are 
excluded. The second group, "pre-change" workers, were hired between 
January 1, 1945 to December 31, 1958 at Rutherglen or to December 31, 
1960 at Eaglescliffe. Bolton employees starting from 1945 are also 
termed pre-change. The cohort of pre-change workers is considered 
incomplete since those leaving 1946-1949 could not be included and 
because of gaps in the later records. For those who started after 1953 
and for all men staying 5+ years, this subcohort of pre-change workers 
is considered complete. The third group, "post-change" workers, 
started after the process changes at Eaglescliffe and Rutherglen became 
fully effective and are considered a "complete" cohort. A "control" 
group of workers from a nearby fertilizer facility, who never worked in 
or near the chromate plant, was assembled.
    A total of 2,607 employees met the cohort entrance criteria. As of 
December 31, 1988, 1,477 were alive, 997 dead, 54 emigrated and 79 
could not be traced (total lost to follow-up: 133). SMRs were 
calculated using the mortality rates for England and Wales and the 
mortality rates for Scotland. Causes of death were ascertained for all 
but three decedents and deaths were coded to the revision of the 
International Classification of Diseases in effect at the time of 
death. Lung cancer in this study is defined as those deaths where the 
underlying cause of death is coded as 162 (carcinoma of the lung) or 
239.1 (lung neoplasms of unspecified nature) in the 9th revision of the 
ICD. Two deaths fell into the latter category. The authors attempted to 
adjust the national mortality rates to allow for differences based upon 
area and social class.
    There were 12 lung cancer deaths at Bolton, 117 at Rutherglen, 75 
at Eaglescliffe and one among staff for a total of 205 lung cancer 
deaths. A statistically significant excess of lung cancer deaths (175 
deaths) among early and pre-change workers is seen at Rutherglen and 
Eaglescliffe for both the adjusted and unadjusted SMRs. For Rutherglen, 
for the early period based upon 68 observed deaths, the adjusted SMR 
was 230 while the unadjusted SMR was 347 (for both SMRs p< 0.001). For 
the 41 pre-change lung cancer deaths at Rutherglen, the adjusted SMR 
was 160 while the unadjusted SMR was 242 (for both SMRs p< 0.001). At 
Eaglescliffe, there were 14 lung cancer deaths in the early period 
resulting in an adjusted SMR of 196 and an unadjusted SMR of 269 (for 
both SMRs p< 0.05). For the pre-change period at Eaglescliffe, the 
adjusted SMR was 195 and the unadjusted was 267 (p< 0.001 for both 
SMRs). At Bolton there is a non-significant excess among pre-change 
men. There are no apparent excesses in the post-change groups, the 
staff groups or in the non-exposed fertilizer group.
    There is a highly significant overall excess of nasal cancers with 
two cases at Eaglescliffe and two cases at Rutherglen (O=4, 
Eadjusted=0.26; SMR=1538). All four men with nasal cancer had more than 
20 years of exposure to chromates.
    Aw reported on two case-control studies conducted at the previously 
studies Eaglescliffe plant (Ex. 245). In 1960, the plant, converted 
from a "high-lime" to a "no-lime" process, reducing the likelihood 
of calcium chromate formation. As of March 1996, 2,672 post-change 
workers had been employed, including 891 office personnel. Of the post-
change plant personnel, 56% had been employed for more than one year. 
Eighteen lung cancer cases were identified among white male post-change 
workers (13 deceased; five alive). Duration of employment for the cases 
ranged from 1.5 to 25 years with a mean of 14.4. Sixteen of the lung 
cancer cases were smokers.
    In the first case-control study reported, the 15 lung cancer cases 
identified up to September 1991 were matched to controls by age and 
hire date (five controls per case). Cases and controls were compared 
based upon their job categories within the plant. The results showed 
that cases were more likely to have worked in the kiln area than the 
controls. Five of the 15 cases had five or more years in the kiln area 
where Cr(VI) exposure occurred vs. six of the 75 controls. A second 
case-control study utilized the 18 lung cancer cases identified in post 
change workers up to March 1996. Five controls per case were matched by 
age (+/-5 years), gender and hire date. Both cases and controls had a 
minimum of one year of employment. A job exposure matrix was being 
constructed that would allow the investigators to "estimate exposure 
to hexavalent chromates for each worker in the study for all the jobs 
done since the start of employment at the site until 1980." Starting 
in 1970 industrial hygiene sampling was performed to determine exposure 
for all jobs at the plant. Cr(VI) exposure levels for the period 
between 1960 and 1969 were being estimated based on the recall of 
employees regarding past working conditions relative to current 
conditions from a questionnaire. The author stated that preliminary 
analysis suggests that the maximum recorded or estimated level of 
exposure to Cr(VI) for the cases was higher than that of the controls. 
However, specific values for the estimated Cr(VI) exposures were not 
reported.
    Korallus et al. conducted a study of 1,140 active and retired 
workers with a minimum of one year of employment between January 1, 
1948 and March 31, 1979 at two German chromate production plants (Ex. 
7-26). Workers employed prior to January 1, 1948 (either active or 
retired) and still alive at that date were also included in the cohort. 
The primary source for determining cause of death was medical
records. Death certificates were used only when medical records could 
not be found. Expected deaths were calculated using the male population 
of North Rhineland-Westphalia. Elevated SMRs for cancer of the 
respiratory system (50 lung cancers and one laryngeal cancer) were seen 
at both plants (O=21; E=10.9; SMR=192 and O=30; E=13.4; SMR=224).
    Korallus et al. reported an update of the study. The cohort 
definition was expanded to include workers with one year of employment 
between January 1, 1948 and December 31, 1987 (Ex. 7-91). One thousand 
four hundred and seventeen workers met the cohort entrance criteria and 
were followed through December 31, 1988. While death certificates were 
used, where possible, to obtain cause of death, a majority of the cause 
of death data was obtained from hospital, surgical and general 
practitioner reports and autopsies because of Germany's data protection 
laws. Smoking data for the cohort were incomplete.
    Process modifications at the two plants eliminated the high-lime 
process by January 1, 1958 at one location and January 1, 1964 at the 
second location. In addition, technical measures were introduced which 
led to reductions in the workplace air concentrations of chromate 
dusts. Cohort members were divided into pre- and post-change cohorts, 
with subcohorts in the pre-change group. SMRs were computed with the 
expected number of deaths derived from the regional mortality rates 
(where the plants are located). One plant had 695 workers (279 in the 
pre-change group and 416 in the post change group). The second plant 
had 722 workers (460 in the pre-change group and 262 in the post-change 
group). A total of 489 deaths were ascertained (225 and 264 deaths). Of 
the cohort members, 6.4% were lost to follow-up.
    Lung cancer is defined as deaths coded 162 in the 9th revision of 
the International Classification of Diseases. There were 32 lung cancer 
deaths at one plant and 43 lung cancer deaths at the second plant. Lung 
cancer SMRs by date of entry (which differ slightly by plant) show 
elevated but declining SMRs for each plant, possibly due to lower 
Cr(VI) exposure as a result of improvements in production process. The 
lung cancer SMR for those hired before 1948 at Plant 1 is statistically 
significant (O=13; SMR=225; 95% CI: 122-382). The overall lung cancer 
SMR for Plant 1 is also statistically significantly elevated based upon 
32 deaths (SMR=175; 95% CI: 120-246). At Plant 2, the only lung cancer 
SMR that is not statistically significant is for those hired after 1963 
(based upon 1 death). Lung cancer SMRs for those hired before 1948 
(O=23; SMR=344; 95% CI: 224-508) and for those hired between 1948 and 
1963 (O=19; SMR=196; 95% CI: 1.24-2.98) are statistically significantly 
elevated. The overall lung cancer SMR at Plant 2 based upon 43 deaths 
is 239 (95% CI: 177-317). No nasal cavity neoplasms were found. A 
statistically significant SMR for stomach cancer was observed at Plant 
2 (O=12; SMR=192; 95% CI: 104-324).
    Recently, the mortality experience of the post-change workers 
identified by Korallus et al. was updated in a study by Birk et al. 
(Ex. 48-4). The study cohort consisted of 901 post-change male workers 
from two German chromate production plants (i.e. 472 workers and 262 
workers, respectively) employed for at least one year. Review of 
employment records led to the addition of employees to the previous 
Korallus cohort. Mortality experience of the cohort was evaluated 
through 1998. A total of 130 deaths were ascertained, of which 22 were 
due to cancer of the lung. Four percent of the cohort was lost to 
follow-up. Specific cause of death could not be determined for 14 
decedents. The mean duration of Cr(VI) exposure was 10 years and the 
mean time since first exposure was 17 years. The proportion of workers 
who ever smoked was 65 percent.
    The cohort lacked sufficient job history information and air 
monitoring data to develop an adequate job-exposure matrix required to 
estimate individual airborne exposures (Ex. 48-1-2). Instead, the 
researchers used the over 12,000 measurements of urinary chromium from 
routine biomonitoring of plant employees collected over the entire 
study period to derive individual cumulative urinary chromium estimates 
as an exposure surrogate. The approximate geometric average of all 
urinary chromium measurements in the two German plants from 1960 to 
1998 was 7-8 [mu]g/dl (Ex. 48-1-2, Table 5). There was a general plant-
wide decline in average urinary chromium over time from 30 to 50 [mu]g/
dl in the 1960s to less than 5 [mu]g/dl in the 1990s (Ex. 48-4, Figure 
1). However, there was substantial variation in urinary chromium by 
work location and job group.
    The study reported a statistically significant deficit in all cause 
mortality (SMR=80 95% CI: 67-95) and mortality due to heart disease 
(SMR=66 95% CI: 45-93) based on the age- and calendar year-adjusted 
German national population rates indicating a healthy worker 
population. However, the SMR for lung cancer mortality was elevated 
(SMR=148 95% CI: 93-225) against the same reference population (Ex. 48-
4, Table 2). There was a statistically significant two-fold excess lung 
cancer mortality (SMR=209; 95% CI: 108-365; 12 observed lung cancer 
deaths) among workers in the highest cumulative exposure grouping (i.e. 
>200 [mu]g Cr/L-yr). There was no increase in lung cancer mortality in 
the lower exposure groups, but the number of lung cancer deaths was 
small (i.e. < =5 deaths) and the confidence intervals were wide.
    There were no obvious trends in lung cancer mortality with 
employment duration or time since first employed, but the results were, 
again, limited by the small number of study subjects per group. 
Logistic regression analysis showed that cumulative urinary chromium >= 
200 [mu]g Cr/L-yr was associated with a significantly higher risk of 
lung cancer death (OR=6.9; 95% CI: 2.6-18.2) when compared against 
workers exposed to lower cumulative urinary chromium exposures. This 
risk was unchanged after controlling for smoking status indicating that 
the elevated risks were unlikely to be confounded by smoking. Including 
a peak exposure score to the regression analysis did not result in 
additional risk beyond that associated with cumulative exposure alone. 
Some commenters felt this German post-change cohort provided evidence 
for an exposure threshold below which there is no risk of lung cancer. 
This issue is addressed in Section VI.B.7 of the quantitative risk 
assessment.
    DeMarco et al. conducted a cohort study of chromate production 
workers in northern Italy to assess the existence of excess risk of 
respiratory cancer, specifically lung cancer (Ex. 7-54). The cohort was 
defined as males who worked for a minimum of one year from 1948 to 1985 
and had at least 10 years of follow-up. Five hundred forty workers met 
the cohort definition. Vital status follow-up, carried out through June 
30, 1985, found 427 cohort members alive, 110 dead and three lost to 
follow-up. Analysis utilizing SMRs based on Italian national rates was 
conducted. Of the 110 deaths, 42 were cancer deaths. The statistically 
significant SMR for lung cancer based upon 14 observed deaths with 6.46 
expected was 217 (95% CI: 118-363).
    Exposure estimates were based upon the duration of cumulative 
exposure and upon a risk score (low, medium, high and not assessed) 
assigned to the department in which the worker was primarily employed. 
A committee assigned the scores, based upon knowledge of the production 
process or on industrial hygiene surveys taken in 1974, 1982 and 1984. 
The risk score is a surrogate for the workplace concentrations of Cr(VI)
in the different plant departments. Since no substantial changes had been 
made since World War II, the assumption was made that exposures remained 
relatively stable. Lung cancer SMRs based upon type of exposure increased 
with level of exposure (Low: O=1; E=1.43; SMR=70; Medium: O=5; E=202; SMR=2.48; 
High: O=6; E=1.4; SMR=420; Not Assessed: O=2; E=1.6; SMR=126). Only the SMR 
for those classified as having worked in departments characterized as high 
exposure was statistically significant at the p< 0.05 level.
    A cohort study of workers at a chromium compounds manufacturing 
plant in Tokyo, Japan by Satoh et al. included males employed between 
1918 and 1975 for a minimum of one year and for whom the necessary data 
were available (Ex. 7-27). Date and cause of death data were obtained 
from the death certificate (85%) or from other "reliable" written 
testimony (15%). Of the 1,061 workers identified, 165 were excluded 
from the study because information was missing. A total of 896 workers 
met the cohort inclusion criteria and were followed through 1978. The 
causes of 120 deaths were ascertained. SMRs based on age-cause specific 
mortality for Japanese males were calculated for four different time 
periods (1918-1949; 1950-1959; 1960-1969 and 1970-1978) and for the 
entire follow-up period (1918-1978). An elevated SMR for lung cancer is 
seen for the entire follow-up period (O=26; E=2.746; SMR=950). A 
majority of the lung cancer deaths (20) occurred during the 1970-1978 
interval.
    Results from the many studies of chromate production workers from 
different countries indicate a relationship between exposure to 
chromium and malignant respiratory disease. The epidemiologic studies 
done between 1948 and 1952 by Machle and Gregorius (Ex. 7-2), Mancuso 
and Hueper (Ex. 7-12) and Brinton, et al. (Ex. 7-1) suggest a risk for 
respiratory cancer among chromate workers between 15 and 29 times 
expectation. Despite the potential problems with the basis for the 
calculations of the expectations or the particular statistical methods 
employed, the magnitude of the difference between observed and expected 
is powerful enough to overcome these potential biases.
    It is worth noting that the magnitude of difference in the relative 
risks reported in a mortality study among workers in three chromate 
plants in the U.K. (Ex.7-20) were lower than the relative risks 
reported for chromate workers in the U.S. during the 1950s and 1960s. 
The observed difference could be the result of a variety of factors 
including different working conditions in the two countries, a shorter 
follow-up period in the British study, the larger lost-to-follow-up in 
the British study or the different statistical methods employed. While 
the earlier studies established that there was an excess risk for 
respiratory cancer from exposure to chromium, they were unable to 
specify either a specific chromium compound responsible or an exposure 
level associated with the risk. Later studies were able to use superior 
methodologies to estimate standardized lung cancer mortality ratios 
between chromate production cohorts and appropriate reference 
populations (Exs. 7-14; 7-22; 7-26; 7-99; 7-91). These studies 
generally found statistically increased lung cancer risk of around two-
fold. The studies usually found trends with duration of employment, 
year of hire, or some production process change that tended to 
implicate chromium exposure as the causative agent.
    Some of the most recent studies were able to use industrial hygiene 
data to reconstruct historical Cr(VI) exposures and show statistically 
significant associations between cumulative airborne Cr(VI) and lung 
cancer mortality (Exs. 23; 31-22-11; Ex. 31-18-4). Gibb et al. found 
the significant association between Cr(VI) and lung cancer was evident 
in models that accounted for smoking. The exposure'response 
relationship from these chromate production cohorts provide strong 
evidence that occupational exposure to Cr(VI) dust can increase cancer 
in the respiratory tract of workers.
    The Davies, Korallus, (German cohort), Luippold (2003), and 
Luippold (2005) studies examine mortality patterns at chromate 
producing facilities where one production process modification involved 
conversion from a high-lime to a low-lime or a lime-free process (Exs. 
7-99; 7-91; 31-18-4). In addition to process modification, technical 
improvements also were implemented that lowered Cr(VI) exposure. One of 
the plants in the Davies study retained the high-lime process and is 
not discussed. The lung cancer SMRs for one British plant and both of 
the German plants decline from early, to pre-change to post change time 
periods. In the remaining British plants, the lung cancer SMR is 
basically identical for the early and pre-change period, but does 
decline in the post-change time period. The lung cancer SMR in the 
Luippold 2003 cohort also declined over time as the amount of lime was 
reduced in the roasting process. Other modifications at the Painesville 
plant that reduced airborne Cr(VI) exposure, such as installation of 
covered conveyors and conversion from batch to continuous process, 
occurred at the same time (Ex. 35-61). The workers in the Luippold 
(2005) study were not exposed to Cr(VI) in facilities using a high-lime 
process. This study did not show excess risk; however, this may be a 
consequence of short follow-up time (<  20 years for most workers) or 
the small size of the study (<  4 expected lung cancers), as discussed 
further in Section VI.B.7. In general, it is not clear whether reduced 
levels of the high-lime byproduct, calcium chromate, or the roasting/
leaching end product, sodium dichromate, that resulted from the various 
process changes is the reason for the decrease in lung cancer SMRs in 
these cohorts. It should be noted that increased lung cancer risk was 
experienced by workers at the Baltimore plant (e.g., Hayes and Gibb 
cohorts) even though early air monitoring studies suggest that a high 
lime process was probably not used at this facility (Ex. 7-17).
2. Evidence From Chromate Pigment Production Workers
    Chromium compounds are used in the manufacture of pigments to 
produce a wide range of vivid colors. Lead and zinc chromates have 
historically been the predominant hexavalent chromium pigments, 
although others such as strontium and barium chromate have also been 
produced. These chromates vary considerably in their water solubility 
with lead and barium chromates being the most water insoluble. All of 
the above chromates are less water-soluble than the highly water-
soluble sodium chromate and dichromate that usually serve as the 
starting material for chromium pigment production. The reaction of 
sodium chromate or dichromate with the appropriate zinc or lead 
compound to form the corresponding lead or zinc chromate takes place in 
solution. The chromate pigment is then precipitated, separated, dried, 
milled, and packaged. Worker exposures to chromate pigments are 
greatest during the milling and packaging stages.
    There have been a number of cohort studies of chromate pigment 
production workers from the United States, the United Kingdom, France, 
Germany, the Netherlands, Norway and Japan. Most of the studies found 
significantly elevated lung cancers in workers exposed to Cr(VI) 
pigments over many years when compared against standardized reference 
populations. In general, the studies of chromate pigment workers lack 
the historical exposure data found in some of the chromate production 
cohorts. The consistently higher lung cancers across several worker 
cohorts exposed to the less water-soluble Cr(VI) compounds complements 
the lung cancer findings from the studies of workers producing highly 
water soluble chromates and adds to the further evidence that occupational 
exposure to Cr(VI) compounds should be regarded as carcinogenic. A summary 
of selected human epidemiologic studies in chromate production workers is 
presented in Table V-2.
BILLING CODE 4510-26-P

Click here to view table V-2

BILLING CODE 4510-26-C
    Langard and Vigander updated a cohort study of lung cancer 
incidence in 133 workers employed by a chromium pigment production 
company in Norway (Ex. 7-36). The cohort was originally studied by 
Langard and Norseth (Ex. 7-33). Twenty four men had more than three 
years of exposure to chromate dust. From 1948, when the company was 
founded, until 1951, only lead chromate pigment was produced.
From 1951 to 1956, both lead chromate and zinc chromate pigments were 
produced and from 1956 to the end of the study period in 1972 only zinc 
chromate was produced. Workers were exposed to chromates both as the 
pigment and its raw material, sodium dichromate.
    The numbers of expected lung cancers in the workers were calculated 
using the age-adjusted incidence rates for lung cancer in the Norwegian 
male population for the period 1955-1976. Follow-up using the Norwegian 
Cancer Registry through December 1980, found the twelve cancers of 
which seven were lung cancers. Six of the seven lung cancers were 
observed in the subcohort of 24 workers who had been employed for more 
than three years before 1973. There was an increased lung cancer 
incidence in the subcohort based on an observed to expected ratio of 44 
(O=6; E=0.135). Except for one case, all lung cancer cases were exposed 
to zinc chromates and only sporadically to other chromates. Five of the 
six cases were known to be smokers or ex-smokers. Although the authors 
did not report any formal statistical comparisons, the extremely high 
age-adjusted standardized incidence ratio suggests that the results 
would likely be statistically significant.
    Davies reported on a cohort study of English chromate pigment 
workers at three factories that produced chromate pigments since the 
1920s or earlier (Ex. 7-41). Two of the factories produced both zinc 
and lead chromate. Both products were made in the same sheds and all 
workers had mixed exposure to both substances. The only product at the 
third factory was lead chromate.
    Cohort members are defined as males with a minimum of one year of 
employment first hired between 1933 and 1967 at plant A; 1948 and 1967 
at plant B and 1946-1961 at plant C. The analysis excludes men who 
entered employment later than 1967 because of the short follow-up 
period. Three hundred and ninety six (396) men from Factory A, 136 men 
from Factory B and 114 men from Factory C were followed to mid-1977. 
Ninety-four workers with 3-11 months employment during 1932-1945 at 
Factory A were also included. Expectations were based upon calendar 
time period-, gender- and age-specific national cancer death rates for 
England and Wales. The author adjusted the death rates for each factory 
for local differences, but the exact methods of adjustment were not 
explicit.
    Exposure to chromates was assigned as high for those in the dry 
departments where pigments were ground, blended and packed; medium for 
those in the wet departments where precipitates were washed, pressed 
and stove dried and in maintenance or cleaning which required time in 
various departments; or low for those jobs which the author states 
involved "slight exposure to chromates such as most laboratory jobs, 
boiler stoking, painting and bricklaying" (Ex. 7-41, p. 159). The high 
and medium exposure categories were combined for analytical purposes.
    For those entering employment from 1932 to 1954 at Factory A, there 
were 18 lung cancer deaths in the high/medium exposure group, with 8.2 
deaths expected. The difference is significant at p< .01. In the low 
exposure group, the number of observed and expected lung cancer deaths 
was equal (two deaths). There were no lung cancer deaths at Factory A 
for those hired between 1955-1960 and 1961-1967.
    For those entering employment between 1948 and 1967 at Factory B, 
there were seven observed lung cancer deaths in the high/medium 
exposure group with 1.4 expected which is statistically significant at 
p< .001. At Factory C (which manufactured only lead chromate), there was 
one death in the high/medium exposure group and one death in the low 
exposure group for those beginning employment between 1946 and 1967.
    The author points out that:

    There has been no excess lung cancer mortality amongst workers 
with chromate exposure rated as "low", nor among those exposed 
only to lead chromate. High and medium exposure-rated workers who in 
the past had mixed exposure to both lead and zinc chromate have 
experienced a marked excess of lung cancer deaths, even if employed 
for as little as one year (Ex. 7-41, p. 157).

    It is the author's opinion that the results "suggest that the 
manufacture of zinc chromate may involve a lung cancer hazard" (Ex. 7-
41, p. 157).
    Davies updated the lung cancer mortality at the three British 
chromate pigment production factories (Ex. 7-42). The follow-up was 
through December 31, 1981. The cohort was expanded to include all male 
workers completing one year of service by June 30, 1975 but excluded 
office workers.
    Among workers at Factory A with high and medium exposure, mortality 
was statistically significantly elevated over the total follow-up 
period among entrants hired from 1932 to 1945 (O/E=2.22). A similar, 
but not statistically significant, excess was seen among entrants hired 
from 1946 to 1954 (O/E=2.23). The results for Factory B showed 
statistically significantly elevated lung cancer mortality among 
workers classified with medium exposures entering service during the 
period from 1948 to 1960 (O/E=3.73) and from 1961 to 1967 (O/E=5.62). 
There were no lung cancer deaths in the high exposure group in either 
time period. At Factory C, analysis by entry date (early entrant and 
the period 1946-1960) produced no meaningful results since the number 
of deaths was small. When the two periods are combined, the O/E was 
near unity. The author concluded that in light of the apparent absence 
of risk at Factory C, "it seems reasonable to suggest that the hazard 
affecting workers with mixed exposures at factories A and B * * * is 
attributable to zinc chromates" (Ex. 7-42, p. 166). OSHA disagrees 
with this conclusion, as discussed in section V.9.
    Davies also studied a subgroup of 57 chromate pigment workers, 
mostly employed between 1930 and 1945, who suffered clinical lead 
poisoning (Ex. 7-43). Followed through 1981, there was a statistically 
significantly elevated SMR for lung cancer based upon four cases (O=4; 
E=2.8; SMR=145).
    Haguenoer studied 251 French zinc and lead chromate pigment workers 
employed for six months or more between January 1, 1958 and December 
31, 1977 (Ex. 7-44). As of December 31, 1977, 50 subjects were 
identified as deceased. Cause of death was obtained for 30 of the 50 
deaths (60%). Lung cancer mortality was significantly elevated based on 
11 fatalities (SMR=461; 95% CI: 270-790). The mean time from first 
employment until detection of cancer was 17 years. The mean duration of 
employment among cases was 15 years.
    The Haguenoer cohort was followed up in a study by Deschamps et al. 
(Ex. 234). Both lead and zinc chromate pigments were produced at the 
plant until zinc chromate production ceased in 1986. The cohort 
consisted of 294 male workers employed for at least six months between 
1958 and 1987. At the end of the follow-up, 182 cohort members were 
alive, 16 were lost to follow-up and 96 were dead. Because of French 
confidentiality rules, the cause of death could not be obtained from 
the death certificate; instead physicians and hospital records were 
utilized. Using cause of death data from sources other than death 
certificates raises the potential for misclassification bias. Cause of 
death could not be obtained for five decedents. Data on smoking habits 
was not available for a number of workers and was not used in the 
analysis.
    Since individual work histories were not available, the authors 
made the assumption that the exposure level was the same for all 
workers during their employment at the plant. Duration of employment 
was used as a surrogate for exposure. Industrial hygiene measurements 
taken in 1981 provide some idea of the exposure levels at the plant. 
In the filtration department, Cr(VI) levels were between 2 and 3 [mu]g/m\3\; 
in the grinding department between 6 and 165 [mu]g/m\3\; in the drying and 
sacking department between 6 and 178 [mu]g/m\3\; and in the sacks 
marking department more than 2000 [mu]g/m\3\.
    The expected number of deaths for the SMR analysis was computed 
from age-adjusted death rates in the northern region of France where 
the plant was located. There was a significant increase in lung cancer 
deaths based on 18 fatalities with five expected (SMR=360; 95% CI: 213-
568). Using duration of employment as a surrogate for exposure, 
statistically significant SMRs were seen for the 10-15 years of 
exposure (O=6, SMR=720, 95% CI: 264-1568), 15-20 years (O=4, SMR=481, 
95% CI: 131-1231), and 20+ years (O=6, SMR=377, 95% CI: 1.38-8.21) time 
intervals. There was a significantly elevated SMR for brain cancer 
based upon two deaths (SMR=844, 95% CI: 102-3049). There was a non-
statistically significant increase for digestive tract cancer (O=9, 
SMR=130) consisting of three esophageal cancers, two stomach cancers 
and four colon cancers.
    Equitable Environmental Health, Inc., on behalf of the Dry Color 
Manufacturers Association, undertook a historical prospective mortality 
study of workers involved in the production of lead chromate (Exs. 2-D-
3; 2-D-1). The cohort was defined as male employees who had been 
exposed to lead chromate for a minimum of six months prior to December 
1974 at one of three facilities in West Virginia, Kentucky or New 
Jersey. The New Jersey facility had a unit where zinc chromate was 
produced dating back to 1947 (Ex. 2-D-3). Most workers rotated through 
this unit and were exposed to both lead and zinc chromates. Two men 
were identified at the New Jersey facility with exposure solely to lead 
chromate; no one with exposure only to zinc chromate was identified.
    Subsequent review of the data found that the Kentucky plant also 
produced zinc chromates from the late 1930s to early 1964. During the 
period 1961-1962, zinc chromates accounted for approximately 12% of 
chromate production at the plant. In addition, strontium chromate and 
barium chromate also were produced at the plant.
    The cohort consisted of 574 male employees from all three plants 
(Ex. 2-D-1). Eighty-five deaths were identified with follow up through 
December 1979. Six death certificates were not obtained. SMRs were 
reported based on U.S. white male death rates. There were 53 deaths 
from the New Jersey plant including a statistically significant SMR for 
cancer of the trachea, bronchus and lung based upon nine deaths (E=3.9; 
SMR=231; 95% CI: 106-438). One lung cancer decedent worked solely in 
the production of lead chromates. Three of the lung cancer deaths were 
black males. In addition, there were six deaths from digestive system 
cancers, five of which were stomach cancers reported at the New Jersey 
plant. The SMR for stomach cancer was statistically significantly 
elevated (O=5; E=0.63; SMR=792; 99% CI: 171-2243). There were 21 deaths 
from the West Virginia plant, three of which were cancer of the 
trachea, bronchus and lung (E=2.3; SMR=130; 95% CI: 27-381). There were 
11 deaths at the Kentucky plant, two of which were cancer of the 
trachea, bronchus and lung (E=0.9; SMR=216; 95% CI: 26-780).
    Sheffet et al. examined the lung cancer mortality among 1,946 male 
employees in a chromate pigment factory in Newark, NJ, who were exposed 
to both lead chromate and zinc chromate pigments (Ex. 7-48). The men 
worked for a minimum of one month between January 1, 1940 and December 
31, 1969. As of March 31, 1979, a total of 321 cohort members were 
identified as deceased (211 white males and 110 non-white males). Cause 
of death could not be ascertained for 37 white males and 12 non-white 
males. The proportion of the cohort lost to follow up was high (15% of 
white males and 20% of non-white males).
    Positions at the plant were classified into three categories 
according to intensity of exposure: high (continuous exposure to 
chemical dust), moderate (occasional exposure to chemical dust or to 
dry or wet pigments) and low (infrequent exposure by janitors or office 
workers). Positions were also classified by type of chemical exposure: 
chromates, other inorganic substances, and organics. The authors state 
that in almost all positions individuals "who were exposed to any 
chemicals were also exposed to hexavalent chromium in the form of 
airborne lead and zinc chromates (Ex. 7-48, p. 46)." The proportion of 
lead chromate to zinc chromate was approximately nine to one. 
Calculations, based upon air samples during later years, give an 
estimate for the study period of more than 2000 [mu]g airborne 
chromium/m\3\ for the high exposure category, between 500 and 2000 
[mu]g airborne chromium/m\3\ and less than 100 [mu]g airborne chromium/
m\3\ for the low exposure category. Other suspected carcinogens present 
in the workplace air at much lower levels were nickel sulfate and 
nickel carbonate.
    Because of the large proportion of workers lost to follow-up (15% 
of white males and 20% of non-white males) and the large numbers of 
unknown cause of death (21% of white males and 12% of non-white males), 
the authors calculated three separate mortality expectations based upon 
race-, gender-, age-, and time-specific U.S. mortality ratios. The 
first expectation was calculated upon the assumption that those lost to 
follow-up were alive at the end of the study follow-up period. The 
second expectation was calculated on the assumption that those whose 
vital status was unknown were lost to follow-up as of their employment 
termination date. The third expectation was calculated excluding those 
of unknown vital status from the cohort. Deaths with unknown cause were 
distributed in the appropriate proportions among known causes of death 
which served as an adjustment to the observed deaths. The adjusted 
deaths were used in all of the analyses.
    A statistically significant ratio for lung cancer deaths among 
white males (O/E=1.6) was observed when using the assumption that 
either the lost to follow-up were assumed lost as of their termination 
date or were excluded from the cohort (assumptions two and three 
above). The ratio for lung cancer deaths for non-white males results in 
an identical O/E of 1.6 for all three of the above scenarios, none of 
which was statistically significant.
    In addition, the authors also conducted Proportionate Mortality 
Ratio (PMR) and Proportionate Cancer Mortality Ratio (PCMR) analyses. 
For white males, the lung cancer PMR was 200 and the lung cancer PCMR 
was 160 based upon 25.5 adjusted observed deaths (21 actual deaths). 
Both were statistically significantly elevated at the p< .05 level. For 
non-white males, the lung cancer PMR was 200 and the lung cancer PCMR 
was 150 based upon 11.2 adjusted observed deaths (10 actual deaths). 
The lung cancer PMR for non-white males was statistically significantly 
elevated at the p< .05 level. Statistically significantly elevated PMRs 
and PCMRs for stomach cancer in white males were reported (PMR=280; 
PCMR=230) based upon 6.1 adjusted observed deaths (five actual).
    The Sheffet cohort was updated in a study by Hayes et al. (Ex. 7-
46). The follow up was through December 31, 1982. Workers employed as 
process operators or in other jobs which involved direct exposure to 
chromium dusts were classified as having exposure to chromates. Airborne 
chromium concentrations taken in "later years" were estimated to be 
>500 [mu]g g/m\3\ for "exposed" jobs and >2000 [mu]g/m\3\ for 
"highly exposed" jobs.
    The cohort included 1,181 white and 698 non-white males. Of the 453 
deaths identified by the end of the follow-up period, 41 were lung 
cancers. For the entire study group, no statistically significant 
excess was observed for lung cancer (SMR=116) or for cancer at any 
other site. Analysis by duration of employment found a statistically 
significant trend (p=.04) for lung cancer SMRs (67 for those employed 
< 1 year; 122 for those employed 1-9 years and 151 for those employed 
10+ years).
    Analysis of lung cancer deaths by duration of employment in 
chromate dust associated jobs found no elevation in risk for subjects 
who never worked in these jobs (SMR=92) or for subjects employed less 
than one year in these jobs (SMR=93). For those with cumulative 
employment of 1-9 and 10+ years in jobs with chromate dust exposure, 
the SMRs were 176 (nine deaths) and 194 (eight deaths) respectively.
    Frentzel-Beyme studied the mortality experience of 1,396 men 
employed for more than six months in one of five factories producing 
lead and zinc chromate pigments located in Germany and the Netherlands 
(Ex. 7-45). The observed deaths from the five factories were compared 
with the expected deaths calculated on the basis of mortality figures 
for the region in which the plant was located. Additional analysis was 
conducted on relevant cohorts which included workers with a minimum of 
10 years exposure, complete records for the entire staff, and exclusion 
of foreign nationals. Jobs were assigned into one of three exposure 
categories: High (drying and milling of the filtered pigment paste), 
medium (wet processes including precipitation of the pigment, filtering 
and maintenance, craftsmen and cleaning) and low or trivial exposure 
(storage, dispatch, laboratory personnel and supervisors).
    There were 117 deaths in the entire cohort of which 19 were lung 
cancer deaths (E=9.3). The lung cancer SMRs in the relevant cohort 
analyses were elevated at every plant; however, in only one instance 
was the increased lung cancer SMR statistically significant, based upon 
three deaths (SMR=386, p< 0.05). Analysis by type of exposure is not 
meaningful due to the small number of lung cancer deaths per plant per 
exposure classification.
    Kano et al. conducted a study of five Japanese manufacturers who 
produced lead chromates, zinc chromate, and/or strontium chromate to 
assess if there was an excess risk of lung cancer (Ex. 7-118). The 
cohort consisted of 666 workers employed for a minimum of one year 
between 1950 and 1975. At the end of 1989, 604 subjects were alive, 
five lost to follow-up and 57 dead. Three lung cancer deaths were 
observed in the cohort with 2.95 expected (SMR=102; 95% CI: 0.21-2.98). 
Eight stomach cancer deaths were reported with a non-statistically 
significant SMR of 120.
    Following the publication of the proposed rule, the Color Pigment 
Manufacturers Association requested that OSHA reconsider its 
preliminary conclusions with respect to the health effects of lead 
chromate color pigments (Ex. 38-205). They relied on the Davies (Ex. 7-
43), Cooper [Equitable Environmental Health, Inc] (Ex. 2-D-1) and Kano 
(Ex. 14-1-B) epidemiologic studies as the only available data on worker 
cohorts exposed to lead chromate in the absence of other chromates 
commonly found in pigment production (e.g., zinc chromate). The CPMA's 
comments regarding the Davies, Cooper and Kano studies and OSHA's 
response to them are discussed in section V.B.9.a.
3. Evidence from Workers in Chromium Plating
    Chrome plating is the process of depositing chromium metal onto the 
surface of an item using a solution of chromic acid. The items to be 
plated are suspended in a diluted chromic acid bath. A fine chromic 
acid mist is produced when gaseous bubbles, released by the 
dissociation of water, rise to the surface of the plating bath and 
burst. There are two types of chromium electroplating. Decorative or 
"bright" involves depositing a thin (0.5-1 [mu]m) layer of chromium 
over nickel or nickel-type coatings to provide protective, durable, 
non-tarnishable surface finishes. Decorative chrome plating is used for 
automobile and bicycle parts. Hard chromium plating produces a thicker 
(exceeding 5 [mu]m) coating which makes it resistant and solid where 
friction is usually greater, such as in crusher propellers and in 
camshafts for ship engines. Limited air monitoring indicates that 
Cr(VI) levels are five to ten times higher during hard plating than 
decorative plating (Ex. 35-116).
    There are fewer studies that have examined the lung cancer 
mortality of chrome platers than of soluble chromate production and 
chromate pigment production workers. The largest and best described 
cohort studies investigated chrome plating cohorts in the United 
Kingdom (Exs. 7-49; 7-57; 271; 35-62). They generally found elevated 
lung cancer mortality among the chrome platers, especially those 
engaged in chrome bath work, when compared to various reference 
populations. The studies of British chrome platers are summarized in 
Table V-3.
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BILLING CODE 4510-26-C
    Cohort studies of chrome platers in Italy, the United States, and 
Japan are also discussed in this subsection. Co-exposure to nickel, 
another suspected carcinogen, during plating operations can complicate 
evaluation of an association between Cr(VI) and an increased risk of 
lung cancer in chrome platers. Despite this, the International Agency 
for Research on Cancer concluded that the epidemiological
studies provide sufficient evidence for carcinogenicity of Cr(VI) as 
encountered in the chromium plating industry; the same conclusion 
reached for chromate production and chromate pigment production (Exs. 
18-1; 35-43). The findings implicate the highly water-soluble chromic 
acid as an occupational carcinogen. This adds to the weight of evidence 
that water-soluble (e.g., sodium chromates, chromic acid) and water-
insoluble forms (e.g., lead and zinc chromates) of Cr(VI) are able to 
cause cancer of the lower respiratory tract.
    Royle reported on a cohort mortality study of 1,238 chromium 
platers employed for a minimum of three consecutive months between 
February 20, 1969 and May 31, 1972 in 54 plating plants in West Riding, 
Yorkshire, England (Ex. 7-49). A control population was enumerated from 
other departments of the larger companies where chromium plating was 
only a portion of the companies' activities and from the former and 
current employees of two industrial companies in York where information 
on past workers was available. Controls were matched for gender, age 
(within two years) and date last known alive. In addition, 229 current 
workers were matched for smoking habits.
    As of May 1974, there were 142 deaths among the platers (130 males 
and 12 females) and 104 deaths among the controls (96 males and 8 
females). Among the male platers, there were 24 deaths from cancer of 
the lung and pleura compared to 13 deaths in the control group. The 
difference was not statistically significant. There were eight deaths 
from gastrointestinal cancer among male platers versus four deaths in 
the control group. The finding was not statistically significant.
    The Royle cohort was updated by Sorahan and Harrington (Ex. 35-62). 
Chrome plating was the primary activity at all 54 plants, however 49 of 
the plants used nickel and 18 used cadmium. Also used, but in smaller 
quantities according to the authors, were zinc, tin, copper, silver, 
gold, brass or rhodium. Lead was not used at any of the plants. Four 
plants, including one of the largest, only used chromium. Thirty-six 
chrome platers reported asbestos exposure versus 93 comparison workers.
    Industrial hygiene surveys were carried out at 42 plants during 
1969-1970. Area air samples were done at breathing zone height. With 
the exception of two plants, the chromic acid air levels were less than 
30 [mu]g/m\3\. The two exceptions were large plants, and in both the 
chromic acid levels exceeded 100 [mu]g/m\3\.
    The redefined cohort consisted of 1087 platers (920 men and 167 
women) from 54 plants employed for a minimum of three months between 
February 1969 and May 31, 1972 who were alive on May 31, 1972. 
Mortality data were also available for a comparison group of 1,163 
workers (989 men and 174 women) with no chromium exposure. Both groups 
were followed for vital status through 1997.
    The lung cancer SMR for male platers was statistically significant 
(O=60; E=32.5; SMR=185; 95% CI: 141-238). The lung cancer SMR for the 
comparison group, while elevated, was not statistically significant 
(O=47; E=36.9; SMR=127; 95% CI: 94-169). The only statistically 
significant SMR in the comparison group was for cancer of the pleura 
(O=7; E=0.57; SMR=1235; 95% CI: 497-2545).
    Internal regression analyses were conducted comparing the mortality 
rates of platers directly with those of the comparison workers. For 
these analyses, lung cancers mentioned anywhere on the death 
certificate were considered cases. The redefinition resulted in four 
additional lung cancer cases in the internal analyses. There was a 
statistically significant relative risk of 1.44 (p< 0.05) for lung 
cancer mortality among chrome platers that was slightly reduced to 1.39 
after adjustment for smoking habits and employment status. There was no 
clear trend between lung cancer mortality and duration of Cr(VI) 
exposure. However, any positive trend may have been obscured by the 
lack of information on worker employment post-1972 and the large 
variation in chromic acid levels among the different plants.
    Sorahan reported the experience of a cohort of 2,689 nickel/
chromium platers from the Midlands, U.K. employed for a minimum of six 
months between 1946 and 1975 and followed through December 1983 (Ex. 7-
57). There was a statistically significant lung cancer SMR for males 
(O=63; E=40; SMR=158; p< 0.001). The lung cancer SMR for women, while 
elevated (O=9; E=8.1; SMR=111), was not statistically significant. 
Other statistically significant cancer SMRs for males included: stomach 
(O=21; E=11.3; SMR=186; p< 0.05); liver (O=4; E=0.6; SMR=667; p< 0.01); 
and nasal cavities (O=2; E=0.2; SMR=1000; p< 0.05). While there were 
several elevated SMRs for women, none were statistically significant. 
There were nine lung cancers and one nasal cancer among the women.
    Analysis by type of first employment (i.e., chrome bath workers vs. 
other chrome work) resulted in a statistically significant SMR for lung 
cancer of 199 (O=46; E=23.1; p< 0.001) for chrome bath workers and a SMR 
of 101 for other chrome work. The SMR for cancer of the stomach for 
male chrome bath workers was also statistically significantly elevated 
(O=13; E=6.3; SMR=206; p< 0.05); for stomach cancer in males doing other 
chrome work, the SMR was 160 with 8 observed and 5 expected. Both of 
the nasal cancers in males and the one nasal cancer in women were 
chrome bath workers. The nasal cancer SMR for males was statistically 
significantly elevated (O=2; E=0.1; SMR=2000; p< 0.05).
    Regression analysis was used to examine evidence of association of 
several types of cancers and Cr(VI) exposure duration among the cohort. 
There was a significant positive association between lung cancer 
mortality and exposure duration as a chrome bath worker controlling for 
gender as well as year and age at the start of employment. There was no 
evidence of an association between other cancer types and duration of 
Cr(VI) exposure. There was no positive association between duration of 
exposure to nickel bath work and cancer of the lung. The two largest 
reported SMRs were for chrome bath workers 10-14 years (O=13; E=3.8; 
SMR=342; p< 0.001) and 15-19 years (O=12; E=4.9; SMR=245; p< 0.01) after 
starting employment. The positive associations between lung cancer 
mortality and duration of chrome bath work suggests Cr(VI) exposure may 
be responsible for the excess cancer risk.
    Sorahan et al. reported the results of a follow-up to the nickel/
chromium platers study discussed above (Ex. 271). The cohort was 
redefined and excluded employees whose personnel records could not be 
located (650); those who started chrome work prior to 1946 (31) and 
those having no chrome exposure (236). The vital status experience of 
1,762 workers (812 men and 950 women) was followed through 1995. The 
expected number of deaths was based upon the mortality of the general 
population of England and Wales.
    There were 421 deaths among the men and 269 deaths among the women, 
including 52 lung cancers among the men and 17 among the women. SMRs 
were calculated for different categories of chrome work: Period from 
first chrome work; year of starting chrome work, and cumulative 
duration of chrome work categories. Poison regression modeling was 
employed to investigate lung cancer in relation to type of chrome work 
and cumulative duration of work.
    A significantly elevated lung cancer SMR was seen for male workers 
with some period of chrome bath work (O=40; E=25.4; SMR=157; 95% CI: 113-
214, p< 0.01). Lung cancer was not elevated among male workers engaged 
in other chrome work away from the chromic acid bath (O=9; E=13.7; 
SMR=66; 95% CI: 30-125). Similar lung cancer mortality results were 
found for female chrome bath workers (O=15; E=8.6; SMR=175; 95% CI: 98-
285; p< 0.06). After adjusting for sex, age, calendar year, year 
starting chrome work, period from first chrome work, and employment 
status, regression modeling showed a statistically significant positive 
trend (p< 0.05) between duration of chrome bath work and lung cancer 
mortality risk. The relative lung cancer risk for chrome bath workers 
with more than five years of Cr(VI) exposure (i.e., relative to the 
risk of those without any chrome bath work) was 4.25 (95% CI: 1.83-
9.37).
    Since the Sorahan cohort consists of nickel/chromium workers, the 
question arises of the potential confounding of nickel. In the earlier 
study, 144 of the 564 employees with some period of chrome bath work 
had either separate or simultaneous periods of nickel bath employment. 
According to the authors, there was no clear association between cancer 
deaths from stomach, liver, respiratory system, nose and larynx, and 
lung and bronchus and the duration of nickel bath employment. In the 
follow-up report, the authors re-iterate this result stating, 
"findings for lung cancer in a cohort of nickel platers (without any 
exposure to chrome plating) from the same factory are unexceptional" 
(Ex. 35-271, p. 241).
    Silverstein et al. reported the results of a cohort study of hourly 
employees and retirees with at least 10 years of credited pension 
service in a Midwestern plant manufacturing hardware and trim 
components for use primarily in the automobile industry (Ex. 7-55). Two 
hundred thirty eight deaths occurred between January 1, 1974 and 
December 31, 1978. Proportional Mortality Ratio (PMR) analysis adjusted 
for race, gender, age and year of death was conducted. For white males, 
the PMR for cancer of the lung and pleura was 1.91 (p< 0.001) based upon 
28 deaths. For white females, the PMR for cancer of the lung and pleura 
was 3.70 (p< 0.001) based upon 10 deaths.
    White males who worked at the plant for less than 15 years had a 
lung cancer PMR of 1.65. Those with 15 or more years at the plant had a 
lung cancer PMR of 2.09 (p< 0.001). For white males with less than 22.5 
years between hire and death (latency) the lung cancer PMR was 1.78 
(p< 0.05) and for those with 22.5 or more years, the PMR was 2.11 
(p< 0.01).
    A case-control analysis was conducted on the Silverstein cohort to 
examine the association of lung cancer risk with work experience. 
Controls were drawn from cardiovascular disease deaths (ICD 390-458, 
8th revision). The 38 lung cancer deaths were matched to controls for 
race and gender. Odds ratios (ORs) were calculated by department 
depending upon the amount of time spent in the department (ever/never; 
more vs. less than one year; and more vs. less than five years). Three 
departments showed increasing odds ratios with duration of work; 
however, the only statistically significant result was for those who 
worked more than five years in department 5 (OR=9.17, p=0.04, Fisher's 
exact test). Department 5 was one of the major die-casting and plating 
areas of the plant prior to 1971.
    Franchini et al. conducted a mortality study of employees and 
retirees from nine chrome plating plants in Parma, Italy (Ex. 7-56). 
Three plants produced hard chrome plating. The remaining six plants 
produced decorative chromium plates. A limited number of airborne 
chromium measurements were available. Out of a total of 10 measurements 
at the hard chrome plating plants, the air concentrations of chromium 
averaged 7 [mu]g/m\3\ (range of 1-50 [mu]g/m\3\) as chromic acid near 
the baths and 3 [mu]g/m\3\ (range of 0-12 [mu]g/m\3\) in the middle of 
the room.
    The cohort consisted of 178 males (116 from the hard chromium 
plating plants and 62 from the bright chromium plating plants) who had 
worked for at least one year between January 1, 1951 and December 31, 
1981. In order to allow for a 10-year latency period, only those 
employed before January 1972 were included in further analysis. There 
were three observed lung cancer deaths among workers in the hard chrome 
plating plants, which was significantly greater than expected (O=3; 
E=0.6; p< 0.05). There were no lung cancer deaths among decorative 
chrome platers.
    Okubo and Tsuchiya conducted a study of plating firms with five or 
more employees in Tokyo (Exs. 7-51; 7-52). Five hundred and eighty nine 
firms were sent questionnaires to ascertain information regarding 
chromium plating experience. The response rate was 70.5%. Five thousand 
one hundred seventy platers (3,395 males and 1,775 females) met the 
cohort entrance criteria and were followed from April 1, 1970 to 
September 30, 1976. There were 186 deaths among the cohort; 230 people 
were lost to follow-up after retirement. The cohort was divided into 
two groups: Chromium platers who worked six months or more and a 
control group with no exposure to chromium (clerical, unskilled 
workers). There were no deaths from lung cancer among the chromium 
platers.
    The Okubo cohort was updated by Takahashi and Okubo (Ex. 265). The 
cohort was redefined to consist of 1,193 male platers employed for a 
minimum of six months between April 1970 and September 1976 in one of 
415 Tokyo chrome plating plants and who were alive and over 35 years of 
age on September 30, 1976. The only statistically significant SMR was 
for lung cancer for all platers combined (O=16; E=8.9; SMR=179; 95% CI: 
102-290). The lung cancer SMR for the chromium plater subcohort was 187 
based upon eight deaths and 172 for the nonchromium plater subcohort, 
also based upon eight deaths. The cohort was followed through 1987. 
Itoh et al. updated the Okubo metal plating cohort through December 
1992 (Ex. 35-163). They reported a lung cancer SMR of 118 (95% CI: 99-
304).
4. Evidence From Stainless Steel Welders
    Welding is a term used to describe the process for joining any 
materials by fusion. The fumes and gases associated with the welding 
process can cause a wide range of respiratory exposures which may lead 
to an increased risk of lung cancer. The major classes of metals most 
often welded include mild steel, stainless and high alloy steels and 
aluminum. The fumes from stainless steel, unlike fumes from mild steel, 
contain nickel and Cr(VI). There are several cohort and case-control 
studies as well as two meta analyses of welders potentially exposed to 
Cr(VI). In general, the studies found an excess number of lung cancer 
deaths among stainless steel welders. However, few of the studies found 
clear trends with Cr(VI) exposure duration or cumulative Cr(VI). In 
most studies, the reported excess lung cancer mortality among stainless 
steel welders was no greater than mild steel welders, even though 
Cr(VI) exposure is much greater during stainless steel welding. This 
weak association between lung cancer and indices of exposure limits the 
evidence provided by these studies. Other limitations include the co-
exposures to other potential lung carcinogens, such as nickel, 
asbestos, and cigarette smoke, as well as possible healthy worker 
effects and exposure misclassification in some studies, which may 
obscure a relationship betweeen Cr(VI) and lung cancer risk. These 
limitations are discussed further in sections VI.B.5, VI.E.3, and 
VI.G.4.
Nevertheless, these studies add some further support to the much 
stronger link between Cr(VI) and lung cancer found in soluble chromate 
production workers, chromate pigment production workers, and chrome 
platers. The key studies are summarized in Table V-4.
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BILLING CODE 4510-26-C
    Sjogren et al. reported on the mortality experience in two cohorts 
of welders (Ex. 7-95). The cohort characterized as "high exposure"
consisted of 234 male stainless steel welders with a minimum of 5 years 
of employment between 1950 and 1965. An additional criterion for 
inclusion in the study was assurance from the employer that asbestos 
had not been used or had been used only occasionally and never in a 
dust-generating way. The cohort characterized as "low exposure" 
consisted of 208 male railway track welders working at the Swedish 
State Railways for at least 5 years between 1950 and 1965. In 1975, air 
pollution in stainless steel welding was surveyed in Sweden. The median 
time weighted average (TWA) value for Cr(VI) was 110 [mu]g 
CrO3/m\3\ (57 [mu]g/m\3\ measured as CrVI). The highest 
concentration was 750 [mu]g CrO3/m\3\ (390 [mu]g/m\3\ 
measured as CrVI) found in welding involving coated electrodes. For 
gas-shielded welding, the median Cr(VI) concentration was 10 [mu]g 
CrO3/m\3\ (5.2 [mu]g/m\3\ measured as CrVI) with the highest 
concentration measured at 440 [mu]g CrO3/m\3\ (229 [mu]g/
m\3\ measured as CrVI). Follow-up for both cohorts was through December 
1984. The expected number of deaths was based upon Swedish male death 
rates. Of the 32 deaths in the "high exposure" group, five were 
cancers of the trachea, bronchus and lung (E=2.0; SMR=249; 95% CI: 
0.80-5.81). In the low exposure group, 47 deaths occurred, one from 
cancer of the trachea, bronchus and lung.
    Polednak compiled a cohort of 1,340 white male welders who worked 
at the Oak Ridge nuclear facilities from 1943 to 1977 (Ex. 277). One 
thousand fifty-nine cohort members were followed through 1974. The 
cohort was divided into two groups. The first group included 536 
welders at a facility where nickel-alloy pipes were welded; the second 
group included 523 welders of mild steel, stainless steel and aluminum 
materials. Smoking data were available for 33.6% of the total cohort. 
Expectations were calculated based upon U.S. mortality rates for white 
males. There were 17 lung cancer deaths in the total cohort (E=11.37; 
SMR=150; 95% CI: 87-240). Seven of the lung cancer deaths occurred in 
the group which routinely welded nickel-alloy materials (E=5.65; 
SMR=124; 95% CI: 50-255) versus 10 lung cancer deaths in the "other" 
welders (E=6.12; SMR=163; 95% CI: 78-300).
    Becker et al. compiled a cohort of 1,213 stainless steel welders 
and 1,688 turners from 25 German metal processing factories who had a 
minimum of 6 months employment during the period 1950-1970 (Exs. 227; 
250; 251). The data collected included the primary type of welding 
(e.g., arc welding, gas-shielded welding, etc.) used by each person, 
working conditions, average daily welding time and smoking status. The 
most recent follow-up of the cohort was through 1995. Expected numbers 
were developed using German mortality data. There were 268 deaths among 
the welders and 446 deaths among the turners. An elevated, but non-
statistically significant, lung cancer SMR (O=28; E=23; SMR=121.5; 95% 
CI: 80.7-175.6) was observed among the welders. There were 38 lung 
cancer deaths among the turners with 38.6 expected, resulting in a SMR 
slightly below unity. Seven deaths from cancer of the pleura (all 
mesotheliomas) occurred among the welders with only 0.6 expected 
(SMR=1,179.9; 95% CI: 473.1-2,430.5), compared to only one death from 
cancer of the pleura among the turners, suggesting that the welders had 
exposure to asbestos. Epidemiological studies have shown that asbestos 
exposure is a primary cause of pleural mesotheliomas.
    The International Agency for Research on Cancer (IARC) and the 
World Health Organization (WHO) cosponsored a study on welders. IARC 
and WHO compiled a cohort of 11,092 male welders from 135 companies in 
nine European countries to investigate the relationship between the 
different types of exposure occurring in stainless steel, mild steel 
and shipyard welding and various cancer sites, especially lung cancer 
(Ex. 7-114). Cohort entrance criteria varied by country. The expected 
number of deaths was compiled using national mortality rates from the 
WHO mortality data bank.
    Results indicated the lung cancer deaths were statistically 
significant in the total cohort (116 cases; E=86.81; SMR=134; 95% CI: 
110-160). Cohort members were assigned to one of four subcohorts based 
upon type of welding activity. While the lung cancer SMRs were elevated 
for all of the subcohorts, the only statistically significant SMR was 
for the mild steel-only welders (O=40; E=22.42; SMR=178; 95% CI: 127-
243). Results for the other subgroups were: shipyard welders (O=36; 
E=28.62; SMR=126; 95% CI: 88-174); ever stainless steel welders (O=39; 
E=30.52; SMR=128; 95% CI: 91-175); and predominantly stainless steel 
welders (O=20; E=16.25; SMR=123; 95% CI: 75-190). When analyzed by 
subcohort and time since first exposure, the SMRs increased over time 
for every group except shipyard welders. For the predominantly 
stainless steel welder subcohort, the trend to increase with time was 
statistically significant (p < .05).
    An analysis was conducted of lung cancer mortality in two stainless 
steel welder subgroups (predominantly and ever) with a minimum of 5 
years of employment. Cumulative Cr(VI) was computed from start of 
exposure until 20 years prior to death. A lung cancer SMR of 170, based 
upon 14 cases, was observed in the stainless steel ever subgroup for 
those welders with >=0.5 mg-years/m\3\ Cr(VI) exposure; the lung cancer 
SMR for those in the < 0.5 mg-years/m\3\ Cr(VI) exposure group was 123 
(based upon seven cases). Neither SMR was statistically significant. 
For the predominantly stainless steel welders, which is a subset of the 
stainless steel ever subgroup, the corresponding SMRs were 167 (>=0.5 
mg-years/m\3\ Cr(VI) exposure) based upon nine cases and 191 (< 0.5 mg-
years/m\3\ Cr(VI) exposure) based upon three cases. Neither SMR was 
statistically significant.
    In conjunction with the IARC/WHO welders study, Gerin et al. 
reported the development of a welding process exposure matrix relating 
13 combinations of welding processes and base metals used to average 
exposure levels for total welding fumes, total chromium, Cr(VI) and 
nickel (Ex. 7-120). Quantitative estimates were derived from the 
literature supplemented by limited monitoring data taken in the 1970s 
from only 8 of the 135 companies in the IARC/WHO mortality study. An 
exposure history was constructed which included hire and termination 
dates, the base metal welded (stainless steel or mild steel), the 
welding process used and changes in exposure over time. When a detailed 
welding history was not available for an individual, the average 
company welding practice profile was used. In addition, descriptions of 
activities, work force, welding processes and parameters, base metals 
welded, types of electrodes or rods, types of confinement and presence 
of local exhaust ventilation were obtained from the companies.
    Cumulative dose estimates in mg/m\3\ years were generated for each 
welder's profile (number of years and proportion of time in each 
welding situation) by applying a welding process exposure matrix 
associating average concentrations of welding fumes (mg/m\3\) to each 
welding situation. The corresponding exposure level was multiplied by 
length of employment and summed over the various employment periods 
involving different welding situations. No dose response relationship 
was seen for exposure to Cr(VI) for either those who were "ever 
stainless steel welders" or those who were "predominantly stainless 
steel welders". The authors note that if their exposure estimates are 
correct, the study had the power to detect a significant result in the 
high exposure group for Cr(VI). However, OSHA believes that there is 
likely to be substantial exposure misclassification in this study, as 
discussed further in section VI.G.4.
    The IARC/WHO multicenter study is the sole attempt to undertake 
even a semi-quantified exposure analysis of stainless steel welders' 
potential exposure to nickel and Cr(VI) for <5 and >=0.5 mg-years/
m3 Cr(VI) exposures. The IARC/WHO investigators noted that 
there was more than a twofold increase in SMRs between the long (>=20 
years since first exposure) and short (< 20 years since first exposure) 
observation groups for the predominantly stainless steel welders 
"suggesting a relation of lung cancer mortality with the occupational 
environment for this group" (Ex. 7-114, p. 152). The authors conclude 
that the increase in lung cancer mortality does not appear to be 
related to either duration of exposure or cumulative exposure to total 
fume, chromium, Cr(VI) or nickel.
    Moulin compiled a cohort of 2,721 French male welders and an 
internal comparison group of 6,683 manual workers employed in 13 
factories (including three shipyards) with a minimum of one year of 
employment from 1975 to 1988 (Ex. 7-92). Three controls were selected 
at random for each welder. Smoking data were abstracted from medical 
records for 86.6% of welders and 86.5% of the controls. Smoking data 
were incorporated in the lung cancer mortality analysis using methods 
suggested by Axelson. Two hundred and three deaths were observed in the 
welders and 527 in the comparison group. A non-statistically 
significant increase was observed in the lung cancer SMR (O=19; 
E=15.33; SMR=124; 95% CI: 0.75-1.94) for the welders. In the control 
group, the lung cancer SMR was in deficit (O=44; E=46.72; SMR=94; 95% 
CI: 0.68-1.26). The resulting relative risk was a non-significant 1.3. 
There were three deaths from pleural cancer in the comparison group and 
none in the welders, suggesting asbestos exposure in the comparison 
group. The welders were divided into four subgroups (shipyard welders, 
mild steel only welders, ever stainless steel welders and stainless 
steel predominantly Cr(VI) welders). The highest lung cancer SMR was 
for the mild steel welders O=9; SMR of 159). The lowest lung cancer 
SMRs were for ever stainless steel welders (O=3; SMR= 92) and for 
stainless steel predominantly Cr(VI) welders (O=2; SMR= 103). None of 
the SMRs are statistically significant.
    Hansen conducted a study of cancer incidence among 10,059 male 
welders, stainless steel grinders and other metal workers from 79 
Danish companies (Ex. 9-129). Cohort entrance criteria included: alive 
on April 1, 1968; born before January 1, 1965; and employed for at 
least 12 months between April 1, 1964 and December 31, 1984. Vital 
status follow-up found 9,114 subjects alive, 812 dead and 133 
emigrated. A questionnaire was sent to subjects and proxies for 
decedents/emigrants in an attempt to obtain information about lifetime 
occupational exposure, smoking and drinking habits. The overall 
response rate was 83%. The authors stated that no major differences in 
smoking habits were found between exposure groups with or without a 
significant excess of lung cancer.
    The expected number of cancers was based on age-adjusted national 
cancer incidence rates from the Danish Cancer Registry. There were 
statistically significantly elevated Standardized Incidence Ratios 
(SIRs) for lung cancer in the welding (any kind) group (O=51; E=36.84; 
SIR=138; 95% CI: 103-181) and in the mild steel only welders (O=28; 
E=17.42; SIR=161; 95% CI: 107-233). The lung cancer SIR for mild steel 
ever welders was 132 (O=46; E=34.75; 95% CI: 97-176); for stainless 
steel ever welders 119 (O=23; E=19.39; 95% CI: 75-179) and for 
stainless steel only welders 238 (O=5; E=2.10; 95% CI: 77-555).
    Laurtitsen reported the results of a nested case-control conducted 
in conjunction with the Hansen cancer incidence study discussed above 
(Exs. 35-291; 9-129). Cases were defined as the 94 lung cancer deaths. 
Controls were defined as anyone who was not a case, but excluded deaths 
from respiratory diseases other than lung cancer (either as an 
underlying or a contributing cause of death), deaths from "unknown 
malignancies" and decedents who were younger than the youngest case. 
There were 439 decedents eligible for use as controls.
    The crude odds ratio (OR) for welding ever (yes/no) was 1.7 (95% 
CI: 1.0-2.8). The crude OR for mild steel welding only was 1.3 (95% CI: 
0.8-2.3) and for stainless steel welding only the crude OR was 1.3 (95% 
CI: 0.3-4.3). When analyzed by number of years exposed, "ever" 
stainless steel welding showed no relationship with increasing number 
of years exposed. The highest odds ratio (2.9) was in the lowest 
category (1-5 years) based upon seven deaths; the lowest odds ratio was 
in the highest category (21+ years) based upon three deaths.
    Kjuus et al. conducted a hospital-based case-control study of 176 
male incident lung cancer cases and 186 controls (matched for age, +/-5 
years) admitted to two county hospitals in southeast Norway during 
1979-1983 (Ex. 7-72). Subjects were classified according to exposure 
status of main occupation and number of years in each exposure category 
and assigned into one of three exposure groups according to potential 
exposure to respiratory carcinogens and other contaminants. A 
statistically significantly elevated risk ratio for lung cancer 
(adjusted for smoking) for the exposure factor "welding, stainless, 
acid proof" of 3.3 (p< 0.05) was observed based upon 16 lung cancer 
deaths. The unadjusted odds ratio is not statistically significant 
(OR=2.8). However, the appropriateness of the analysis is questionable 
since the exposure factors are not discrete (a case or a control may 
appear in multiple exposure factors and therefore is being compared to 
himself). In addition, the authors note that several exposure factors 
were highly correlated and point out specifically that one-half of the 
cases "exposed to either stainless steel welding fumes or fertilizers 
also reported moderate to heavy asbestos exposure." When put into a 
stepwise logistic regression model, exposure to stainless steel fumes, 
which was initially statistically significant, loses its significance 
when smoking and asbestos are first entered into the model.
    Hull et al. conducted a case-control study of lung cancer in white 
male welders aged 20-65 identified through the Los Angeles County tumor 
registry (Southern California Cancer Surveillance Program) for the 
period 1972 to 1987 (Ex. 35-243). Controls were welders 40 years of age 
or older with non-pulmonary malignancies. Interviews were conducted to 
obtain information about sociodemographic data, smoking history, 
employment history and occupational exposures to specific welding 
processes, metals welded, asbestos and confined space welding. 
Interviews were completed for 90 (70%) of the 128 lung cancer cases and 
116 (66%) of the controls. Analysis was conducted using 85 deceased 
cases and 74 deceased controls after determining that the subject's 
vital status influenced responses to questions concerning occupational 
exposures. The crude odds ratio (ever vs. never exposed) for stainless 
steel welding, based upon 34 cases, was 0.9 (95% CI: 0.3-1.4). For 
manual metal arc welding on stainless steel, the crude odds ratio
was 1.3 (95% CI: 0.6-2.3) based upon 61 cases.
    While the relative risk estimates in both cohort and case-control 
of stainless steel welders are elevated, none are statistically 
significant. However, when combined in two meta-analyses, a small but 
statistically significant increase in lung cancer risk was reported. 
Two meta-analyses of welders have been published. Moulin carried out a 
meta-analysis of epidemiologic studies of lung cancer risk among 
welders, taking into account the role of asbestos and smoking (Ex. 35-
285). Studies published between 1954 and 1994 were reviewed. The 
inclusion criteria were clearly defined: only the most recent updates 
of cohort studies were used and only the mortality data from mortality/
morbidity studies were included. Studies that did not provide the 
information required by the meta-analysis were excluded.
    Five welding categories were defined (shipyard welding, non-
shipyard welding, mild steel welding, stainless steel welding and all 
or unspecified welding). The studies were assigned to a welding 
category (or categories) based upon the descriptions provided in the 
paper's study design section. The combined relative risks (odds ratios, 
standardized mortality ratios, proportionate mortality ratios and 
standardized incidence ratios) were calculated separately for the 
population-based studies, case-control studies, and cohort studies, and 
for all the studies combined.
    Three case-control studies (Exs. 35-243; 7-120; 7-72) and two 
cohort studies (Exs. 7-114; 35-277) were included in the stainless 
steel welding portion of the meta-analysis. The combined relative risk 
was 2.00 (O=87; 95% CI: 1.22-3.28) for the case-control studies and 
1.23 (O=27; 95% CI: 0.82-1.85) for the cohort studies. When all five 
studies were combined, the relative risk was 1.50 (O=114; 95% CI: 1.10-
2.05).
    By contrast, the combined risk ratio for the case-control studies 
of mild steel welders was 1.56 (O=58; 95% CI: 0.82-2.99) (Exs. 7-120; 
35-243). For the cohort studies, the risk ratio was 1.49 (O=79; 95% CI: 
1.15-1.93) (Exs. 35-270; 7-114). For the four studies combined, the 
risk ratio was 1.50 (O=137; 95% CI: 1.18-191). The results for the 
stainless steel welders and the mild steel welders are basically the 
same.
    The meta-analysis by Sjogren of exposure to stainless steel welding 
fumes and lung cancer included studies published between 1984 and 1993, 
which took smoking and potential asbestos exposure into account (Ex. 7-
113). Five studies met the author's inclusion criteria and were 
included in the meta-analysis: two cohort studies, Moulin et al. (Ex. 
35-283) and Sjogren et al. (Ex. 7-95); and three case-control studies, 
Gerin, et al. (Ex. 7-120, Hansen et al. (Ex. 9-129) and Kjuus et al. 
(Ex. 7-72). The calculated pooled relative risk for welders exposed to 
stainless steel welding fumes was 1.94 (95% CI: 1.28-2.93).
5. Evidence from Ferrochromium Workers
    Ferrochromium is produced by the electrothermal reduction of 
chromite ore with coke in the presence of iron in electric furnaces. 
Some of the chromite ore is oxidized into Cr(VI) during the process. 
However, most of the ore is reduced to chrome metal. The manufacture of 
ferroalloys results in a complex mixture of particles, fumes and 
chemicals including nickel, Cr(III) and Cr(VI). Polycyclic aromatic 
hydrocarbons (PAH) are released during the manufacturing process. The 
co-exposure to other potential lung carcinogens combined with the lack 
of a statistically significant elevation in lung cancer mortality among 
ferrochromium workers were limitations in the key studies. 
Nevertheless, the observed increase in the relative risks of lung 
cancer add some further support to the much stronger link between 
Cr(VI) and lung cancer found in soluble chromate production workers, 
chromate pigment production workers, and chrome platers. The key 
studies are summarized in Table V-5.
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    Langard et al. conducted a cohort study of male workers producing 
ferrosilicon and ferrochromium for more than one year between 1928 and 
1977 at a plant located on the west coast of Norway (Exs. 7-34; 7-37). The 
cohort and study findings are summarized in Table V.5. Excluded from 
the study were workers who died before January 1, 1953 or had an 
unknown date of birth. The cohort was defined in the 1980 study as 976 
male employees who worked for a minimum of one year prior to January 1, 
1960. In the 1990 study, the cohort definition was expanded to include 
those hired up to 1965.
    Production of ferrosilicon at the plant began in 1928 and 
ferrochromium production began in 1932. Job characterizations were 
compiled by combining information from company personnel lists and 
occupational histories contained in medical records and supplemented 
with information obtained via interview with long-term employees. Ten 
occupational categories were defined. Workers were assigned to an 
occupational category based upon the longest time in a given category.
    Industrial hygiene studies of the plant from 1975 indicated that 
both Cr(III) and Cr(VI) were present in the working environment. The 
ferrochromium furnance operators were exposed to measurements of 0.04-
0.29 mg/m3 of total chromium. At the charge floor the mean 
concentration of total chromium was 0.05 mg/m3, 11-33% of 
which was water soluble. The water soluble chromium was considered to 
be in the hexavalent state.
    Both observed and expected cases of cancer were obtained via the 
Norwegian Cancer Registry. The observation period for cancer incidence 
was January 1, 1953 to December 31, 1985. Seventeen incident lung 
cancers were reported in the 1990 study (E=19.4; SIR=88). A deficit of 
lung cancer incidence was observed in the ferrosilicon group (O=2; 
E=5.8; SIR=35). In the ferrochromium group there were a significant 
excess of lung cancer; 10 observed lung cancers with 6.5 expected 
(SIR=154).
    Axelsson et al. conducted a study of 1,932 ferrochromium workers to 
examine whether exposure in the ferrochromium industry could be 
associated with an increased risk of developing tumors, especially lung 
cancer (Ex. 7-62). The study cohort and findings are summarized in 
Table V.5. The study cohort was defined as males employed at a 
ferrochromium plant in Sweden for at least one year during the period 
January 1, 1930 to December 31, 1975.
    The different working sites within the industry were classified 
into four groups with respect to exposure to Cr(VI) and Cr(III). 
Exposure was primarily to metallic and trivalent chromium with 
estimated levels ranging from 0-2.5 mg/m3. Cr(VI) was also 
present in certain operations with estimated levels ranging from 0-0.25 
mg/m3. The highest exposure to Cr(VI) was in the arc-furnace 
operations. Cr(VI) exposure also occurred in a chromate reduction 
process during chromium alum production from 1950-1956. Asbestos-
containing materials had been used in the plant. Cohort members were 
classified according to length and place of work in the plant.
    Death certificates were obtained and coded to the revision of the 
International Classification of Diseases in effect at the time of 
death. Data on cancer incidence were obtained from the Swedish National 
Cancer Registry. Causes of death in the cohort for the period 1951-1975 
were compared with causes of death for the age-adjusted male population 
in the county in which the plant was located.
    There were seven cases of cancers of the trachea, bronchus and lung 
and the pleura with 5.9 expected (SIR=119) for the period 1958-1975. 
Four of the seven cases in the lung cancer group were maintenance 
workers and two of the four cases were pleural mesotheliomas. In the 
arc furnace group, which was thought to have the highest potential 
exposure to both Cr(III) and Cr(VI), there were two cancers of the 
trachea, bronchus and lung and the pleura. One of the cases was a 
mesothelioma. Of the 380 deaths that occurred during the period 1951-
1975, five were from cancer of the trachea, bronchus and lung and the 
pleura (E=7.2; SMR=70). For the "highly" exposed furnace workers, 
there was one death from cancer of the trachea, bronchus and lung and 
the pleura.
    Moulin et al. conducted a cohort mortality study in a French 
ferrochromium/stainless steel plant to determine if exposure to 
chromium compounds, nickel compounds and polycyclic aromatic 
hydrocarbons (PAHs) results in an increased risk of lung cancer (Ex. 
282). The cohort was defined as men employed for at least one year 
between January 1, 1952 and December 31, 1982; 2,269 men met the cohort 
entrance criteria. No quantitative exposure data were available and no 
information on the relative amounts of Cr(VI) and Cr(III) was provided. 
In addition, some workers were also exposed to other carcinogens, such 
as silica and asbestos. The authors estimated that 75.7% of the cohort 
had been exposed to combinations of PAH, nickel and chromium compounds. 
Of the 137 deaths identified, the authors determined 12 were due to 
cancer of the trachea, bronchus and lung (E=8.56; SMR=140; 95% CI: 
0.72-2.45). Eleven of the 12 lung cancers were in workers employed for 
at least one year in the ferrochromium or stainless steel production 
workshops (E=5.4; SMR=204; 95% CI: 1.02-3.64).
    Pokrovskaya and Shabynina conducted a cohort mortality study of 
male and female workers employed "some time" between 1955 and 1969 at 
a chromium ferroalloy production plant in the U.S.S.R (Ex. 7-61). 
Workers were exposed to both Cr(III) and Cr(VI) as well as to benzo [a] 
pyrene. Neither the number of workers nor the number of cancer deaths 
by site were provided. Death certificates were obtained and the deaths 
were compared with municipal mortality rates by gender and 10 year age 
groups. The investigators state that they were able to exclude those in 
the comparison group who had chromium exposures in other industries. 
The lung cancer SMR for male chromium ferroalloy workers was 440 in the 
30-39 year old age group and 660 in the 50-59 year old age group 
(p=0.001). There were no lung cancer deaths in the 40-49 and the 60-69 
year old age groups. The data suggest that these ferrochromium workers 
may have been had an excess risk of lung cancer.
    The association between Cr(VI) exposure in ferrochromium workers 
and the incidence of respiratory tract cancer these studies is 
difficult to assess because of co-exposures to other potential 
carcinogens (e.g., asbestos, PAHs, nickel, etc.), absence of a clear 
exposure-response relationship and lack of information on smoking. 
There is suggestive evidence of excess lung cancer mortality among 
Cr(VI)-exposed ferrochromium workers in the Norwegian (Langard) cohort 
when compared to a similar unexposed cohort of ferrosilicon workers. 
However, there is little consistency for this finding in the Swedish 
(Axelsson) or French (Moulin) cohorts.
6. Evidence From Workers in Other Industry Sectors
    There are several other epidemiological studies that do not fit 
into the five industry sectors previously reviewed. These include 
worker cohorts in the aerospace industry, paint manufacture, and 
leather tanning operations, among others. The two cohorts of aircraft 
manufacturing workers are summarized in Table V-6. All of the cohorts 
had some Cr(VI) exposure, but certain cohorts may have included a 
sizable number of workers with little or no exposure to Cr(VI). This 
creates an additional complexity in assessing whether the study 
findings support a Cr(VI) etiology for cancer of the respiratory system.
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    Alexander et al. conducted a cohort study of 2,429 aerospace 
workers with a minimum of six months of cumulative employment in jobs 
involving chromate exposure during the period 1974 through 1994 (Ex. 31-16-3). 
Exposure estimates were based on industrial hygiene measurements and work 
history records. Jobs were classified into categories of "high" 
(spray painters, decorative painters), "moderate" (sanders/maskers, 
maintenance painters) and "low" (chrome platers, surface processors, 
tank tenders, polishers, paint mixers) exposure. Each exposure category 
was assigned a summary TWA exposure based upon the weighted TWAs and 
information from industrial hygienists. The use of respiratory 
protection was accounted for in setting up the job exposure matrix. The 
index of cumulative total chromium exposure (reported as [mu]g/m\3\ 
chromate TWA-years) was computed by multiplying the years in each job 
by the summary TWAs for each exposure category.
    In addition to cumulative chromate exposure, chromate exposure jobs 
were classified according to the species of chromate. According to the 
authors, in painting operations the exposure is to chromate pigments 
with moderate and low solubility such as zinc chromate, strontium 
chromate and lead chromate; in sanding and polishing operations the 
same chromate pigments exist as dust; while platers and tank tenders 
are exposed to chromium trioxide, which is highly soluble.
    Approximately 26% of the cohort was lost to follow-up. Follow-up on 
the cohort was short (average 8.9 years per cohort member). Cases were 
identified through the Cancer Surveillance System (CSS) at the Fred 
Hutchinson Cancer Research Center in Seattle, Washington. CSS records 
primary cancer diagnoses in 13 counties in western Washington. Expected 
numbers were calculated using race-, gender-, age- and calendar-
specific rates from the Puget Sound reference population for 1974 
through 1994. Fifteen lung cancer cases were identified with an overall 
standardized incidence ratio (SIR) of 80 (95% CI: 0.4-1.3). The SIRs 
for lung cancer by cumulative years of employment in the "high 
exposure" painting job category were based upon only three deaths in 
each of the cumulative years categories (<5 and >=5); years of 
employment was inversely related to the risk of lung cancer. For those 
in the "low exposure" category, the SIRs were 130 for those who 
worked less than five years in that category (95% CI: 0.2-4.8) and 190 
for those who worked five years or more (95% CI: 0.2-6.9). However, 
there were only two deaths in each category. The SIR for those who 
worked >=5 years was 270 (95% CI: 0.5-7.8), but based only on three 
deaths.
    Boice et al. conducted a cohort mortality study of 77,965 workers 
employed for a minimum of one year on or after January 1960 in aircraft 
manufacturing (Ex. 31-16-4). Routine exposures to Cr(VI) compounds 
occurred primarily while operating plating and coating process 
equipment or when using chromate based primers or paints. According to 
the authors, 3,634 workers, or 8% of the cohort, had the potential for 
routine exposure to chromate and 3,809 workers, or 8.4%, had the 
potential for intermittent exposure to chromate. Limited chromate air 
sampling was conducted between 1978 and 1991. The mean full shift air 
measurement was 1.5 [mu]g CrO3/m\3\ (0.78 [mu]g Cr(VI)/m\3\) 
indicating fairly low airborne Cr(VI) in the plant (Ex. 47-19-5).
    Follow up of the cohort was through 1996. Expectations were 
calculated based on the general population of California for white 
workers, while general population rates for the U.S. were used for non-
white workers. For the 3,634 cohort members who had potential for 
routine exposure to chromates, the lung cancer SMR (race and gender 
combined) was 102 based upon 87 deaths (95% CI: 82-126). There was a 
slight non-significant positive trend (p value >2.0) for lung cancer 
with duration of potential exposure. The SMR was 108 (95% CI: 75-157) 
for workers exposed to chromate for >=5 years. Among the painters, 
there were 41 deaths from lung cancer yielding a SMR of 111 (95% CI: 
80-151). For those who worked as a process operator or plater the SMR 
for lung cancer was 103 based upon 38 deaths (95% CI: 73-141).
    OSHA believes the Alexander (Ex. 31-16-3) and the Boice et al. (Ex. 
31-16-4) studies have several limitations. The Alexander cohort has few 
lung cancers (due in part to the young age of the population) and lacks 
smoking data. The authors note that these factors "[limit] the overall 
power of the study and the stability of the risk estimates, especially 
in exposure-related subanalyses" (Ex. 31-16-3, p. 1256). Another 
limitation of the study is the 26.3% of cohort members lost to follow-
up. Boice et al. is a large study of workers in the aircraft 
manufacturing industry, but was limited by a lack of Cr(VI) exposure 
measurement during the 1960s and most of the 1970s. I was also limited 
by a substantial healthy worker survivor effect that may have masked 
evidence of excess lung cancer mortality in Cr(VI) exposed workers (Ex. 
31-16-4). These studies are discussed further in section VI, including 
section VI.B.6 (Alexander cohort) and section VI.G.4.a (Alexander and 
Boice cohorts).
    Dalager et al. conducted a proportionate mortality study of 977 
white male spray painters potentially exposed to zinc chromate in the 
aircraft maintenance industry who worked at least three months and 
terminated employment within ten years prior to July 31, 1959 (Ex. 7-
64). Follow-up was through 1977. The expected numbers of deaths were 
obtained by applying the cause-specific proportionate mortality of U.S. 
white males to the total numbers of deaths in the study group by five 
year age groups and five year time intervals. Two hundred and two 
deaths were observed. There were 21 deaths from cancer of the 
respiratory system (PMR=184), which was statistically significant. The 
Proportionate Cancer Mortality Ratio for cancer of the respiratory 
system was not statistically significant (PCMR= 146). Duration of 
employment as a painter with the military as indicated on the service 
record was used as an estimate of exposure to zinc chromate pigments, 
which were used as a metal primer. The PMRs increased as duration of 
employment increased (< 5 years, O=9, E=6.4, PMR=141; 5-9 years, O=6, 
E=3, PMR=200; and 10+ years, O=6, E=2, PMR=300) and were statistically 
significant for those who worked 10 or more years.
    Bertazzi et al. studied the mortality experience of 427 workers 
employed for a minimum of six months between 1946 and 1977 in a plant 
manufacturing paint and coatings (Ex. 7-65). According to the author, 
chromate pigments represented the "major exposure" in the plant. The 
mortality follow-up period was 1954-1978. There were eight deaths from 
lung cancer resulting in a SMR of 227 on the local standard (95% CI: 
156-633) and a SMR of 334 on the national standard (95% CI: 106-434). 
The authors were unable to differentiate between exposures to different 
paints and coatings. In addition, asbestos was used in the plant and 
may be a potential confounding exposure.
    Morgan conducted a cohort study of 16,243 men employed after 
January 1, 1946 for at least one year in the manufacture of paint or 
varnish (Ex. 8-4). Analysis was also conducted for seven subcohorts, 
one of which was for work with pigments. Expectations were calculated 
based upon the mortality experience of U.S. white males. The SMR for 
cancer of the trachea, bronchus and lung was below unity based upon 150 
deaths. For the pigment subcohort, the SMR for cancer of the trachea, 
bronchus and lung was 117 based upon 43 deaths. In a follow-up study of 
the subcohorts, case-control analyses were conducted for several causes 
of death including lung cancer (Ex. 286). The details of matching were not 
provided. The authors state that no significant excesses of lung cancer 
risk by job were found. No odds ratios were presented.
    Pippard et al. conducted a cohort mortality study of 833 British 
male tannery workers employed in 1939 and followed through December 31, 
1982 (Ex. 278). Five hundred and seventy three men worked in tanneries 
making vegetable tanned leathers and 260 men worked in tanneries that 
made chrome tanned leathers. The expected number of deaths was 
calculated using the mortality rates of England and Wales as a whole. 
The lung cancer SMR for the vegetable tanned leather workers was in 
deficit (O=31; E=32.6; 95% CI: 65-135), while the lung cancer SMR for 
the chrome tanned leather workers was slightly elevated but not 
statistically significant (O=13; E=12; SMR=108; 95% CI: 58-185).
    In a different study of two U.S. tanneries, Stern et al. 
investigated mortality in a cohort of all production workers employed 
from January 1, 1940 to June 11, 1979 at tannery A (N=2,807) and from 
January 1, 1940 to May 1, 1980 at tannery B (N=6,558) (Ex. 7-68). Vital 
status was followed through December 31, 1982. There were 1,582 deaths 
among workers from the two tanneries. Analyses were conducted employing 
both U.S. mortality rates and the mortality rates for the state in 
which the plant is located. There were 18 lung/pleura cancer deaths at 
tannery A and 42 lung/pleura cancer deaths at tannery B. The lung 
cancer/pleura SMRs were in deficit on both the national standard and 
the state standard for both tanneries. The authors noted that since the 
1940s most chrome tanneries have switched to the one-bath tanning 
method in which Cr(VI) is reduced to Cr(III).
    Blot et al. reported the results of a cohort study of 51,899 male 
workers of the Pacific Gas & Electric Company alive in January 1971 and 
employed for at least six months before the end of 1986 (Ex. 239). A 
subset of the workers were involved in gas generator plant operations 
where Cr(VI) compounds were used in open and closed systems from the 
1950s to early 1980s. One percent of the workers (513 men) had worked 
in gas generator jobs, with 372 identified from post-1971 listing at 
the company's three gas generator plants and 141 from gas generator job 
codes. Six percent of the cohort members (3,283) had trained at one of 
the gas generator plants (Kettleman).
    SMRs based on national and California rates were computed. Results 
in the paper are based on the California rates, since the overall 
results reportedly did not differ substantially from those using the 
national rates. SMRs were calculated for the entire cohort and for 
subsets defined by potential for gas generator plant exposure. No 
significant cancer excesses were observed and all but one cancer SMR 
was in deficit. There were eight lung cancer deaths in the gas 
generator workers (SMR=81; 95% CI: 0.35-1.60) and three lung cancer 
deaths among the Kettleman trainees (SMR=57; 95% CI: 0.12-1.67). There 
were no deaths from nasal cancer among either the gas generator workers 
or the Kettleman trainees. The risk of lung cancer did not increase 
with length of employment or time since hire.
    Rafnsson and Johannesdottir conducted a study of 450 licensed 
masons (cement finishers) in Iceland born between 1905 and 1945, 
followed from 1951 through 1982 (Ex. 7-73). Stonecutters were excluded. 
Expectations were based on the male population of Iceland. The SMR for 
lung cancer was 314 and is statistically significant based upon nine 
deaths (E=2.87; 95% CI: 1.43-5.95). When a 20 year latency was factored 
into the analysis, the lung cancer SMR remained statistically 
significant (O=8; E=2.19; SMR=365; 95% CI: 1.58-7.20).
    Svensson et al. conducted a cohort mortality study of 1,164 male 
grinding stainless steel workers employed for three months or more 
during the period 1927-1981 (Ex.266). Workers at the facility were 
reportedly exposed to chromium and nickel in the stainless steel 
grinding process. Records provided by the company were used to assign 
each worker to one of three occupational categories: those considered 
to have high exposure to chromium, nickel as well as total dust, those 
with intermediate exposure, and those with low exposure. Mortality 
rates for males in Blekinge County, Sweden were used as the reference 
population. Vital status follow-up was through December 31, 1983. A 
total of 194 deaths were observed (SMR=91). No increased risk of lung 
cancer was observed (SMR=92). The SMR for colon/rectum cancer was 2.47, 
but was not statistically significant.
    Cornell and Landis studied the mortality experience of 851 men who 
worked in 26 U.S. nickel/chromium alloy foundries between 1968 and 1979 
(Ex. 7-66). Standardized Proportionate Mortality Ratio (SPMR) analyses 
were done using both an internal comparison group (foundry workers not 
exposed to nickel/chromium) and the mortality experience of U.S. males. 
The SPMR for lung cancer was 105 (O=60; E=56.9). No nasal cancer deaths 
were observed.
    Brinton et al. conducted a case-control study of 160 patients 
diagnosed with primary malignancies of the nasal cavity and sinuses at 
one of four hospitals in North Carolina and Virginia between January 1, 
1970 and December 31, 1980 (Ex. 8-8). For each case determined to be 
alive at the time of interview, two hospital controls were selected 
matched on vital status, hospital, year of admission (2 
years), age (5 years), race and state economic area or 
county or usual residence. Excluded from control selection were 
malignant neoplasms of the buccal cavity and pharynx, esophagus, nasal 
cavity, middle ear and accessory sinuses, larynx, and secondary 
neoplasms. Also excluded were benign neoplasms of the respiratory 
system, mental disorders, acute sinusitis, chronic pharyngitis and 
nasopharyngitis, chronic sinusitis, deflected nasal septum or nasal 
polyps. For those cases who were deceased at the time of interview, two 
different controls were selected. One control series consisted of 
hospital controls as described previously. The second series consisted 
of decedents identified through state vital statistics offices matched 
for age (5 years), sex, race, county of usual residence and 
year of death. A total of 193 cases were identified and 160 case 
interviews completed. For those exposed to chromates, the relative risk 
was not significantly elevated (OR=5.1) based upon five cases. 
According to the authors, chromate exposure was due to the use of 
chromate products in the building industry and in painting, rather than 
the manufacture of chromates.
    Hernberg et al. reported the results of a case-control study of 167 
living cases of nasal or paranasal sinus cancer diagnosed in Denmark, 
Finland and Sweden between July 1, 1977 and December 31, 1980 (Exs. 8-
7; 7-71). Controls were living patients diagnosed with malignant tumors 
of the colon and rectum matched for country, gender and age at 
diagnosis (3 years) with the cases. Both cases and controls 
were interviewed by telephone to obtain occupational histories. 
Patients with work-related exposures during the ten years prior to 
their illness were excluded. Sixteen cases reported exposure to 
chromium, primarily in the "stainless steel welding" and "nickel" 
categories, versus six controls (OR=2.7l; 95% CI: 1.1-6.6).
7. Evidence From Experimental Animal Studies
    Most of the key animal cancer bioassays for chromium compounds were 
conducted before 1988. These studies have been critically reviewed by the 
IARC in the Monograph Chromium, Nickel, and Welding (Ex. 35-43). OSHA 
reviewed the key animal cancer bioassays in the NPRM (69 FR at 59341-59347)
and requested any additional data in experimental animals that were considered 
important to evaluating the carcinogenicity of Cr(VI). The discussion below 
describes these studies along with any new study information received 
during the public hearing and comment periods.
    In the experimental studies, Cr(VI) compounds were administered by 
various routes including inhalation, intratracheal instillation, 
intrabronchial implantation, and intrapleural injection, as well as 
intramuscular and subcutaneous injection. For assessing human health 
effects from occupational exposure, the most relevant route is 
inhalation. However, as a whole, there were very few inhalation 
studies. In addition to inhalation studies, OSHA is also relying on 
intrabronchial implantation and intratracheal instillation studies for 
hazard identification because these studies examine effects directly 
administered to the respiratory tract, the primary target organ of 
concern, and they give insight into the relative potency of different 
Cr(VI) compounds. In comparison to studies examining inhalation, 
intrabronchial implantation, and intratracheal instillation, studies 
using subcutaneous injection and intramuscular administration of Cr(VI) 
compounds were of lesser significance but were still considered for 
hazard identification.
    In its evaluation, OSHA took into consideration the exposure 
regimen and experimental conditions under which the experiments were 
performed, including the exposure level and duration; route of 
administration; number, species, strain, gender, and age of the 
experimental animals; the inclusion of appropriate control groups; and 
consistency in test results. Some studies were not included if they did 
not contribute to the weight of evidence, lacked adequate 
documentation, were of poor quality, or were less relevant to 
occupational exposure conditions (e.g., some intramuscular injection 
studies).
    The summarized animal studies are organized by Cr(VI) compound in 
order of water solubility as defined in section IV on Chemical 
Properties (i.e., Cr(VI) compounds that are highly soluble in water; 
Cr(VI) compounds that are slightly soluble in water, and Cr(VI) 
compounds that insoluble in water). Solubility is an important factor 
in determining the carcinogenicity of Cr(VI) compounds (Ex. 35-47).
a. Highly Water Soluble Cr(VI) Compounds
    Multiple animal carcinogenicity studies have been conducted on 
highly water soluble sodium dichromate and chromic acid. The key 
studies are summarized in Table V-7.
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Chromic acid (Chromium trioxide). In a study by Adachi et al., ICR/JcI 
mice were exposed by inhalation to 3.63 mg/m\3\ for 30 minutes per day, 
two days per week for up to 12 months (Ex. 35-26-1). The mice were 
observed for an additional six months. The authors used a miniaturized 
chromium electroplating system to generate chromic acid for the study. 
The authors found there were elevations in lung adenomas at 10-14
months (3/14 vs. 0/10) and lung adenocarcinomas at 15-18 months (2/19 
vs. 0/10), but the results were not statistically significant. The 
small number of animals (e.g. 10-20 per group) used in this study 
limited its power to detect all but a relatively high tumor incidence 
(e.g. >20%) with statistical precision. Statistically significant 
increases in nasal papillomas were observed in another study by Adachi 
et al., in which C57B1 mice were exposed by inhalation to 1.81 mg/m\3\ 
chromic acid for 120 min per day, two days per week for up to 12 months 
(Ex. 35-26). At 18 months, the tumor incidence was 6/20 in exposed 
animals vs. 0/20 in the control animals (p< 0.05).
    In separate but similar studies, Levy et al. and Levy and Venitt, 
using similar exposure protocol, conducted bronchial implantation 
experiments in which 100 male and female Porton-Wistar rats were dosed 
with single intrabronchial implantations of 2 mg chromic acid (1.04 mg 
Cr(VI)) mixed 50:50 with cholesterol in stainless steel mesh pellets 
(Exs. 11-2; 11-12). The authors found no statistically significant 
increases in lung tumors, although Levy et al. found a bronchial 
carcinoma incidence of 2/100 in exposed rats compared with 0/100 in 
control rats. Levy and Venitt found a bronchial carcinoma incidence of 
1/100 accompanied by a statistically significant increase in squamous 
metaplasia, a lesion believed capable of progressing to carcinoma. 
There was no statistically significant increase in the incidence of 
squamous metaplasia in control rats or rats treated with Cr(III) 
compounds in the same study. This finding suggests that squamous 
metaplasia is specific to Cr(VI) and is not evoked by a non-specific 
stimuli, the implantation procedure itself, or treatment with Cr(III) 
containing materials.
    Similar to Levy et al. and Levy and Venitt studies, Laskin et al. 
gave a single intrabronchial implantation of 3-5 mg chromic acid mixed 
50:50 with cholesterol in stainless steel mesh pellets to 100 male and 
female Porton-Wistar rats (Ex. 10-1). The rats were observed for 2 
years. No tumors were identified in the treated or control animals (0/
100 vs. 0/24).
    Sodium dichromate. Glaser et al. exposed male Wistar rats to 
aerosolized sodium dichromate by inhalation for 22-23 hours per day, 
seven days per week for 18 months (Exs. 10-10; 10-11). The rats were 
held for an additional 12 months at which point the study was 
terminated. Lung tumor incidences among groups exposed to 25, 50, and 
100 [mu]g Cr(VI)/m\3\ were 0/18, 0/18, and 3/19, respectively, vs. 0/37 
for the control animals. Histopathology revealed one adenocarcinoma and 
two adenomas in the highest group. The slightly elevated tumor 
incidence at the highest dose was not statistically significant. A 
small number of animals (20 per group) were used in this study limiting 
its power to detect all but a relatively high tumor incidence (e.g. 
>20%) with statistical precision. In addition, the administered doses 
used in this study were fairly low, such that the maximum tolerated 
dose (i.e., the maximum dose level that does not lead to moderate 
reduction in body weight gain) may not have been achieved. Together, 
these factors limit the interpretation of the study.
    In an analysis prepared by Exponent and submitted by the Chrome 
Coalition, Exponent stated that "inhalation studies of Glaser et al. 
support a position that exposures to soluble Cr(VI) at concentrations 
at least as high as the current PEL (i.e., 52 [mu]g/m\3\) do not cause 
lung cancer" (Ex. 31-18-1, page 2). However, it should be noted that 
the Glaser et al. studies found that 15% (\3/19\) of the rats exposed 
to an air concentration just above the current PEL developed lung 
tumors, and that the elevated tumor incidence was not statistically 
significant in the highest dose group because the study used a small 
number of animals. OSHA believes the Glaser study lacks the statistical 
power to state with sufficient confidence that Cr(VI) exposure does not 
cause lung cancer at the current PEL, especially when given the 
elevated incidence of lung tumors at the next highest dose level.
    Steinhoff et al. studied the carcinogenicity of sodium dichromate 
in Sprague-Dawley rats (Ex. 11-7). Forty male and 40 female Sprague-
Dawley rats were divided into two sets of treatment groups. In the 
first set, doses of 0.01, 0.05 or 0.25 mg/kg body weight in 0.9% saline 
were instilled intratracheally five times per week. In the second set 
of treatment groups, 0.05, 0.25 or 1.25 mg/kg body weight in 0.9% 
saline doses were instilled intratracheally once per week. Duration of 
exposure in both treatment groups was 30 months. The total cumulative 
dose for the lowest treatment group of animals treated once per week 
was the same as the lowest treatment group treated five times per week. 
Similarly, the medium and high dose groups treated once per week had 
total doses equivalent to the medium and high dose animals treated five 
times per week, respectively. No increased incidence of lung tumors was 
observed in the animals dosed five times weekly. However, in the 
animals dosed once per week, tumor incidences were 0/80 in control 
animals, 0/80 in the 0.05 mg/kg exposure group, 1/80 in the 0.25 mg/kg 
exposure group and 14/80 in the 1.25 mg/kg exposure group (p < 0.01). 
The tumors were malignant in 12 of the 14 animals in the 1.25 mg/kg 
exposure group. Tracheal instillation at the highest dose level (i.e. 
1.25 mg/kg) caused emphysematous lesions and pulmonary fibrosis in the 
lungs of Cr(VI)-treated rats. A similar degree of lung damage did not 
occur at the lower dose levels. Exponent commented that the Steinhoff 
and Glaser results are evidence that the risk of lung cancer from 
occupational exposure does not exist below a threshold Cr(VI) air 
concentration of approximately 20 [mu]g/m\3\ (Ex. 38-233-4). This 
comment is addressed in Section VI.G.2.c.
    In separate but similar studies, Levy et al. and Levy and Venitt 
implanted stainless steel mesh pellets filled with a single dose of 2 
mg sodium dichromate (0.80 mg Cr(VI)) mixed 50:50 with cholesterol in 
the bronchi of male and female Porton-Wistar rats (Exs. 11-2; 11-12). 
Control groups (males and females) received blank pellets or pellets 
loaded with cholesterol. The rats were observed for two years. Levy et 
al. and Levy and Venitt reported a bronchial tumor incidence of 1/100 
and 0/89, respectively, for exposed rats. However, the latter study 
reported a statistically significant increase in squamous metaplasia, a 
lesion believed capable of progressing to carcinoma, among exposed rats 
when compared to unexposed rats. There were no bronchial tumors or 
squamous metaplasia in any of the control animals and no significant 
increases in lung tumors were observed in the two studies.
b. Slightly Water Soluble Cr(VI) Compounds
    Animal carcinogenicity studies have been conducted on slightly 
water soluble calcium chromate, strontium chromate, and zinc chromates. 
The key studies are summarized in Table V-8.
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     Calcium chromate. Nettesheim et al. conducted the only available 
inhalation carcinogenicity study with calcium chromate showing 
borderline statistical significance for increased lung adenomas in 
C57B1/6 mice exposed to 13 mg/m\3\ for 5 hours per day, 5 days per week 
over the life of the mice. The tumor incidences were 6/136 in exposed 
male mice vs. 3/136 in control male mice and 8/136 in exposed female 
mice vs. 2/136 in control female mice (Ex. 10-8).
    Steinhoff et al. observed a statistically significant increase in 
lung tumors in Sprague-Dawley rats exposed by intratracheal 
instillation to 0.25 mg/kg body weight calcium chromate in 0.9% saline 
five times weekly for 30 months (Ex. 11-7). Tumors were found in 6/80 
exposed animals vs. 0/80 in unexposed controls (p< 0.01). Increased 
incidence of lung tumors was also observed in those rats exposed to 
1.25 mg/kg calcium chromate once per week (14/80 vs. 0/80 in controls) 
for 30 months. At the highest dose, the authors observed 11 adenomas, 
one adenocarcinoma, and two squamous carcinomas. The total administered 
doses for both groups of dosed animals (1 x 1.25 mg/kg and 5 x 0.25 mg/
kg) were equal, but the tumor incidence in the rats exposed once per 
week was approximately double the incidence in rats exposed to the same 
weekly dose divided into five smaller doses. The authors suggested that 
the dose-rate for calcium chromate compounds may be important in 
determining carcinogenic potency and that limiting higher single 
exposures may offer greater protection against carcinogenicity than 
reducing the average exposure alone.
    Snyder et al. administered Cr(VI)-contaminated soil of defined 
aerodynamic diameter (2.9 to 3.64 micron) intratracheally to male 
Sprague-Dawley rats (Ex. 31-18-12). For the first six weeks of 
treatment, the rats were instilled with weekly suspensions of 1.25 mg 
of material per kg body weight, followed by 2.5 mg/kg every other week, 
until treatments were terminated after 44 weeks. The investigation 
included four exposure groups: control animals (50 rats), rats 
administered Cr(VI)-contaminated soil (50 rats), rats administered 
Cr(VI)-contaminated soil supplemented with calcium chromate (100 rats), 
and rats administered calcium chromate alone (100 rats). The total 
Cr(VI) dose for each group was: control group (0.000002 mg Cr(VI)/kg), 
soil alone group (0.324 mg Cr(VI)/kg), soil plus calcium chromate group 
(7.97 mg Cr(VI)/kg), and calcium chromate alone group (8.70 mg Cr(VI)/
kg). No primary tumors were observed in the control group or the 
chromium contaminated soil group. Four primary tumors of the lung were 
found in the soil plus calcium chromate group and one primary lung 
tumor was observed in the group treated with calcium chromate alone; 
however, these incidences did not reach statistical significance.
    Statistically significant increases in the incidence of bronchial 
carcinoma in rats exposed to calcium chromate through intrabronchial 
instillation were reported by Levy et al. (Ex. 11-2) and Levy and 
Venitt (Ex. 11-12). These studies, using a similar protocol, implanted 
a single dose of 2 mg calcium chromate (0.67 mg Cr(VI)) mixed 50:50 
with cholesterol in stainless steel pellets into the bronchi of Porton-
Wistar rats. Levy et al. and Levy and Venitt found bronchial carcinoma 
incidences of 25/100 and 8/84, respectively, following a 24-month 
observation. The increased incidences were statistically significant 
when compared to the control group. Levy and Venitt also reported 
statistically significant increases in squamous metaplasia in the 
calcium chromate-treated rats (Ex. 11-12).
    Laskin et al. observed 8/100 tumors in rats exposed to a single 
dose of 3-5 mg calcium chromate mixed with cholesterol in stainless 
steel mesh pellets implanted in the bronchi (Ex. 10-1). Animals were 
observed for a total of 136 weeks. The sex, strain, and species of the 
rats were not specified in the study. Tumor incidence in control 
animals was 0/24. Although tumor incidence did not reach statistical 
significance in this study, OSHA agrees with the IARC evaluation that 
the incidences are due to calcium chromate itself rather than 
background variation.
    Strontium chromate. Strontium chromate was tested by intrabronchial 
implantation and intrapleural injection. In a study by Levy et al., two 
strontium chromate compounds mixed 50:50 with cholesterol in stainless 
steel mesh pellets were administered by intrabronchial instillation of 
a 2 mg (0.48 mg Cr(VI)) dose into 100 male and female Porton-Wistar 
rats (Ex. 11-2). Animals were observed for up to 136 weeks. The 
strontium chromate compounds induced bronchial carcinomas in 43/99 (Sr, 
42.2%; CrO4, 54.1%) and 62/99 rats (Sr, 43.0%; Cr, 24.3%)], 
respectively, compared to 0/100 in the control group. These results 
were statistically significant. The strontium chromates produced the 
strongest carcinogenic response out of the 20 Cr(VI) compounds tested 
by the intrabronchial implantation protocol. Boeing Corporation 
commented that the intrabronchial implantation results with strontium 
chromate should not be relied upon in an evaluation of carcinogenicity 
and that the data is inconsistent with other Cr(VI) studies (Ex. 38-
106-2, p. 26). This comment is discussed in the Carcinogenic Effects 
Conclusion Section V.B.9 dealing with the carcinogenicity of slightly 
soluble Cr(VI) compounds.
    In the study by Hueper, strontium chromate was administered by 
intrapleural injection (doses unspecified) lasting 27 months (Ex. 10-
4). Local tumors were observed in 17/28 treated rats vs. 0/34 for the 
untreated rats. Although the authors did not examine the statistical 
significance of tumors, the results clearly indicate a statistical 
significance.
    Zinc chromate compounds. Animal studies have been conducted to 
examine several zinc chromates of varying water solubilities and 
composition. In separate, but similarly conducted studies, Levy et al. 
and Levy and Venitt studied two zinc chromate powders, zinc potassium 
chromate, and zinc tetroxychromate (Exs. 11-2; 11-12). Two milligrams 
of the compounds were administered by intrabronchial implantation to 
100 male and female Porton-Wistar rats. Zinc potassium chromate (0.52 
mg Cr(VI)) produced a bronchial tumor incidence of 3/61 which was 
statistically significant (p< 0.05) when compared to a control group 
(Ex. 11-12). There was also an increased incidence of bronchial tumors 
(5/100, p=0.04; 3/100, p=0.068) in rats receiving the zinc chromate 
powders (0.44 mg Cr(VI)). Zinc tetroxychromate (0.18 mg Cr(VI)) did not 
produce a statistically significant increase in tumor incidence (1/100) 
when compared to a control group. These studies show that most slightly 
water soluble zinc chromate compounds elevated incidences of tumors in 
rats.
    Basic potassium zinc chromate was administered to mice, guinea pigs 
and rabbits via intratracheal instillation (Ex. 35-46). Sixty-two 
Strain A mice were given six injections of 0.03 ml of a 0.2% saline 
suspension of the zinc chromate at six week intervals and observed 
until death. A statistically significant increase in tumor incidence 
was observed in exposed animals when compared to controls (31/62 vs. 7/
18). Statistically significant effects were not observed among guinea 
pigs or rabbits. Twenty-one guinea pigs (sex and strain not given) 
received six injections of 0.3 ml of a 1% suspension of zinc chromate 
at three monthly intervals and observed until death. Results showed 
pulmonary adenomas in only 1/21 exposed animals vs. 0/18 in controls. 
Seven rabbits (sex and strain not given) showed no increase in lung 
tumors when given 3-5 injections of 1 ml of a saline suspension of 10 
mg zinc chromate at 3-month intervals. However, as noted by IARC, the 
small numbers of animals used in the guinea pig and rabbit experiments 
(as few as 13 guinea pigs and 7 rabbits per group) limit the power of 
the study to detect increases in cancer incidence.
    Hueper found that intrapleural injection of slightly water soluble 
zinc yellow (doses were unspecified) resulted in statistically significant 
increases in local tumors in rats (sex, strain, and age of rat 
unspecified; dose was unspecified). The incidence of tumors in exposed 
rats was 22/33 vs. 0/34 in controls (Ex. 10-4).
    Maltoni et al. observed increases in the incidence of local tumors 
after subcutaneous injection of slightly water soluble zinc yellow in 
20 male and 20 female Sprague-Dawley rats (statistical significance was 
not evaluated) (Ex. 8-37). Tumor incidences were 6/40 in 20% 
CrO3 dosed animals at 110 weeks and 17/40 in 40% 
CrO3 dosed animals at 137 weeks compared to 0/40 in control 
animals.
c. Water Insoluble Cr(VI) Compounds
    There have been a number of animal carcinogenicity studies 
involving implantation or injection of principally water insoluble 
zinc, lead, and barium chromates. The key studies are summarized in 
Table V-9.
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    Lead chromate and lead chromate pigments. Levy et al. examined the 
carcinogenicity of lead chromate and several lead chromate-derived 
pigments in 100 male and female Porton-Wistar rats after a single 
intrabronchial implantation followed by a two year observation period 
(Ex. 11-12). The rats were dosed with two mg of a lead chromate 
compound and lead chromate pigments, which were mixed 50:50 with
cholesterol in stainless steel mesh pellets and implanted in the 
bronchi of experimental animals. The lead chromate and lead chromate 
pigment compositions consisted of the following: lead chromate (35.8% 
CrO4; 0.32 mg Cr(VI)), primrose chrome yellow (12.6% Cr; 
0.25 mg Cr(VI)), molybdate chrome orange (12.9% Cr; 0.26 mg Cr(VI)), 
light chrome yellow (12.5% Cr; 0.25 mg Cr(VI)), supra LD chrome yellow 
(26.9% CrO3; 0.28 mg Cr(VI)), medium chrome yellow (16.3% 
Cr; 0.33 mg Cr(VI)) and silica encapsulated medium chrome yellow (10.5% 
Cr; 0.21 mg Cr(VI)). No statistically significant tumors were observed 
in the lead chromate group compared to controls (1/98 vs. 0/100), 
primrose chrome yellow group (1/100 vs. 0/100), and supra LD chrome 
yellow group (1/100 vs. 0/100). The authors also noted no tumors in the 
molybdate chrome orange group, light chrome yellow group, and silica 
encapsulated medium chrome yellow group.
    Maltoni (Ex. 8-25), Maltoni (Ex. 5-2), and Maltoni et al. (Ex. 8-
37) examined the carcinogenicity of lead chromate, basic lead chromate 
(chromium orange) and molybdenum orange in 20 male and 20 female 
Sprague-Dawley rats by a single subcutaneous administration of the lead 
chromate compound in water. Animals were observed for 117 to 150 weeks. 
After injection of 30 mg lead chromate, local injection site sarcomas 
were observed in 26/40 exposed animals vs. 0/60 and 1/80 in controls. 
Although the authors did not examine the statistical significance of 
sarcomas, the results clearly indicate a statistical significance. 
Animals injected with 30 mg basic lead chromate (chromium orange) were 
found to have an increased incidence of local injection site sarcomas 
(27/40 vs. 0/60 and 1/80 in controls). Animals receiving 30 mg 
molybdenum orange in 1 ml saline were also found to have an increased 
incidence of local injection site sarcomas (36/40 vs. 0/60 controls).
    Carcinogenesis was observed after intramuscular injection in a 
study by Furst et al. (Ex. 10-2). Fifty male and female Fischer 344 
rats were given intramuscular injections of 8 mg lead chromate in 
trioctanoin every month for nine months and observed up to 24 months. 
An increase in local tumors at the injection site (fibrosarcomas and 
rhabdomyosarcomas) was observed (31/47 in treated animals vs. 0/22 in 
controls). These rats also had an increased incidence of renal 
carcinomas (3/23 vs. 0/22 in controls), but IARC noted that the renal 
tumors may be related to the lead content of the compound. In the same 
study, 3 mg lead chromate was administered to 25 female NISH Swiss 
weanling mice via intramuscular injection every 4 months for up to 24 
months. In the exposed group, the authors observed three lung 
alveologenic carcinomas after 24 months of observation and two 
lymphomas after 16 months of observation. Two control groups were used: 
an untreated control group (22 rats) and a vehicle injected control 
group (22 rats). The authors noted that one alveologenic carcinoma and 
one lymphoma were observed in each control group. The Color Pigment 
Manufacturers Association (CPMA) commented that the lack of elevated 
tumor incidence in the intrabronchial implantation studies confirmed 
that lead chromate was not carcinogenic and that the positive injection 
studies by the subcutaneous, intrapleural, and intramuscular routes 
were of questionable relevance (Ex. 38-205, p. 93). This comment is 
further discussed in the Carcinogenic Effects Conclusion Section V.B.9 
dealing with the carcinogenicity of lead chromate.
    Barium chromate. Barium chromate was tested in rats via 
intrabronchial, intrapleural and intramuscular administration. No 
excess lung or local tumors were observed (Ex. 11-2; Ex. 10-4; Ex. 10-
6).
    d. Summary. Several Cr(VI) compounds produced tumors in laboratory 
animals under a variety of experimental conditions using different 
routes of administration. The animals were generally given the test 
material(s) by routes other than inhalation (e.g., intratracheal 
administration, intramuscular injection, intrabronchial implantation, 
and subcutaneous injection). Although the route of administration may 
have differed from that found in an occupational setting, these studies 
have value in the identification of potential health hazards associated 
with Cr(VI) and in assessing the relative potencies of various Cr(VI) 
compounds.
    OSHA believes that the results from Adachi et al. (Ex. 35-26-1), 
Adachi et al. (Ex. 35-26), Glaser et al. (Ex. 10-4), Glaser et al. (Ex. 
10-10), Levy et al. (Ex. 11-2), and Steinhoff et al. (Ex. 11-7) studies 
provide valuable insight on the carcinogenic potency of Cr(VI) 
compounds in laboratory animals. Total dose administered, dose rate, 
amount of dosage, dose per administration, number of times 
administered, exposure duration and the type of Cr(VI) compound are 
major influences on the observed tumor incidence in animals. It was 
found that slightly water soluble calcium, strontium, and zinc 
chromates showed the highest incidence of lung tumors, as indicated in 
the results of the Steinhoff and Levy studies, even when compared to 
similar doses of the more water soluble sodium chromates and chromic 
acid compounds. The highly insoluble lead chromates did not produce 
lung tumors by the intrabronchial implantation procedure but did 
produce tumors by subcutaneous injection and intramuscular injection.
8. Mechanistic Considerations
    Mechanistic information can provide insight into the biologically 
active form(s) of chromium, its interaction with critical molecular 
targets, and the resulting cellular responses that trigger neoplastic 
transformation. There has been considerable scientific study in recent 
years of Cr(VI)-initiated cellular and molecular events believed to 
impact development of respiratory carcinogenesis. Much of the research 
has been generated using in vitro techniques, cell culture systems, and 
animal administrations. The early mechanistic data were reviewed by 
IARC in 1990 (Ex. 35-43). Recent experimental research has identified 
several biological steps critical to the mode of action by which Cr(VI) 
transforms normal lung cells into a neoplastic phenotype. These are: 
(a) Cellular uptake of Cr(VI) and its extracellular reduction, (b) 
intracellular Cr(VI) reduction to produce biologically active products, 
(c) damage to DNA, and (d) activation of signaling pathways in response 
to cellular stress. Each step will be described in detail below.
    a. Cellular Uptake and Extracellular Reduction. The ability of 
different Cr(VI) particulate forms to be taken up by the 
bronchoalveolar cells of the lung is an essential early step in the 
carcinogenic process. Particle size and solubility are key physical 
factors that influence uptake into these cells. Large particulates (>10 
[mu]m) are generally deposited in the upper nasopharygeal region of the 
respiratory tract and do not reach the bronchoalveolar region of the 
lungs. Smaller Cr(VI) particulates will increasingly reach these lower 
regions and come into contact with target cells.
    Once deposited in the lower respiratory tract, solubility of Cr(VI) 
particulates becomes a major influence on disposition. Highly water 
soluble Cr(VI), such as sodium chromate and chromic acid, rapidly 
dissolves in the fluids lining the lung epithelia and can be taken up 
by lung cells via facilitated diffusion mediated by sulfate/phosphate 
anion transport channels (Ex. 35-148). This is because Cr(VI) exists in 
a tetrahedral configuration as a chromate oxyanion similar to the 
physiological anions, sulfate and phosphate (Ex. 35-231). Using cultured
human epithelial cells, Liu et al. showed that soluble Cr(VI) uptake was 
time- and dose-dependant over a range of 1 to 300 [mu]m in the medium with 
30 percent of the Cr(VI) transported into the cells within two hours and 
67 percent at 16 hours at the lowest concentration (Ex. 31-22-18).
    Water insoluble Cr(VI) particulates do not readily dissolve into 
epithelial lining fluids of the bronchoalveolar region. This has led to 
claims that insoluble chromates, such as lead chromate pigments, are 
not bioavailable and, therefore, are unable to cause carcinogenesis 
(Ex. 31-15). However, several scientific studies indicate that 
insoluble Cr(VI) particulates can come in close contact with the 
bronchoalveolar epithelial cell surface, allowing enhanced uptake into 
cells. Wise et al. showed that respirable lead chromate particles 
adhere to the surface of rodent cells in culture causing cell-enhanced 
dissolution of the chromate ion as well as phagocytosis of lead 
chromate particles (Exs. 35-68; 35-67). The intracellular accumulation 
was both time- and dose-dependant. Cellular uptake resulted in damage 
to DNA, apoptosis (i.e., form of programmed cell death), and neoplastic 
transformation (Ex. 35-119). Singh et al. showed that treatment of 
normal human lung epithelial cells with insoluble lead chromate 
particulates (0.4 to 2.0 [mu]g/cm\2\) or soluble sodium chromate (10 
[mu]M) for 24 hours caused Cr(VI) uptake, Cr-DNA adduct formation, and 
apoptosis (Ex. 35-66). The proximate genotoxic agent in these cell 
systems was determined to be the chromate rather than the lead ions 
(Ex. 35-327). Elias et al. reported that cell-enhanced particle 
dissolution and uptake was also responsible for the cytotoxicity and 
neoplastic transformation in Syrian hamster embryo cells caused by 
Cr(VI) pigments, including several complex industrial chrome yellow and 
molybdate orange pigments (Ex. 125). These studies are key experimental 
evidence in the determination that water-insoluble Cr(VI) compounds, as 
well as water soluble Cr(VI) compounds, are to be regarded as 
carcinogenic agents. This determination is further discussed in the 
next section (see V.B.9).
    Reduction to the poorly permeable Cr(III) in the epithelial lining 
fluid limits cellular uptake of Cr(VI). Ascorbic acid and glutathione 
(GSH) are believed to be the key molecules responsible for the 
extracellular reduction. Cantin et al. reported high levels of GSH in 
human alveolar epithelial lining fluid and Susuki et al. reported 
significant levels of ascorbic acid in rat lung lavage fluids (Exs. 35-
147; 35-143). Susuki and Fukuda studied the kinetics of soluble Cr(VI) 
reduction with ascorbic acid and GSH in vitro and following 
intratracheal instillation (Ex. 35-90). They reported that the rate of 
reduction was proportional to Cr(VI) concentration with a half-life of 
just under one minute to several hours. They found the greatest 
reduction rates with higher levels of reductants. Ascorbic acid was 
more active than GSH. Cr(VI) reduction was slower in vivo than 
predicted from in vitro and principally involved ascorbic acid, not 
GSH. This research indicates that extracellular Cr(VI) reduction to 
Cr(III) is variable depending on the concentration and nature of the 
reductant in the epithelial fluid lining regions of the respiratory 
tract. De Flora et al. determined the amount of soluble Cr(VI) reduced 
in vitro by human bronchiolar alveolar fluid and pulmonary alveolar 
macrophage fractions over a short period and used these specific 
activities to estimate an "overall reducing capacity" of 0.9-1.8 mg 
Cr(VI) and 136 mg Cr(VI) per day per individual, respectively (Ex. 35-
140).
    De Flora, Jones, and others have interpreted the extracellular 
reduction data to mean that very high levels of Cr(VI) are required to 
"overwhelm" the reductive defense mechanism before target cell uptake 
can occur and, as such, impart a "threshold" character to the 
exposure-response (Exs. 35-139; 31-22-7). However, the threshold 
capacity concept does not consider that facilitated lung cell uptake 
and extracellular reduction are dynamic and parallel processes that 
happen concurrently. If their rates are comparable then some cellular 
uptake of Cr(VI) would be expected, even at levels that do not 
"overwhelm" the reductive capacity. Based on the in vitro kinetic 
data, it would appear that such situations are plausible, especially 
when concentrations of ascorbic acid are low. Unfortunately, there has 
been little systematic study of the dose-dependence of Cr(VI) uptake in 
the presence of physiological levels of ascorbate and GSH using 
experimental systems that possess active anion transport capability. 
The implications of extracellular reduction on the shape of Cr(VI) 
dose--lung cancer response curve is further discussed in Section 
VI.G.2.c.
    Wise et al. did study uptake of a single concentration of insoluble 
lead chromate particles (0.8 [mu]g/cm2) and soluble sodium 
chromate (1.3 [mu]M) in Chinese hamster ovary cells co-treated with a 
physiological concentration (1mM) of ascorbate (Ex. 35-68). They found 
that the ascorbate substantially reduced, but did not eliminate, 
chromate ion uptake over a 24 hour period. Interestingly, ascorbate did 
not affect phagocytic uptake of lead chromate particles, although it 
eliminated the Cr(VI)-induced clastogenesis (e.g., DNA strand breakage 
and chromatid exchange) as measured under their experimental 
conditions.
    Singh et al. suggested that cell surface interactions with 
insoluble lead chromate particulates created a concentrated 
microenvironment of chromate ions resulting in higher intracellular 
levels of chromium than would occur from soluble Cr(VI) (Ex. 35-149). 
Cell membrane-enhanced uptake of Cr(VI) is consistent with the 
intratracheal and intrabronchial instillation studies in rodents that 
show greater carcinogenicity with slightly soluble (e.g., calcium 
chromate and strontium chromate) than with the highly water-soluble 
chromates (e.g., sodium chromate and chromic acid) (Ex. 11-2).
    Finally, Cr(VI) deposited in the tracheobronchial and alveolar 
regions of the respiratory tract is cleared by the mucocilliary 
escalator (soluble and particulate Cr(VI)) and macrophage phagocytosis 
(particulate Cr(VI) only). In most instances, these clearance processes 
take hours to days to completely clear Cr(VI) from the lung, but it can 
take considerably longer for particulates deposited at certain sites. 
For example, Ishikawa et al. showed that some workers had substantial 
amounts of chromium particulates at the bifurcations of the large 
bronchii for more than two decades after cessation of exposure (Ex. 35-
81). Mancuso reported chromium in the lungs of six chromate production 
workers who died from lung cancer (as cited in Ex. 35-47). The interval 
between last exposure to Cr(VI) until autopsy ranged from 15 months to 
16 years. Using hollow casts of the human tracheobronchial tree and 
comparing particle deposition with reported occurrence of bronchogenic 
tumors, Schlesinger and Lippman were able to show good correlations 
between sites of greatest deposition and increased incidence of 
bronchial tumors (Ex. 35-102).
    b. Intracellular Reduction of Cr(VI). Once inside the cell, the 
hexavalent chromate ion is rapidly reduced to intermediate oxidation 
states, Cr(V) and Cr(IV), and the more chemically stable Cr(III). 
Unlike Cr(VI), these other chromium forms are able to react with DNA 
and protein to generate a variety of adducts and complexes. In 
addition, reactive oxygen species (ROS) are produced during the 
intracellular reduction of Cr(VI) that are also capable of damaging 
DNA. These reactive intermediates, and not Cr(VI) itself, are considered
to be the ultimate genotoxic agents that initiate the carcinogenic process.
    After crossing the cell membrane, Cr(VI) compounds can be non-
enzymatically converted to Cr(III) by several intracellular reducing 
factors (Ex. 35-184). The most plentiful electron donors in the cell 
are GSH, and other thiols, such as cysteine, and ascorbate. Connett and 
Wetterhahn showed that a Cr(VI)-thioester initially forms in the 
presence of GSH (Ex. 35-206). A two-phase reduction then occurs with 
rapid conversion to Cr(V) and glutathionyl radical followed by 
relatively slower reduction to Cr(III) that requires additional 
molecules of GSH. Depletion of cellular GSH and other thiols is 
believed to retard complete reduction of Cr(VI) to Cr(III), allowing 
buildup of intermediates Cr(V) and Cr(IV). The molecular kinetics of 
the Cr(VI) to Cr(III) reduction with ascorbate is less well understood 
but can also involve intermediate formation of Cr(V) and free radicals 
(Ex. 35-184).
    Another important class of intracellular Cr(VI) reductions are 
catalyzed by flavoenzymes, such as GSH reductase, lipoyl dehydrogenase, 
and ferredoxin-NADP oxidoreductase. The most prominent among these is 
GSH reductase that uses NADPH as a cofactor in the presence of 
molecular oxygen (O2) to form Cr(V)-NADPH complexes. During 
the reaction, O2 undergoes one electron reduction to the 
superoxide radical (O2-) which produces hydrogen 
peroxide (H2O2) through the action of the enzyme 
superoxide dismutase. The Cr(V)-NADPH can then react with 
H2O2 to regenerate Cr(VI) giving off hydroxyl 
radicals, a highly reactive oxygen species, by a Fenton-like reaction. 
It is, therefore, possible for a single molecule of Cr(VI) to produce 
many molecules of potentially DNA damaging ROS through a repeated 
reduction/oxidation cycling process. Shi and Dalal used electron spin 
resonance (ESR) to establish formation of Cr(V)-NADPH and hydroxyl 
radical in an in vitro system (Ex. 35-169; 35-171). Sugiyama et al. 
reported Cr(V) formation in cultured Chinese hamster cells treated with 
soluble Cr(VI) (Ex.35-133). Using a low frequency ESR, Liu et al. 
provided evidence of Cr(V) formation in vivo in mice injected with 
soluble Cr(VI) (Ex. 35-141-28).
    Several studies have documented that Cr(VI) can generate Cr(V) and 
ROS in cultured human lung epithelial cells and that this reduction/
oxidation pathway leads to DNA damage, activation of the p53 tumor 
suppressor gene and stress-induced transcription factor NF-[kappa]B, 
cell growth arrest, and apptosis (Exs. 35-125; 35-142; 31-22-18; 35-
135). Leonard et al. used ESR spin trapping, catalase, metal chelators, 
free radical scavengers, and O2-free atmospheres to show 
that hydroxyl radical generation involves a Fenton-like reaction with 
soluble potassium dichromate (Ex. 31-22-17) and insoluble lead chromate 
(Ex.35-137) in vitro. Liu et al. showed that the Cr(IV)/Cr(V) compounds 
are also able to generate ROS with H2O2 in a 
Fenton reduction/oxidation cycle in vitro (Ex. 35-183).
    Although most intracellular reduction of Cr(VI) is believed to 
occur in the cytoplasm, Cr(VI) reduction can also occur in mitochondria 
and the endoplasmic reticulum. Cr(VI) reduction can occur in the 
mitochondria through the action of the electron transport complex (Ex. 
35-230). The microsomal cytochrome P-450 system in the endoplasmic 
reticulum also enzymatically reduces Cr(VI) to Cr(V), producing ROS 
through reduction/oxidation cycling as described above (Ex. 35-171).
    c. Genotoxicity and Damage to DNA. A large number of studies have 
examined multiple types of genotoxicity in a wide range of experimental 
test systems. Many of the specific investigations have been previously 
reviewed by IARC (Ex. 35-43), Klein (Ex. 35-134), ATSDR (Ex. 35-41), 
and the K.S. Crump Group (Ex. 35-47) and will only be briefly 
summarized here. The body of evidence establishes that both soluble and 
insoluble forms of Cr(VI) cause structural DNA damage that can lead to 
genotoxic events such as mutagenisis, clastogenisis, inhibition of DNA 
replication and transcription, and altered gene expression, all of 
which probably play a role in neoplastic transformation. The reactive 
intermediates and products that occur from intracellular reduction of 
Cr(VI) cause a wide variety of DNA lesions. The type(s) of DNA damage 
that are most critical to the carcinogenic process is an area of active 
investigation.
    Many Cr(VI) compounds are mutagenic in bacterial and mammalian test 
systems (Ex. 35-118). In the bacterial Salmonella typhimurium strains, 
soluble Cr(VI) caused base pair substitutions at A-T sites as well as 
frame shift mutations (Ex. 35-161). Nestmann et al. also reported 
forward and frame shift mutations in Salmonella typhimurium with pre-
solubilized lead chromate (Ex. 35-162). Several Cr(VI) compounds have 
produced mutagenic responses at various genetic loci in mammalian cells 
(Ex. 12-7). Clastogenic damage, such as sister chromatid exchange and 
chromosomal aberrations, have also been reported for insoluble Cr(VI) 
and soluble Cr(VI) (Exs. 35-132; 35-115). Mammalian cells undergo 
neoplastic transformation following treatment with soluble Cr(VI) or 
insoluble Cr(VI), including a number of slightly soluble zinc and 
insoluble lead chromate pigments (Exs. 12-5; 35-186).
    Genotoxicity has been reported from Cr(VI) administration to 
animals in vivo. Soluble Cr(VI) induced micronucleated erythrocytes in 
mice following intraperitoneal (IP) administration (Ex. 35-150). It 
also increased the mutation frequency in liver and bone marrow 
following IP administration to lacZ transgenic mice (Exs. 35-168; 35-
163). Izzotti et al. reported DNA damage in the lungs of rats exposed 
to soluble Cr(VI) by intratracheal instillation (Ex. 35-170). 
Intratracheal instillation of soluble Cr(VI) produced a time- and dose-
dependant elevation in mutant frequency in the lung of Big Blue 
transgenic mice (Ex. 35-174). Oral administration of soluble Cr(VI) in 
animals did not produce genotoxicity in several studies probably due to 
route-specific differences in absorption. OSHA is not aware of 
genotoxicity studies from in vivo administration of insoluble Cr(VI). 
Studies of chromosomal and DNA damage in workers exposed to Cr(VI) vary 
in their findings. Some studies reported higher levels of chromosomal 
aberrations, sister chromatid exchanges, or DNA strand breaks in 
peripheral lymphocytes of stainless steel welders (Exs. 35-265; 35-160) 
and electroplaters (Ex. 35-164). Other studies were not able to find 
excess damage in DNA from the blood lymphocytes of workers exposed to 
Cr(VI) (Exs. 35-185; 35-167). These reports are difficult to interpret 
since co-exposure to other genotoxic agents (e.g., other metals, 
cigarette smoke) likely existed and the extent of Cr(VI) exposures were 
not known.
    Because of the consistent positive response across multiple assays 
in a wide range of experimental systems from prokaryotic organisms 
(e.g., bacteria) to human cells in vitro and animals in vivo, OSHA 
regards Cr(VI) as an agent able to induce carcinogenesis through a 
genotoxic mode of action. Both soluble and insoluble forms of Cr(VI) 
are reported to cause genotoxicity and neoplastic transformation. On 
the other hand, Cr(III) compounds do not easily cause genotoxicity in 
intact cellular systems, presumably due to the inability of Cr(III) to 
penetrate cell membranes (Exs. 12-7; 35-186).
    There has been a great deal of research to identify the types of 
damage to DNA caused by Cr(VI), the reactive intermediates that are 
responsible for the damage, and the specific genetic lesions critical to 
carcinogenesis. It was shown that Cr(VI) was inactive in DNA binding assays 
with isolated nuclei or purified DNA (Ex. 35-47). However, Cr(III) was able 
to produce DNA protein cross-links, sister chromatid exchanges, and chromosomal 
aberrations in an acellular system. Zhitkovich et al. showed that incubation of 
Chinese hamster ovary cells with soluble Cr(VI) produced ternary complexes of 
Cr(III) cross-linked to cysteine, other amino acids, or glutathione and 
the DNA phosphate backbone (Ex. 312). Utilizing the pSP189 shuttle 
vector plasmid, they showed these DNA-Cr(III)-amino acid cross-links 
were mutagenic when introduced in human fibroblasts (Ex. 35-131).
    Another research group showed that plasmid DNA treated with Cr(III) 
produced intrastrand crosslinks and the production of these lesions 
correlated with DNA polymerase arrest (Ex. 35-126). The same 
intrastrand crosslinks and DNA polymerase arrest could also be induced 
by Cr(VI) in the presence of ascorbate as a reducing agent to form 
Cr(III) (Ex. 35-263). These results were confirmed in a cell system by 
treating human lung fibroblasts with soluble Cr(VI), isolating genomic 
DNA, and demonstrating dose-dependent guanine-specific arrest in a DNA 
polymerase assay (Ex. 35-188). Cr(V) may also form intrastrand 
crosslinks since Cr(V) interacts with DNA in vitro (Ex. 35-178). The 
Cr(V)-DNA crosslinks are probably readily reduced to Cr(III) in cell 
systems. Intrastrand crosslinks have also been implicated in inhibition 
of RNA polymerase and DNA topoisomerase, leading to cell cycle arrest, 
apoptosis and possibly other disturbances in cell growth that 
contribute to the carcinogenic pathway (Ex. 35-149).
    DNA strand breaks and oxidative damage result from the one electron 
reduction/oxidation cycling of Cr(VI), Cr(V), and Cr(IV). Shi et al. 
showed that soluble Cr(VI) in the presence of ascorbate and 
H2O2 caused DNA double strand breaks and 8-
hydroxy deoxyguanine (8-OHdG, a marker for oxidative DNA damage) in 
vitro (Ex. 35-129). Leonard et al. showed that the DNA strand breaks 
were reduced by several experimental conditions including an 
O2-free atmosphere, catabolism of H2O2 
by catalase, ROS depletion by free radical scavengers, and chelation of 
Cr(V). They concluded that the strand breaks and 8-OHdG resulted from 
DNA damage caused by hydroxyl radicals from Cr(VI) reduction/oxidation 
cycling (Ex. 31-22-17). Generation of ROS-dependant DNA damage could 
also be shown with insoluble Cr(VI) (Ex. 35-137). DNA strand breaks and 
related damage caused by soluble Cr(VI) have been reported in Chinese 
hamster cells (Ex. 35-128), human fibroblasts (Ex. 311), and human 
prostate cells (Ex. 35-255). Pretreatment of Chinese hamster cells with 
a metal chelator suppressed Cr(V) formation from Cr(VI) and decreased 
DNA strand breaks (Ex. 35-197). Chinese hamster cells that developed 
resistance to H2O2 damage also had reduced DNA 
strand breaks from Cr(VI) treatment compared to the normal phenotype 
(Ex. 35-176).
    Several researchers have been able to modulate Cr(VI)-induced DNA 
damage using cellular reductants such as ascorbate, GSH and the free 
radical scavenger tocopherol (vitamin E). This has provided insight 
into the relationships between DNA damage, reduced chromium forms and 
ROS. Sugiyama et al. showed that Chinese hamster cells pretreated with 
ascorbate decreased soluble Cr(VI)-induced DNA strand damage (e.g., 
alkali-labile sites), but enhanced DNA-amino acid crosslinks (Ex. 35-
133). Standeven and Wetterhahn reported that elimination of ascorbate 
from rat lung cytosol prior to in vitro incubation with soluble Cr(VI) 
completely inhibited Cr-DNA binding (Ex. 35-180). However, not all 
types of Cr-DNA binding are enhanced by ascorbate. Bridgewater et al. 
found that high ratios of ascorbate to Cr(VI) actually decreased 
intrastrand crosslinks in vitro while low ratios induced their 
formation (Ex. 35-263). This finding is consistent with research by 
Stearns and Watterhahn who showed that excessive ascorbate relative to 
Cr(VI) leads to two-electron reduction of Cr(III) and formation of 
Cr(III)-DNA monoadducts and DNA-Cr(III)-amino acid crosslinks (Ex. 35-
166). Low amounts of ascorbate primarily cause one-electron reduction 
to intermediates Cr(V) and Cr(IV) that form crosslinks with DNA and ROS 
responsible for DNA strand breaks, alkali-labile sites, and clastogenic 
damage. This explains the apparent paradox that extracellular Cr(VI) 
reduction by ascorbate to Cr(III) reduces Cr(VI)-induced DNA binding 
but intracellular Cr(VI) reduction by ascorbate to Cr(III) enhances Cr-
DNA binding. The aforementioned studies used soluble forms of Cr(VI), 
but Blankenship et al. showed that ascorbate pretreatment inhibited 
chromosomal aberrations in Chinese hamster ovary cells caused by both 
insoluble lead chromate particles as well as soluble Cr(VI) (Ex. 35-
115). Pretreatment with the free radical scavenger tocopherol also 
inhibits chromosomal aberrations and alkali-labile sites in Cr(VI)-
treated cells (Exs. 35-115; 35-128).
    Studies of the different types of DNA damage caused by Cr(VI) and 
the modulation of that damage inside the cell demonstrate that Cr(VI) 
itself is not biologically active. Cr(VI) must undergo intracellular 
reduction to Cr(V), Cr(IV), and Cr(III) before the damage to DNA can 
occur. The evidence suggests that Cr(III) can cause DNA-Cr-amino acid, 
DNA-Cr-DNA crosslinks and Cr-DNA monoadducts. Cr(V) and possibly Cr(IV) 
contribute to intrastrand crosslinks and perhaps other Cr-DNA binding. 
ROS generated during intracellular reduction of Cr(VI) lead to lesions 
such as chromosomal aberrations, DNA strand breaks, and oxidative DNA 
damage. The specific DNA lesions responsible for neoplastic 
transformation have yet to be firmly established so all forms of DNA 
damage should, at this time, be regarded as potential contributors to 
carcinogenicity.
    d. Cr(VI)-induced Disturbances in the Regulation of Cell 
Replication. Recent research has begun to elucidate how Cr(VI)-induced 
oxidative stress and DNA lesions trigger cell signaling pathways that 
regulate the cell growth cycle. The complex regulation of the cell 
growth cycle by Cr(VI) involves activation of the p53 protein and other 
transcription factors that respond to oxidative stress and DNA damage. 
The cellular response ranges from a temporary pause in the cell cycle 
to terminal growth arrest (i.e., viable cells that have lost the 
ability to replicate) and a programmed form of cell death, known as 
apoptosis. Apoptosis involves alterations in mitochondrial 
permeability, release of cytochrome c and the action of several kinases 
and caspases. Less is known about the molecular basis of terminal 
growth arrest. Terminal growth arrest and apoptosis serve to eliminate 
further growth of cells with unrepaired Cr(VI)-induced genetic damage. 
However, it is believed that cells which escape these protective 
mechanisms and regain replicative competence eventually become 
resistant to normal growth regulation and can transform to a neoplastic 
phenotype (Exs. 35-121; 35-122; 35-120).
    Blankenship et al. first described apoptosis as the primary mode of 
cell death following a two hour treatment of Chinese hamster ovary 
cells with high concentrations (>150 [mu]M) of soluble Cr(VI) (Ex. 35-
144). Apoptosis also occurs in human lung cells following short-term 
treatment with soluble Cr(VI)(Ex. 35-125) as well as longer term treatment
(e.g., 24 hours) with lower concentrations of soluble Cr(VI) (e.g., 10 [mu]M)
and insoluble Cr(VI) in the form of lead chromate (Ex. 35-166). Ye et al. 
found that the Cr(VI) treatment that caused apoptosis also activated expression
of p53 protein (Ex. 35-125). This apoptotic response was substantially 
reduced in a p53-deficient cell line treated with Cr(VI), suggesting 
that the p53 activation was required for apoptosis. Other studies using 
p53 null cells from mice and humans confirmed that Cr(VI)-induced 
apoptosis is p53-dependent (Ex. 35-225).
    The p53 protein is a transcription factor known to be activated by 
DNA damage, lead to cell cycle arrest, and regulate genes responsible 
for either DNA repair or apoptosis. Therefore, it is likely that the 
p53 activation is a response to the Cr(VI)-induced DNA damage. 
Apoptosis (i.e., programmed cell death) is triggered once the Cr(VI)-
induced DNA damage becomes too extensive to successfully repair. In 
this manner, apoptosis serves to prevent replication of genetically 
damaged cells.
    Several researchers have gone on to further elucidate the molecular 
pathways involved in Cr(VI)-induced apoptosis. ROS produced by 
intracellular Cr(VI) reduction/oxidation cycling have been implicated 
in the activation of p53 and apoptosis (Exs. 35-255; 35-122). Using 
specific inhibitors, Pritchard et al. showed that mitochondrial release 
of cytochrome c is critical to apoptotic death from Cr(VI) (Ex. 35-
159). Cytochrome c release from mitochondria could potentially result 
from either direct membrane damage caused by Cr(VI)-induced ROS or 
indirectly by enhanced expression of the p53-dependent apoptotic 
proteins, Bax and Nova, known to increase mitochondrial membrane 
permeability.
    Cr(VI) causes cell cycle arrest and reduces clonogenic potential 
(i.e., normal cell growth) at very low concentrations (e.g., 1 [mu]M) 
where significant apoptosis is not evident. Xu et al. showed that human 
lung fibroblasts treated with low doses of Cr(VI) caused guanine-
guanine intrastrand crosslinks, guanine-specific polymerase arrest, and 
inhibited cell growth at the G1/S phase of the cell cycle 
(Ex. 35-188). Zhang et al. described a dose-dependent increase in 
growth arrest at the G2/M phase of the cell cycle in a human 
lung epithelial cell line following 24 hour Cr(VI) treatment over a 
concentration range of 1 to 10 [mu]M (Ex. 35-135). The cell cycle 
arrest could be partially eliminated by reducing production of Cr(VI)-
induced ROS. Apoptosis was not detected in these cells until a 
concentration of 25 [mu]M Cr(VI) had been reached. These data suggest 
that low cellular levels of Cr(VI) are able to cause DNA damage and 
disrupt the normal cell growth cycle.
    Pritchard et al. studied the clonogenicity over two weeks of human 
fibroblasts treated 24 hours with soluble Cr(VI) concentrations from 1 
to 10 [mu]M (Ex. 35-120). They reported a progressive decline in cell 
growth with increasing Cr(VI) concentration. Terminal growth arrest 
(i.e., viable cells that have lost the ability to replicate) was 
primarily responsible for the decrease in clonogenic survival below 4 
[mu]M Cr(VI). At higher Cr(VI) concentrations, apoptosis was 
increasingly responsible for the loss in clonogenicity. Pritchard et 
al. and other research groups have suggested that a subset of cells 
that continue to replicate following Cr(VI) exposure could contain 
unrepaired genetic damage or could have become intrinsically resistant 
to processes (e.g., apoptosis, terminal growth arrest) that normally 
control their growth (Exs. 35-121; 35-122; 35-120). These surviving 
cells would then be more prone to neoplastic progression and have 
greater carcinogenic potential.
    e. Summary. Respirable chromate particulates are taken up by target 
cells in the bronchoalveolar region of the lung, become intracellularly 
reduced to several reactive genotoxic species able to damage DNA, 
disrupt normal regulation of cell division and cause neoplastic 
transformation. Scientific studies indicate that both water soluble and 
insoluble Cr(VI) can be transported into the cell. In fact, cell 
surface interactions with slightly soluble and insoluble chromates may 
create a concentrated microenvironment of chromate ion, especially in 
the case of the slightly soluble Cr(VI) compounds that more readily 
dissociate. The higher concentration of chromate ion in close proximity 
to the lung cells will likely result in higher intracellular Cr(VI) 
than would occur from the highly water-soluble chromates. This is 
consistent with the studies of respiratory tract carcinogenesis in 
animals that indicate the most tumorigenic chromates had low to 
moderate water solubility. Once inside the cell, Cr(VI) is converted to 
several lower oxidation forms able to bind to and crosslink DNA. ROS 
are produced during intracellular reduction/oxidation of Cr(VI) that 
further damage DNA. These structural lesions are functionally 
translated into a impaired DNA replication, mutagenesis, and altered 
gene expression that ultimately lead to neoplastic transformation.
9. Conclusion
    In the NRPM, OSHA preliminarily concluded that the weight of 
evidence supports the determination that all Cr(VI) compounds should be 
regarded as carcinogenic to workers (69 FR at 59351). This conclusion 
included the highly water soluble chromates, such as sodium chromate, 
sodium dichromate, and chromic acid; chromates of slight and 
intermediate water solubility such as calcium chromate, strontium 
chromates, and many zinc chromates (e.g. zinc yellow); and chromates 
that have very low water solubility and are generally considered to be 
water insoluble such as barium chromate and lead chromates. The 
strongest evidence supporting this conclusion comes from the many 
cohort studies reporting excess lung cancer mortality among workers 
engaged in the production of soluble chromates (Exs. 7-14; 31-22-11; 
23; 31-18-4), chromate pigments (Exs. 7-36; 7-42; 7-46), and chrome 
plating (Exs. 35-62; 35-271). Chromate production workers were 
principally exposed to the highly soluble sodium chromate and 
dichromate (Ex. 35-61) although lesser exposure to other chromates, 
such as highly soluble chromic acid and slightly soluble calcium 
chromate probably occurred. Pigment production workers were principally 
exposed Cr(VI) in the form of lead and zinc chromates. Significantly 
elevated lung cancer mortality was found in two British chromium 
electroplating cohorts (Exs. 35-62; 35-271). These workers were exposed 
to Cr(VI) in the form of chromic acid mist. Therefore, significantly 
elevated lung cancer rates have been observed in working populations 
exposed to a broad range of Cr(VI) compounds.
    Cellular research has shown that both highly water soluble (e.g. 
sodium chromate) Cr(VI) and water insoluble (e.g. lead chromate) Cr(VI) 
enter lung cells (see Section V.8.a) and undergo intracellular 
reduction to several lower oxidation forms able to bind to and 
crosslink DNA as well as generate reactive oxygen species that can 
further damage DNA (see Section V.8.b). Soluble and insoluble Cr(VI) 
compounds are reported to cause mutagenesis, clastogenesis, and 
neoplastic transformation across multiple assays in a wide range of 
experimental systems from prokaryotic organisms to human cells in vitro 
and animals in vivo (see Section V.8.c).
    The carcinogenicity of various Cr(VI) compounds was examined after 
instillation in the respiratory tract of rodents. Slightly water 
soluble Cr(VI) compounds, strontium chromate, calcium chromate, and some 
zinc chromates produced a greater incidence of respiratory tract tumors than 
highly water soluble (e.g. sodium dichromate and chromic acid) and 
water insoluble (e.g. barium chromate and lead chromates) Cr(VI) 
compounds under similar experimental protocol and conditions (see 
Section V.7). This likely reflects the greater tendency for chromates 
of intermediate water solubility to provide a persistent high local 
concentration of solubilized Cr(VI) in close proximity to the target 
cell. Highly soluble chromates rapidly dissolve and diffuse in the 
aqueous fluid lining the epithelia of the lung. Thus, these chromates 
are less able to achieve the higher local concentrations within close 
proximity of the lung cell surface than the slightly water soluble 
chromates. However, it has been shown that water-soluble Cr(VI) can 
still enter lung cells, damage DNA, and cause cellular effects 
consistent with carcinogenesis (Ex. 31-22-18; 35-125; 35-135; 35-142). 
Like the slightly water soluble chromates, water insoluble Cr(VI) 
particulates are able to come in close contact with the lung cell 
surface and slowly dissolve into readily absorbed chromate ion. For 
example, water insoluble lead chromate has been shown to enter human 
airway cells both through extracellular solubilization as chromate ion 
(Exs. 35-66; 35-327; 47-12-3) as well as internalization as 
unsolubilized particulate (Exs. 35-66; 47-19-7). However, the rate of 
solubilization and uptake of water insoluble Cr(VI) is expected to be 
more limited than chromates with moderate solubility. Once chromate ion 
is inside lung cells, studies have shown that similar cellular events 
believed critical to initiating neoplastic transformation occur 
regardless of whether the source is a highly soluble or insoluble 
Cr(VI) compound (Ex. 35-327).
a. Public Comment on the Carcinogenicity of Cr(VI) Compounds
    In the NRPM, OSHA requested comment on whether currently available 
epidemiologic and experimental studies supported the determination that 
all Cr(VI) compounds possess carcinogenic potential and solicited 
additional information that should be considered in evaluating relative 
carcinogenic potency of the different Cr(VI) compounds (69 FR 59307). 
Several comments supported the view that sufficient scientific evidence 
exists to regard all Cr(VI) compounds as potential occupational 
carcinogens (Exs. 38-106-2; 38-222; 39-73-2; 40-10-2; 42-2). The AFL-
CIO stated that " * * * the agency has fully demonstrated that Cr(VI) 
is a human carcinogen and that exposed workers are at risk of 
developing lung cancer" (Ex. 38-222). NIOSH stated that "the 
epidemiologic and experimental studies cited by OSHA support the 
carcinogenic potential of all Cr(VI) compounds (i.e. water soluble, 
insoluble, and slightly soluble)" (Ex. 40-10-2, p. 4). Peter Lurie of 
Public Citizen testified:

    As we heard repeatedly in the course of this hearing, scientific 
experts, in fact, agree. They agree that the most reasonable 
approach to the regulation is to consider them all [Cr(VI) 
compounds] to be carcinogenic (Tr. 710).

    Several commenters agreed that the evidence supported the 
qualitative determination that Cr(VI) compounds were carcinogenic but 
wished to make clear that the information was inadequate to support 
quantitative statements about relative potency of the individual 
chromates (Exs. 38-106-2; 40-10-2; 42-2). For example, the Boeing 
Company in their technical comments stated:

    The available data does support the conclusion that the low 
solubility hexavalent chromium compounds [e.g. strontium chromate] 
can cause cancer but evidence to support a quantitative comparison 
of carcinogenic potency based on differences in solubility is 
lacking (Ex. 38-106-2, p. 18).

Pigment Manufacturers' Comments on Carcinogenicity of Lead Chromate--
One group that did not regard all Cr(VI) compounds as occupational 
carcinogens was the color pigment manufacturers who manufacture and 
market lead chromate pigments which are primarily used in industrial 
coatings and colored plastic articles. The color pigment manufacturers 
maintain that their lead chromate products are unreactive in biological 
systems, are not absorbed into the systemic circulation by any route, 
and can not enter lung cells (Ex. 38-205, p. 14). Their principal 
rationale is that lead chromate is virtually insoluble in water, is 
unable to release chromate ion into aqueous media, and therefore, is 
incapable of interacting with biological systems (Exs. 38-205, p. 95; 
38-201-1, p. 9). The color pigment manufacturers assert that their lead 
chromate pigment products are double encapsulated in a resin/plastic 
matrix surrounded by a silica coating and that the encapsulated pigment 
becomes even less "bioavailable" than unencapsulated "less 
stabilized" lead chromates. They believe the extreme stability and 
non-bioavailable nature of their products makes them a non-carcinogenic 
form of Cr(VI) (Ex. 38-205, p. 106).
    According to the Color Pigment Manufacturers Association (CPMA), 
several pieces of scientific evidence support their position, namely, 
the lack of a significant excess of lung cancer mortality in three 
cohorts of pigment workers engaged in the production of water-insoluble 
lead chromate (Ex. 38-205, pp. 88-91) and the lack of statistically 
significant elevated tumor incidence following a single instillation of 
lead chromate in the respiratory tract of rats (Ex. 38-205, pp. 88-92). 
They dismiss as irrelevant other animal studies that produced 
statistically significant increases in tumors when lead chromate was 
repeatedly injected by other routes. In addition, CPMA claims that the 
lead chromate used in cellular studies that report genotoxicity was 
reagent grade, was contaminated with soluble chromate, and was 
inappropriately solubilized using strong acids and bases prior to 
treatment (Exs. 38-205, pp. 93-94; 47-31, pp. 9-13). They are 
especially critical of studies conducted by the Environmental and 
Genetic Toxicology group at the University of Southern Maine that 
report lead chromate particulates to be clastogenic in human lung cells 
(Exs. 34-6-1; 38-205, pp. 98-102 & appendix D; 47-22). Instead, they 
rely on two in vitro studies of lead chromate pigments that report a 
lack of genotoxicity in cultured bacterial and hamster ovary cells, 
respectively (Exs. 47-3 Appendix C; 38-205, p. 94).
    OSHA addresses many of the CPMA claims in other sections of the 
preamble. The bioavailability issue of encapsulated lead chromate is 
addressed in Section V.A.2. The CPMA request to consider the lack of 
excess lung cancer mortality among pigment workers exposed exclusively 
to lead chromate is discussed in Section V.B.2. The CPMA assertions 
that animal studies are evidence that lead chromates are not 
carcinogenic to workers are addressed in Section V.B.7. The studies 
documenting uptake of lead chromate into lung cells are described in 
Section V.B.8.a. Section V.B.8.c describes evidence that lead chromate 
is genotoxic. As requested by CPMA, OSHA will pull these responses 
together and expand on their concerns below.
    Lung Cancer Mortality in Pigments Workers Exposed to Lead 
Chromate--Comments and testimony from NIOSH and others cite evidence of 
excess lung cancer among pigment workers and support the results of 
OSHA's preliminary risk assessment for color pigments in general and 
for lead chromate in particular (Tr. 135-146, 316, 337, Ex. 40-18-1, p. 
2). However, comments submitted by the CPMA and the Dominion Colour 
Corporation (DCC) attributed the excess lung cancer risk observed in 
pigment worker studies to zinc chromate (Tr. 1707, 1747, Exs. 38-201-1, 
p. 13; 38-205, p. 90; 40-7, p. 92). For example, the CPMA stated that:

    When lead chromate and zinc chromate exposures occur 
simultaneously, there appears to be a significant cancer hazard. 
However, when lead chromate pigments alone are the source of 
chromium exposure, a significant carcinogenic response has never 
been found (Ex. 40-7, p. 92).

The latter statement refers to the Davies et al. (1984) study of 
British pigment workers, the Cooper et al. (1983) study of U.S. pigment 
workers, and the Kano et al. (1993) study of pigment workers in Japan, 
all of which calculated separate observed and expected lung cancer 
deaths for workers exposed exclusively to lead chromate (Ex. 38-205, p. 
89). DCC and the Small Business Administration's Office of Advocacy 
similarly stated that the excess lung cancer risk observed among 
workers exposed to both zinc chromate and lead chromate cannot 
necessarily be attributed to lead chromate (Exs. 38-201-1, p. 13; 38-7, 
p. 4).
    OSHA agrees with CPMA and DCC that the excess lung cancer observed 
in most pigment worker studies taken alone cannot be considered 
conclusive evidence that lead chromate is carcinogenic. Given that the 
workers were exposed to both zinc chromate and lead chromate, it is not 
possible to draw strong conclusions about the effects of either 
individual compound using only these studies. However, based on the 
overall weight of available evidence, OSHA believes that the excess 
lung cancer found in these studies is most likely attributable to lead 
chromate as well as zinc chromate exposure. Lead chromate was the 
primary source of Cr(VI) for several worker cohorts with excess lung 
cancer (e.g., Davies et al. (1984), Factory A; Hayes et al. (1989); and 
Deschamps et al. (1995)) (Exs. 7-42; 7-46; 35-234), and as previously 
discussed, there is evidence from animal and mechanistic studies 
supporting the carcinogenicity of both zinc chromate and lead chromate. 
Considered in this context, the elevated risk of lung cancer observed 
in most chromate pigment workers is consistent with the Agency's 
determination that all Cr(VI) compounds--including lead chromate--
should be regarded as carcinogenic.
    Moreover, OSHA disagrees with the CPMA and DCC interpretation of 
the data on workers exposed exclusively to lead chromate. In the 
Preamble to the Proposed Rule, OSHA stated that "[t]he number of lung 
cancer deaths [in the Davies, Cooper, and Kano studies] is too small to 
be meaningful" with respect to the Agency's determination regarding 
the carcinogenicity of lead chromate (FR 69 at 59332). The CPMA 
subsequently argued that:

    [b]y this rationale, OSHA could never conclude that a compound 
such as lead chromate pigment exhibits no carcinogenic potential 
because there can never be enough lung cancer deaths to produce a 
"meaningful" result. This is an arbitrary and obviously biased 
assessment which creates an insurmountable barrier. Since the lead 
chromate pigments did not create an excess of lung cancer, there 
cannot be a significant enough mortality from lung cancer to be 
meaningful (Ex. 38-205, p. 90).

OSHA believes that these comments reflect a misunderstanding of the 
sense in which the Davies, Cooper, and Kano studies are too small to be 
meaningful, and also a misunderstanding of the Agency's position.
    Contrary to CPMA's argument, a study with no excess in lung cancer 
mortality can provide evidence of a lack of carcinogenic effect if the 
confidence limits for the measurement of effect are close to the null 
value. In other words, the measured effect must be close to the null 
and the study must have a high level of precision. In the case of the 
Davies, Cooper, and Kano studies, the standardized mortality ratio 
(SMR) is the measurement of interest and the null value is an SMR of 1. 
Table V.10 below shows that the SMRs for these study populations are 
near or below 1; however, the 95% confidence intervals for the SMRs are 
quite wide, indicating that the estimated SMRs are imprecise. The Kano 
data, for example, are statistically consistent with a "true" SMR as 
low as 0.01 or as high as 2.62. The results of these studies are too 
imprecise to provide evidence for or against the hypothesis that lead 
chromate is carcinogenic.

Click here to view table V-10

    This lack of precision may be partly explained by the small size of 
the studies, as reflected in the low numbers of expected lung cancers. 
However, it is the issue of precision, and not the number of lung 
cancer deaths per se, that led OSHA to state in the preamble to the 
proposed rule that the Davies, Cooper, and Kano studies cannot serve as 
the basis of a meaningful analysis of lead chromate carcinogenicity 
(Exs. 7-42; 2-D-1; 7-118). In contrast, a study population that has 
confidence limits close to or below 1 would provide evidence to support 
the DCC claim that " * * * if lead chromate pigments possess any 
carcinogenic potential at all, it must be extremely small" (Ex. 38-
201-1, p. 14) at the exposure levels experienced by that population. 
While this standard of evidence has not been met in the epidemiological 
literature for pigment workers exposed exclusively to lead chromate 
(i.e., the Davies, Cooper, and Kano studies), it is hardly an 
"insurmountable barrier" that sets up an impossible standard of proof 
for those who contend that lead chromate is not carcinogenic.
    Some comments suggested that the Davies, Cooper, and Kano studies 
should be combined to derive a summary risk measure for exposure to 
lead chromate (see e.g. Ex. 38-201-1, pp. 13-14). However, OSHA 
believes that these studies do not provide a suitable basis of meta-analysis.
There is little information with which to assess factors recognized by 
epidemiologists as key to meta-analysis, for example sources of bias or 
confounding in the individual studies and comparability of exposures and 
worker characteristics across studies, and to verify certain conditions 
required for comparability of SMRs across these studies (see e.g. Modern 
Epidemiology, Rothman and Greenland, p. 655). In addition, the 
inclusion criteria and length of follow-up differ across the three 
studies. Finally, each of the studies is extremely small. Even if it 
were appropriate to calculate a 'summary' SMR based on them, the 
precision of this SMR would not be much improved compared to those of 
the original studies.
    In their written testimony, DCC suggested that OSHA should 
aggregate the data from the Davies, Cooper, and Kano studies in order 
to determine whether there is a discrepancy between the results of 
these three studies, taken together, and OSHA's preliminary risk 
assessment (Ex. 38-201-1, pp. 13-14). DCC performed a calculation to 
compare OSHA's risk model with the observed lung cancer in the three 
cohorts. DCC stated that:

    OSHA estimates a chromate worker's risk of dying from lung 
cancer due to occupational exposure as about one chance in four * * 
* [Assuming that there were about] 200 workers in the Kano study, 
the total in the three studies would be 600. A calculation of one 
quarter would be 150 deaths. To compensate for a working life of 
less than OSHA's 45 years [an assumption of 20 years] provides * * * 
a refined estimate of about 70 deaths. An observed number less than 
this could be due either to exposures already in practice averaging 
much less than the current PEL of 52, or to lead chromate having 
much less potential (if any) for carcinogenicity than other 
chromates. In any event the actual incidence of death from lung 
cancer would appear to be no more than one tenth of OSHA's best 
estimate (Ex. 38-201-1, pp. 15-16).

The method suggested by DCC is not an appropriate way to assess the 
carcinogenicity of lead chromate, to identify a discrepancy between the 
pigment cohort results and OSHA's risk estimates, or to determine an 
exposure limit for lead chromate. Among other problems, DCC's 
calculation does not make a valid comparison between OSHA's risk 
estimates and the results of the Davies, Cooper, and Kano studies. 
OSHA's 'best estimate' of lung cancer risk for any given Cr(VI)-exposed 
population depends strongly on factors including exposure levels, 
exposure duration, population age, and length of follow-up. The 'one in 
four' prediction cited by DCC applies to one specific risk scenario 
(lifetime risk from 45 years of occupational exposure at the previous 
PEL of 52 [mu]g/m\3\). OSHA's best estimate of risk would be lower for 
a population with lower exposures (as noted by DCC), shorter duration 
of exposure, or less than a lifetime of follow-up. Without adequate 
information to adjust for each of these factors, a valid comparison 
cannot be drawn between OSHA's risk predictions and the results of the 
lead chromate cohort studies.
    The importance of accounting for cohort age and follow-up time may 
be illustrated using information provided in the Cooper et al. study. 
As shown in Table V-11 below, approximately three-fourths of the Cooper 
et al. Plant 1 cohort members were less than 60 years old at the end of 
follow-up.

Click here to view table V-11

    For a population of 600 with approximately the same distribution of 
follow-up time as described in the Cooper et al. publication (e.g., 
0.4% of workers are followed to age 84, 2% to age 79, etc.), OSHA's 
risk model predicts about 3-15 excess lung cancers (making the DCC 
assumption that workers are exposed for 20 years at 52 [mu]g/m\3\), 
rather than the 70 deaths calculated by the DCC. If the workers were 
typically exposed for less than 20 years or at levels lower than 52 
[mu]g/m\3\, OSHA s model would predict still lower risk. A precise 
comparison between OSHA's risk model and the observed lung cancer risk 
in the Davies, Cooper and Kano cohorts is not possible without 
demographic, work history and exposure information on the lead chromate 
workers. (In particular, note that year 2000 background lung cancer 
rates were used in the calculation above, as it was not feasible to 
reconstruct appropriate reference rates without work history 
information on the cohorts.) However, this exercise illustrates that 
DCC's assertion of a large discrepancy between OSHA's risk model and 
the available data on workers exposed exclusively to lead chromate is 
not well-founded. To make a valid comparison between the OSHA risk
model and the lung cancer observed in the lead chromate cohorts would 
require more information on exposure and follow-up than is available 
for these cohorts.
    OSHA received comments and testimony from NIOSH and others 
supporting of the Agency's interpretation of the epidemiological 
literature on Cr(VI) color pigments, including lead chromate (Tr. 135-
146, 316, 337, Ex. 40-18-1, p. 2). At the hearing, Mr. Robert Park of 
NIOSH stated that the available studies of workers exposed to chromate 
pigments show " * * * a general pattern of excess [lung cancer] * * * 
" and pointed out that "[i]n several of the studies, lead [chromate] 
was by far the major component of production, like 90 percent * * * So 
I don't think there is any epidemiological evidence at this point that 
gets lead off the hook" (Tr. 337). Regarding the lack of statistically 
significant excess lung cancer in several pigment worker cohorts, Mr. 
Park identified study attributes that may have obscured an excess in 
lung cancer, such as the high percentage of workers lost to follow-up 
among immigrant workers in the Davies et al. study (Tr. 337) or a 
healthy worker effect in the Hayes et al. study (Tr. 316). Dr. Paul 
Schulte of NIOSH explained that

    * * * a lot of these studies that appear to be negative were 
either of low power or had [some] other kind of conflicting 
situation [so] that we can't really consider them truly negative 
studies (Tr. 338).

Dr. Herman Gibb testified that the epidemiological studies relied on by 
CPMA and DCC to question the carcinogenicity of lead chromate have very 
low expected numbers of lung cancer deaths, so they " * * * really 
don't have a lot of ability to be able to detect a risk" (Tr. 135-
136). Public Citizen agreed with OSHA's preliminary conclusion that 
lead chromate is carcinogenic. Based on the major pigment worker 
cohorts identified by OSHA in the Preamble to the Proposed Rule, Public 
Citizen's Health Research Group concluded that

    * * * inadequately-powered studies, the standardized mortality 
ratios for exposed workers are significantly elevated (range 1.5-
4.4) and a relationship between extent of exposure (whether measured 
by duration of exposure or factory) generally emerges; [moreover,] 
[t]hese studies must be placed in the context * * * of the animal 
carcinogenicity studies * * * and the mechanistic studies reviewed 
by OSHA (Ex. 40-18-1, p. 2).

Tumor Incidence in Experimental Animals Administered Lead Chromate--
CPMA also claims that the absence of evidence for carcinogenicity found 
among the three cited cohorts of lead chromate pigment workers " * * * 
is further confirmed by the rat implantation studies of Levy" (Ex. 38-
205, p. 98). They argue that these studies which involved implantation 
into rat lungs " * * * indicated no increased incidence of tumors for 
lead chromate pigment, although more soluble chromates exhibited 
varying degrees of carcinogenicity" (Ex. 38-205, p. 93). They 
dismissed other animal studies involving intramuscular and subcutaneous 
injection of lead chromate which did report increased incidence of 
tumors because they believe these techniques

    * * * are of questionable relevance in relation to human 
workplace exposure conditions in industry, whereas tests involving 
implantation in rat lung * * * are relevant to inhalation in 
industrial exposures (Ex. 38-205, p. 93).

In a more recent submission, CPMA remarked that the intramuscular and 
subcutaneous injection studies with lead chromate were contradictory 
and " * * * problematic in that false positive results frequently 
occur during the study procedure (Ex. 47-31, p. 13).
    The rat implantation studies of Levy involved the surgical 
placement of a Cr(VI)-containing pellet in the left bronchus of an 
anesthetized rat (Exs. 10-1; 11-12; 11-2). This pellet procedure was an 
attempt to deliver Cr(VI) compounds directly to the bronchial 
epithelium and mimic continuous chronic in vivo dosing at the tissue 
target site in order to assess the relative ability of different Cr(VI) 
compounds to induce bronchogenic carcinoma. Histopathological 
evaluation of the rat lung was conducted after a two year exposure 
time. In most cases, approximately 100 rats were implanted with a 
single pellet for each Cr(VI) test compound. The total lifetime dose of 
Cr(VI) received by the animal was generally between 0.2 and 1.0 mg 
depending on the compound. The amount of Cr(VI) that actually leached 
from the cholesterol pellet and remained near the lung tissue was never 
determined. At least 20 different commercially relevant Cr(VI) 
compounds ranging from water insoluble to highly water soluble were 
tested using this intrabronchial implantation protocol.
    The results of these studies are described in preamble section 
V.B.7 and tables V-7, V-8, and V-9. Reagent grade lead chromate and six 
different lead chromate pigments were tested. The lead chromate 
pigments were a variety of different chrome yellows, including a silica 
encapsulated chrome yellow, and molybdenum orange. The incidence of 
bronchogenic cancer in the rats under this set of experimental 
conditions was one percent or less for all the lead chromates tested. 
This incidence was not statistically different from the negative 
controls (i.e. rats implanted with a cholesterol pellet containing no 
test compound) or rats administered either the water-insoluble barium 
chromate or the highly soluble chromic acid and sodium dichromate. The 
percent incidence of bronchogenic cancer in lead chromate-treated rats 
was substantially less than that of rats treated with slightly soluble 
strontium chromates (about 52 percent) and calcium chromate (24 
percent). The type of bronchogenic cancer induced in these experiments 
was almost entirely squamous cell carcinomas.
    OSHA does not agree with the CPMA position that absence of a 
significant tumor incidence in the intrabronchial implantation studies 
confirms that lead chromates lack carcinogenic activity and, therefore, 
should not be subject to the OSHA Cr(VI) standard. The bioassay 
protocol used approximately 100 test animals per experimental group. 
This small number of animals limits the power of the bioassay to detect 
tumor incidence below three to four percent with an acceptable degree 
of statistical confidence. Three of the lead chromates, in fact, 
produced a tumor incidence of about one percent (e.g. 1 tumor in 100 
rats examined) which was not statistically significant. The researchers 
only applied a single 2 mg [approximately 0.3 mg Cr(VI)] dose of lead 
chromate to the bronchus of the rats. Since it was not experimentally 
confirmed that the lead chromate pigments were able to freely leach 
from the cholesterol pellet, the amount of Cr(VI) actually available to 
the lung tissue is not entirely clear. Therefore, OSHA believes a more 
appropriate interpretation of the study findings is that lead chromates 
delivered to the respiratory tract at a dose of about 0.3 mg Cr(VI) 
(maybe lower) lead to a less than three percent tumor incidence.
    However, OSHA agrees that the intrabronchial implantation protocol 
does provide useful information regarding the relative carcinogenicity 
of different Cr(VI) compounds once they are delivered and deposited in 
the respiratory tract. No other study examines the carcinogenicity of 
such a broad range of commercial Cr(VI) compounds under the same 
experimental conditions in the relevant target organ to humans (i.e. 
respiratory tract) following in vivo administration. OSHA agrees with 
CPMA that the results of this study provide credible
evidence that water insoluble lead chromates are less carcinogenic than 
some of the more moderately soluble chromates. Specifically, this 
includes the slightly soluble zinc chromates (e.g. zinc yellow, zinc 
potassium chromates, basic zinc chromates) as well as strontium 
chromate and calcium chromate. Intrabronchial implantation of chromic 
acid and other highly soluble Cr(VI) salts, such as sodium chromates, 
did not induce a significant number of tumors. Therefore, these 
experiments do not indicate lead chromate are less carcinogenic than 
the highly water soluble Cr(VI) compounds.
    If the histopathology data from the intrabronchial implantation is 
examined more closely, all lead chromates increased the incidence of 
squamous metaplasia relative to controls, and, for some lead chromates, 
squamous dysplasia of the bronchial epithelium occurred (Table 2, Ex. 
11-2). Squamous metaplasia and dysplasia are generally considered to be 
transformed cellular states from which a neoplasm (e.g. carcinomas) can 
arise (Ex. 11-12). Increased squamous metaplasia was common among all 
tested Cr(VI) compounds but not among Cr(III)-containing materials or 
the negative controls (Ex. 11-12). The increased metaplasia induced by 
lead chromates is unlikely to be due to bronchial inflammation since 
the degree of inflammation was no greater than that observed in the 
cholesterol-implanted controls (Table 2, Ex. 11-2).
    The squamous metaplasia and dysplasia in the rat lung model 
following low dose lead chromate administration is consistent with a 
low carcinogenic response (e.g. incidence of one percent or less) not 
able to be detected under the conditions of the animal bioassay. This 
explanation is supported by studies (discussed later in the section) 
that show lead chromate can enter lung cells, damage DNA, and cause 
genotoxic events leading to neoplastic transformation.
    Lead chromate carcinogenicity is also supported by the animal 
studies that CPMA dismisses as problematic and of questionable 
relevance. These studies administered lead chromates to rodents by 
either the subcutaneous (Exs. 8-25, 5-2, 8-37) or intramuscular routes 
(Ex. 10-2). While OSHA agrees that these routes may be less relevant to 
occupational inhalation than implantation in the respiratory tract, the 
studies exposed rats to a larger dose of lead chromate. The higher 
amounts of Cr(VI) produced a significant incidence of tumors at the 
injection site (see section V.B.7.c).
    The lead chromate pigments, chrome yellow and chrome orange, 
induced injection site rhabdomyosarcomas and fibrosarcomas in 65 
percent of animals following a single 30 mg injection in a saline 
suspension (Ex. 8-37). The rats received a roughly ten fold higher dose 
of Cr(VI) than in the intrabronchial bioassay. Rats injected with 
saline alone did not develop injection site tumors. Only two percent or 
less of rats receiving equal quantities of the inorganic pigments iron 
yellow and iron red developed these tumors. The iron oxides are not 
considered to be carcinogenic and do not give a significant neoplastic 
response in this bioassay. OSHA has no reason to believe the 
experimental procedure was problematic or given to frequent false 
positives.
    A similarly high incidence (i.e. 70 percent) of the same injection 
site sarcomas were found in an independent study in which rats were 
injected intramuscularly with reagent grade lead chromate once a month 
for nine months (Ex. 10-2). Each injection contained approximately 1.3 
mg of Cr(VI) and the total dose administered was over 30 times higher 
than the intrabronchial implantation. The lead chromate was 
administered in a glycerin vehicle. The vehicle produced less than a 
two percent incidence of injection site sarcomas when administered 
alone.
    Contrary to statements by Eurocolour (Ex. 44-3D), lead chromate did 
produce a low incidence of site-of-contact tumors in rats in an earlier 
study when administered by either intramuscular or intrapleural 
implantation (Ex. 10-4). There was no tumor incidence in the control 
animals. The dose of lead chromate in this early publication was not 
stated.
    Based on the increase in pre-neoplastic changes from the single low 
dose intrabronchial implantation and the high incidence of malignant 
tumors resulting from larger doses administered by subcutaneous and 
intramuscular injection, it is scientifically reasonable to expect that 
larger doses of lead chromate may have produced a higher incidence of 
tumors in the more relevant intrabronchial implantation procedure. The 
highly soluble sodium dichromate produced a small (statistically 
insignificant) incidence of squamous cell carcinoma (i.e. one percent) 
upon single low dose intrabronchial implantation similar to the lead 
chromates (Ex. 11-2). In another study, sodium dichromate caused a 
significant 17 percent increase in the incidence of respiratory tract 
tumors when instilled once a week for 30 months in the trachea of rats 
(Ex. 11-7). The weekly-administered dose for this repeated instillation 
was about \1/5\th the dose of that used in the intrabronchial 
implantation assay but the total administered dose after 30 months was 
about 25 times higher. Rats that received a lower total dose of sodium 
dichromate or the same total dose in more numerous instillations (i.e. 
lower dose rate) developed substantially fewer tumors that were 
statistically indistinguishable from the saline controls. A third study 
found a 15 percent increase (not statistically significant) in lung 
tumor incidence when rats repeatedly inhaled aerosolized sodium 
dichromate for 18 months at the highest air concentrations tested (Ex. 
10-11). These sodium dichromate studies are further described in 
section V.B.7.a. The findings suggest that the lack of significant 
carcinogenic activity in the intrabronchial implantation study 
reflects, in part, the low administered dose employed in the bioassay.
    In his written testimony to OSHA, Dr. Harvey Clewell directly 
addressed the issue of interpreting the absence of carcinogenicity in 
an animal study as it relates to significant risk.

    First, the ability to detect an effect depends on the power of 
the study design. A statistically-based No Observed Adverse Effect 
Level (NOAEL) in a toxicity study does not necessarily mean that 
there is no risk of adverse effect. For example, it has been 
estimated that a NOAEL in a typical animal study can actually be 
associated with the presence of an effect in as many as 10% to 30% 
of the animals. Thus the failure to observe a statistically 
significant increase in tumor incidence at a particular exposure 
does not rule out the presence of a substantial carcinogenic effect 
at that exposure * * *. Similarly the failure of Levy et al. (1986) 
to detect an increase in tumors following intrabronchial 
instillation of lead chromate does not in itself demonstrate a lack 
of carcinogenic activity for that compound. It only demonstrates a 
lower activity than for other compounds that showed activity in the 
same experimental design. Presumably this lower activity is 
primarily due to its low solubility; evidence of solubilization, 
cellular uptake, and carcinogenic activity of this compound [i.e. 
lead chromate] is provided in other studies (Maltoni et al. 1974, 
Furst et al., 1976, Blankenship et al., 1997; Singh et al., 1999; 
Wise et al., 2004) (Ex. 44.5, p. 13-14).

    OSHA agrees with Dr. Clewell that the inability to detect a 
statistically significant incidence of tumors in one study that 
administers a single low dose of lead chromate to a limited number of 
animals is not evidence that this Cr(VI) compound lacks carcinogenic 
activity. This is especially true when there exists an elevation in 
pre-neoplastic lesions and other studies document significant
tumor incidence in animals administered higher doses of lead chromate.
    Cellular Uptake and Genotoxicity of Lead Chromate--CPMA disputes 
the many studies that report lead chromate to be genotoxic or 
clastogenic in cellular test systems (Exs. 35-162; 12-5; 35-119; 35-
188; 35-132; 35-68; 35-67; 35-115; 35-66; 47-22-1; 47-12-3; 35-327; 35-
436). They claim that the studies inappropriately solubilized the lead 
chromate " * * * in non-biological conditions such as strong alkali or 
strong acid that causes the chemical breakdown of the lead chromate 
crystal" (Ex. 38-205, p. 94) and the "lead chromate had been 
dissolved * * * using aggressive substances" (Ex. 38-205, p. 99). In a 
later submission, CPMA states state that some of the cellular studies 
used reagent grade lead chromate that is only >=98 percent pure and may 
contain up to 2 percent soluble chromate (Ex. 47-31, p. 11). They 
speculate that the interactions (e.g. chromate ion uptake, chromosomal 
aberrations, DNA adducts, etc.) described in studies using cell 
cultures treated with lead chromate are either due to the presumed 
contamination of soluble chromate or some other undefined "reactive 
nature" of lead chromate. CPMA adds that " * * * the studies 
referenced by OSHA [that use reagent grade lead chromate] have no 
relevance to occupational exposures to commercial lead chromate 
pigments" (Ex. 38-205, p. 11-12).
    OSHA agrees that studies involving lead chromate pre-solubilized in 
solutions of hydrochloric acid, sodium hydroxide or other strong acids 
and bases prior to treatment with cells are not particularly relevant 
to the inhalation of commercial lead chromate particulates. However, 
several relevant cellular studies have demonstrated that lead chromate 
particulates suspended in biological media and not can enter lung 
cells, damage DNA, and cause altered gene expression as described 
below.
    Beginning in the late 1980s, there has been a consistent research 
effort to characterize the genotoxic potential of lead chromate 
particulate in mammalian cells. The lead chromate was not pre-
solubilized prior to cell treatment in any of these investigations. In 
most of the studies, lead chromate particles were rinsed with water and 
then acetone. The rinses cleansed the particles of water- and acetone-
soluble contaminants before cell treatment. This served to remove any 
potential water-soluble Cr(VI) present that might confound the study 
results. In most instances, the lead chromate particles were filtered, 
stirred or sonicated in suspension to break up the aggregated particles 
into monomeric lead chromate particulates. These lead chromate 
particulates were primarily less than 5 [mu]m in diameter. This is 
consistent with the inhaled particle size expected to deposit in the 
bronchial and alveolar regions of the lung where lung cancer occurs. 
Air-dried lead chromate particulates were introduced to the cell 
cultures in a suspension of either saline-based media or acetone. Lead 
chromate particulate is considered to be insoluble in both solvents so 
significant solubilization is not expected during the process of 
creating a homogenous suspension.
    The initial research showed that lead chromate particulate 
morphologically transformed mouse and hamster embryo cells (Exs. 35-
119; 12-5). One study tested a variety of lead chromate pigments of 
different types (e.g. chrome yellows, chrome oranges, molybdate 
oranges) as well as reagent grade lead chromate (Ex. 12-5). The 
transformed cells displayed neoplastic properties (e.g. growth in soft 
agar) and were tumorigenic when injected into animals (Ex. 35-119; 12-
5). While lead chromate particulate transformed mouse embryo cells, it 
is important to note that lead chromate particulate was not found to be 
mutagenic in these cells suggesting that other types of genetic lesions 
(e.g. clastogenicity) may be involved (Ex. 35-119).
    Follow-on research established that lead chromate particulate 
caused DNA-protein crosslinks, DNA strand breaks, and chromosomal 
aberrations (i.e. chromatid deletions and achromatic lesions combined) 
in mammalian cells rather than DNA nucleotide binding often associated 
with base substitution and frameshift mutations captured in a standard 
Ames assay (Exs. 35-132; 35-188). This distinguishes lead chromate 
particulate from high concentrations of soluble Cr(VI) compounds or 
pre-solubilized lead chromate which can cause these mutations.
    Lead chromate particulate enters mammalian embryo cells by two 
distinct pathways (Ex. 35-68). It partially dissolves in the culture 
medium (i.e. biological saline solution) to form chromate ion, which is 
then transported into the cell. The rate of particle dissolution was 
shown to be time- and concentration-dependent. The measured chromate 
ion concentration was consistent with that predicted from the lead 
chromate solubility constant in water. Lead chromate particulates were 
shown to adhere to the embryo cell surface enhancing chromate ion 
solubilization leading to sustained intracellular chromium levels and 
measurable chromosomal damage (Ex. 35-67).
    Lead chromate particulates are also internalized into embryo cells, 
without dissolution, by a phagocytic process (Ex. 35-68). The lead 
chromate particles appeared to remain undissolved in tight vacuoles 
(i.e. phagosomes) within the cell over a 24 hour period. Treatment of 
embryo cells with lead chromate particulates in the presence of a 
reducing agent (i.e. ascorbate) substantially reduced cellular uptake 
of dissolved chromate ions and the chromosomal damage, but did not 
impact the internalization of lead chromate particulates (Ex. 35-68). 
This suggests that chromosomal damage by lead chromate was the result 
of extracellular particle dissolution and not internalization under the 
particular experimental conditions. Embryo cell treatment with large 
amounts of lead glutamate that produced high intracellular lead in the 
absence of Cr(VI) did not cause chromosomal damage further implicating 
intracellular chromium as the putative clastogenic agent (Ex. 35-67).
    As the ability to maintain human tissue cells in culture improved 
in the 1990s, dissolution and internalization of lead chromate 
particulates, uptake of chromate ion, and the resulting chromosomal 
damage were verified in human lung cells (Exs. 35-66; 47-22-1; 47-12-3; 
35-327; 35-436). Lead chromate particulates are internalized, form 
chromium adducts with DNA, and trigger dose-dependent apoptosis in 
human small airway epithelial cells (Ex. 35-66). They also cause dose-
dependent increases in intracellular chromium, internalized lead 
chromate particulates and chromosomal damage in human lung fibroblasts 
(Exs. 47-22-1; 47-12-3). The chromosomal damage from lead chromate in 
these human lung cells is dependent on the extracellular dissolution 
and cell uptake of the chromate, rather than lead, in a manner similar 
to dilute concentrations of the highly soluble sodium chromate (Ex. 47-
12-3; 35-327). Another water insoluble Cr(VI) compound, barium chromate 
particulate, produces very similar responses in human lung fibroblasts 
(Ex. 35-328). Human lung macrophages can phagocytize lead chromate 
particulates and trigger oxidation-reduction of Cr(VI) to produce 
reactive oxygen species capable of damaging DNA and altering gene 
expression (Ex. 35-436).
    OSHA finds these recent studies to be carefully conceived and 
executed by reputable academic laboratories. The scientific findings 
have been published in well-respected peer reviewed
molecular cancer and toxicology journals, such as Carcinogenesis (Exs. 
12-5, 35-68), Cancer Research (Ex. 35-119), Toxicology and Applied 
Pharmacology (Exs. 35-66; 25-115), and Mutation Research (Exs. 35-132; 
47-22-1; 35-327). Contrary to statements by CPMA, the results indicate 
that lead chromate particulates are able to dissociate in the presence 
of biological media without the aid of aggressive substances. The 
resulting chromate ion is bioavailable to enter lung cells, damage 
genetic material and initiate events critical to carcinogenesis. These 
effects can not be attributed to small amounts of soluble chromate 
contaminants since these substances are usually removed as part of the 
test compound preparation prior to cell treatment.
    As one of the study authors, Dr. John Wise of the University of 
Southern Maine, stated in his post-hearing comments:

    At no time did we dissolve lead chromate particles prior to 
administration. At the initial onset of the administration of lead 
chromate particles in our studies, the cells encountered intact lead 
chromate particles. Any dissolution that occurred was the natural 
result of the fate of lead chromate particles in a biological 
environment (Ex. 47-12, p. 3).

Other scientists concurred that the methods and findings of the 
cellular research with lead chromate were reasonable. Dr. Kathleen 
MacMahon, a biologist from NIOSH stated:

    NIOSH believes that the methods that were used in the [lead 
chromate] studies were credible and we support the results and 
conclusions from those studies (Tr. 342).

Dr. Clewell said:

    As I recall, it [lead chromate particles] was suspended in 
acetone and ultrasonically shaken to reduce it to submicron 
particles, which seems like a reasonably good thing to do. There are 
actually a couple of studies besides the Wise studies that have 
looked at the question of the uptake of lead chromate. I have looked 
at those studies and I don't really see any basic flaws in what they 
did. It is obviously a challenge to reproduce inhalation exposure in 
vitro (Tr. 180-181).

Chromosal Aberrations and Lead Chromate--Several submissions contained 
testimony from another researcher, Dr. Earle Nestmann of CANTOX Health 
Sciences International, that criticized the methodology and findings of 
a study published by the research group at the University of Southern 
Maine (Exs. 34-6-1; 38-205D; 47-12-1; 47-22). Dr. Nestmann viewed as 
inappropriate the practice of combining the chromatid deletions and 
achromatic lesions together as chromosomal aberrations. He indicated 
the standard practice was to score these two types of lesions 
separately and that only the deletions had biological relevance. 
According to Dr. Nestmann, achromatic lesions are chromatid gaps (i.e. 
lesion smaller than the width of one chromatid) that have no 
clastogenic significance and serve to inflate the percentage of cells 
with chromosomal aberrations (i.e. chromatid deletions or breaks). Dr. 
Nestmann criticized the studies for not including a positive control 
group that shows the experimental system responds to a 'true' 
clastogenic effect (i.e. a compound that clearly increases chromosomal 
deletions without contribution from chromatid gaps).
    Dr. John Wise, the Director of the research laboratory at the 
University of Southern Maine, responded that distinguishing chromatid 
gaps from breaks is a subjective distinction (e.g. requiring judgment 
as to the width of a lesion relative to the width of a chromatid) and 
pooling these lesions simply reduces this potential bias (Ex. 47-12; 
47-12-1). He stated that there is no consensus on whether gaps should 
or should not be scored as a chromosomal aberration and that gaps have 
been included as chromosomal aberrations in other publications. Dr. 
Wise also points out that achromatic lesions have not been shown to 
lack biological significance and that the most recent research 
indicates that they may be related to DNA strand breaks, a 
scientifically accepted genotoxic endpoint. Dr. Wise further believed 
that a positive control was unnecessary in his experiments since the 
purpose was not to determine whether lead chromate was a clastogenic 
agent, which had already been established by other research. Rather, 
the purpose of his studies was to assess Cr(VI) uptake and chromosomal 
damage caused by water-insoluble lead chromate compared to that of 
highly water soluble sodium chromate using a relevant in vitro cell 
model (i.e. human lung cells).
    OSHA is not in a position to judge whether achromatic lesions 
should be scored as a chromosomal aberration. However, OSHA agrees with 
Dr. Nestmann that combining gaps and breaks together serves to increase 
the experimental response rate in the studies. Given the lack of 
consensus on the issue, it would have been of value to record these 
endpoints separately. OSHA is not aware of data that show achromatic 
gaps to be of no biological significance. The experimental data cited 
above indicate that soluble and insoluble Cr(VI) compounds clearly 
increase achromatic gaps in a concentration-dependent manner. The 
chromatid lesions (gaps and breaks) may be chromosomal biomarkers 
indicative of genetic damage that is critical to neoplastic 
transformation. Furthermore, OSHA agrees with Dr. Wise that other 
evidence establishes lead chromate as an agent able to cause DNA damage 
and transform cells. The Agency considers the use of sodium chromate-
treated cells in the above set of experiments to be the appropriate 
comparison group and does not find the absence of an additional 
positive control group to be a technical deficiency of the studies. 
OSHA considers the research conducted at the University of Southern 
Maine documenting chromosomal damage in human lung cells following 
treatment with lead chromate particulates to be consistent with results 
from other studies (see Section V.B.8) and, thus, contributes to the 
evidence that water insoluble lead chromate, like other chromates, is 
able to enter lung cells and damage DNA.
    In post-hearing comments, CPMA provided a Canadian research 
laboratory report that tested the lead chromate Pigment Yellow 34 for 
chromosomal aberrations in a hamster embryo cell system (Ex. 47-3, 
appendix C). The research was sponsored by DCC and its representative 
Dr. Nestmann. Lead chromate particles over the concentration range of 
0.1 [mu]/cm2 to 10 [mu]/cm2 were reported to not 
induce chromosomal aberrations under the experimental test conditions. 
Chromatid structural and terminal gaps were not scored as aberrations 
in this study, even though the percentage of cells with these lesions 
increased in a dose-dependent manner from two percent in the absence of 
lead chromate to over thirteen percent in cells treated with 1 [mu]/
cm2 lead chromate pigment particles.
    This result is consistent with other experimental data that show 
lead chromate particulates cause chromosomal lesions when administered 
to mammalian embryo cells (Exs. 35-188; 35-132; 35-68; 35-67). The key 
difference is how the various researchers interpreted the data. The 
George Washington University group (i.e. Pateirno, Wise, Blankenship et 
al.) considered the dose-dependent achromatic lesions (i.e. chromatid 
gaps) as a clastogenic event and included them as chromosomal damage. 
The Canadian test laboratory (i.e. Nucrotechnics) reported achromatic 
lesions but did not score them as chromosomal aberrations. Reporting 
achromatic lesions but not scoring them as chromosomal aberrations is 
consistent with regulatory test guidelines as currently recommended by 
EPA and OECD. The Nucrotechnics data suggest that the tested lead chromate 
pigment caused a similar degree of chromosomal damage (i.e. dose-dependent 
achromatic lesions and chromosomal aberrations combined) in mammalian cells. 
This result was similar to results produced by reagent grade lead chromate in 
previous studies.
    Mutagenicity and Lead Chromate--CPMA also relied on a study that 
reported a lack of mutagenicity for lead chromate pigments in a 
bacterial assay using Salmonella Typhimurium TA 100 (Ex. 11-6). As 
previously mentioned, this assay specifically measures point and 
frameshift mutations usually caused by DNA adduct formation. The assay 
is not sensitive to chromosomal damage, DNA strand breaks, or DNA 
crosslinks most commonly found with low concentrations of Cr(VI) 
compounds. Large amounts (50 to 500 [mu]g/plate) of highly soluble 
sodium dichromate and slightly soluble calcium, strontium, and zinc 
chromates, were found to be mutagenic in the study, but not the water 
insoluble barium chromate and lead chromate pigments. However, 
mutagenicity was observed when the acidic chelating agent, 
nitrilotriacetic acid (NTA), was added to the assay to help solubilize 
the water insoluble Cr(VI) compounds. The chelating agent was unable to 
solubilize sufficient amounts of lead chromate pigments to cause 
bacterial mutagenicity, if these pigments were more than five percent 
encapsulated (weight to weight) with amorphous silica.
    OSHA finds the results of this study to be consistent with the 
published literature that shows Cr(VI) mutagenicity requires high 
concentrations of solubilized chromate ion (Exs. 35-118; 35-161). Large 
amounts of water-soluble and slightly soluble Cr(VI) compounds produce 
a mutagenic response in most studies since these Cr(VI) compounds can 
dissociate to achieve a high concentration of chromate ion. Insoluble 
lead chromate usually needs to be pre-solubilized under acidic or 
alkaline conditions to achieve sufficient chromate ion to cause 
mutagenicity (Ex. 35-162). The above study found highly and slightly 
soluble chromates to be mutagenic as well as water insoluble lead 
chromate pigments pre-solubilized with NTA. The lack of mutagenicity 
for silica encapsulated lead chromate pigments under these experimental 
conditions is likely the result of their greater resistance to acidic 
digestion than unencapsulated lead chromate pigment.
    Failure to elicit a mutagenic response in a bacterial assay, with 
or without NTA, is not a convincing demonstration that chromate ion can 
not partially dissociate from encapsulated lead chromate in biological 
media, enter mammalian cells, and elicit other types of genotoxicity. 
As described above, chromosomal damage, believed to result from DNA 
strand breaks and crosslinks, appears to be the critical genotoxic 
endpoint for low concentrations of Cr(VI) compounds. Research has shown 
that lead chromate and lead chromate pigment particulates in biological 
media can cause chromosomal lesions and cell transformation without the 
aid of strongly acidic or basic substances (Exs. 12-5; 35-119; 35-188; 
35-132; 35-68; 35-67; 47-12-3; 35-327). While silica-encapsulated lead 
chromate pigments have not been as thoroughly investigated as the 
unencapsulated pigments or reagent grade lead chromate, one study 
reported that lead silicochromate particles did have low solubility in 
biological culture media and transformed hamster embryo cells (Ex. 12-
5).
    Information is not available in the record to adequately 
demonstrate the efficiency and stability of the encapsulation process, 
despite OSHA statements that such information would be of value in its 
health effects evaluation and its request for such information (69 FR 
59315-59316, 10/4/2004; Ex. 2A). In the absence of data to the 
contrary, OSHA believes it prudent and plausible that encapsulated lead 
chromate pigments are able to partially dissociate into chromate ion 
available for lung cell uptake and/or be internalized in a manner 
similar to other lead chromate particulates. The resulting 
intracellular Cr(VI) leads to genotoxic damage and cellular events 
critical to carcinogenesis.
    Public Comments on Carcinogenicity of Slightly Water Soluble Cr(VI) 
Compounds--In its written comments to the NPRM, Boeing Corporation 
stated that "there is no persuasive scientific evidence for OSHA's 
repeated assertion that low solubility hexavalent chromium compounds 
[e.g. strontium and zinc chromates] are more potent carcinogens than 
[highly] soluble [Cr(VI)] compounds" (Ex. 38-106, p. 2). Boeing and 
others in the aerospace industry are users of certain slightly soluble 
Cr(VI) compounds, particularly strontium chromate, found in the 
protective coatings applied to commercial and military aircraft.
    Boeing argues that OSHA, along with IARC, ACGIH and others, have 
exclusively relied on intrabronchial implantation studies in animals 
that are both not representative of inhalation exposures in the 
workplace and are not consistent with the available animal inhalation 
data (Ex. 38-106-2, p. 26). Boeing asserts that there is no evidence 
that slightly soluble chromates behave differently in terms of their 
absorption kinetics than highly soluble chromates when instilled in the 
lungs of rats (Ex. 38-106-2, p. 19). Boeing believes the OSHA position 
that slightly soluble Cr(VI) compounds are retained in the lung, 
associate with cells, and cause high uptake or high local 
concentrations to be inconsistent with other data showing these Cr(VI) 
compounds quickly disperse in water (Ex. 38-106-2, p. 26). Boeing 
concludes:

    There is no basis for the conclusion that low solubility [i.e. 
slightly soluble] chromates could be more potent than [highly] 
soluble, and some evidence the opposite may be the case. As a worst 
case OSHA should conclude that there is inadequate evidence to 
conclude that [highly] soluble and low-solubility compounds differ 
in carcinogenic potency. It is critical that OSHA maintain a 
distinction between low-solubility chromates and highly insoluble 
chromates based on this data. (Ex. 38-106-2, p. 26)

    As noted earlier, OSHA as well as other commenters agree with 
Boeing that the animal intrabronchial and intratracheal instillation 
studies are not appropriate for quantitatively predicting lung cancer 
risk to a worker breathing Cr(VI) dust and aerosols. However, many 
stakeholders disagreed with the Boeing view and believed these animal 
studies can be relied upon as qualitative evidence of relative 
carcinogenic potency. CPMA, which relies on the rat intrabronchial 
implantation results as evidence that lead chromate is non-
carcinogenic, states "tests involving implantation in rat lung, as 
carried out by Levy et al. in 1986, are relevant to inhalation in 
industrial exposures" (Ex. 38-205, p. 93). In their opening statement 
NIOSH agreed with the preliminary OSHA determination that "the less 
water soluble [Cr(VI)] compounds may be more potent than the more water 
soluble [Cr(VI)] compounds" (Tr. 299). NIOSH identified the rat 
intrabronchial implantation findings as the basis for their position 
that the slightly soluble Cr(VI) compounds appear to be more 
carcinogenic than the more soluble and insoluble Cr(VI) compounds (Tr. 
334). Dr. Clewell testified that:

    Some animal studies suggest the solubility of hexavalent 
chromium compounds influences their carcinogenic potency with 
slightly soluble compounds having the higher potencies than highly 
soluble or insoluble compounds. However, the evidence is inadequate 
to conclude that specific hexavalent chromium compounds are not 
carcinogenic. Moreover the designs of the studies were not 
sufficient to quantitatively estimate comparative potencies (Ex. 44-5, p. 15).

Respiratory Tract Instillation of Slightly Soluble Cr(VI) Compounds in 
Rats--OSHA agrees that animal intrabronchial and intratracheal 
implantation studies provide persuasive evidence that slightly soluble 
Cr(VI) are more carcinogenic than the highly soluble Cr(VI) compounds. 
As mentioned previously, these studies provide useful information 
regarding the relative carcinogenicity of different Cr(VI) compounds 
once they are delivered and deposited in the respiratory tract. For 
example, one study examined the carcinogenicity of over twenty 
different Cr(VI) compounds in rats, spanning a broad range of 
solubilities, under the same experimental conditions in the relevant 
target organ to humans (i.e. respiratory tract) following in vivo 
administration (Ex. 11-2). A single administration of each Cr(VI) test 
compound was instilled in the lower left bronchus of approximately 100 
rats. The results were dramatic. Roughly 50 and 25 percent of the rats 
receiving the slightly soluble strontium and calcium chromates, 
respectively, developed bronchogenic carcinoma. No other Cr(VI) 
compounds produced more than five percent tumor incidence. The highly 
soluble sodium dichromate under the same experimental conditions caused 
bronchogenic carcinoma in only a single rat.
    The higher relative potency of the slightly soluble calcium 
chromate compared to the highly soluble sodium dichromate was confirmed 
in another study in which each test compound was instilled at a low 
dose level (i.e., 0.25 mg/kg) in the trachea of 80 rats five times 
weekly for 30 months (Ex. 11-7). Using this experimental protocol, 7.5 
percent of the slightly soluble calcium chromate-treated animals 
developed brochioalveolar adenomas while none of the highly soluble 
sodium dichromate-treated rats developed tumors. The tumor incidence at 
this lower dose level occurred in the absence of serious lung pathology 
and is believed to reflect the tumorigenic potential of the two Cr(VI) 
compounds at workplace exposures of interest to OSHA. On the other 
hand, a five-fold higher dose level that caused severe damage and 
chronic inflammation to the rat lungs produced a similar fifteen 
percent lung tumor incidence in both calcium and sodium chromate 
treated rats. OSHA, as well as the study authors, believe the later 
tumor response with the higher dose level did not result from direct 
Cr(VI) interaction with cellular genes, but, instead, was primarily 
driven by the cellular hyperplasia secondary to the considerable damage 
to the lung tissue. Boeing also seems to attribute this result to 
tissue damage stating "most of the tumors were found in areas of 
chronic inflammation and scarring, suggesting an effect that is 
secondary to tissue damage" (Ex. 38-106-2, p. 21).
    OSHA does not agree with some study interpretations advanced by 
Boeing in support of their position that slightly soluble Cr(VI) 
compounds are no more carcinogenic than highly soluble Cr(VI). For 
example, Boeing claims that the intrabronchial implantation experiments 
cannot be relied upon because the results do not correspond to findings 
from animal inhalation studies (Ex. 38-106-2, p. 24-25). The primary 
basis for the Boeing comparison were two rodent bioassays that reported 
tumor incidence from the inhalation of different Cr(VI) compounds (Exs. 
10-8; 10-11). In one study over 200 mice inhaled slightly soluble 
calcium chromate powder for five hours per day, five days per week for 
roughly two years (Ex. 10-8). In the other study, 19 rats inhaled an 
aqueous sodium dichromate liquid aerosol virtually around the clock for 
22 hours a day, seven days a week for eighteen months (Ex. 10-11). The 
two studies reported a similar tumor incidence despite the lower total 
weekly Cr(VI) dose of sodium dichromate in the second study. OSHA 
believes the vastly different experimental protocols employed in these 
studies do not allow for a legitimate comparison of carcinogenic 
potency between Cr(VI) compounds. First, mouse and rat strains can 
differ in their susceptibility to chemical-induced lung tumors. Second, 
the proportion of respirable Cr(VI) may differ between a liquid aerosol 
of aqueous sodium dichromate mist and an aerosol solid calcium chromate 
particles suspended in air. Third, the opportunity for Cr(VI) clearance 
will undoubtedly differ between a Cr(VI) dose inhaled nearly 
continuously (e.g., 22 hours per day, seven days a week) and inhaled 
intermittently (e.g., five hours a day, five days a week) over the 
course of a week. These experimental variables can be expected to have 
a major influence on tumor response and, thus, will obscure a true 
comparison of carcinogenic potency. Boeing acknowledges that "these 
[inhalation] studies used very different protocols and are not directly 
comparable" (Ex. 38-106-2, p.24). On the other hand, slightly soluble 
Cr(VI) compounds were found to cause a greater incidence of lung tumors 
than highly soluble Cr(VI) compounds in two independent studies in 
which the test compounds were instilled under the same dosing regime in 
the same rodent models in research specifically designed to assess 
relative Cr(VI) carcinogenic potency (Exs. 11-2; 11-7). Therefore, OSHA 
believes any apparent lack of correspondence between animal inhalation 
and instillation studies is due to an inability to compare inhalation 
data from vastly different experimental protocols and should not 
diminish the relevance of the instillation findings.
    Epidemiological Studies of Slightly Soluble Cr(VI) Compounds--
Boeing further argues that the greater carcinogenic potency experienced 
by rats intrabronchially instilled with slightly soluble chromates 
compared to rats instilled with highly soluble and water-insoluble 
Cr(VI) compounds "do not correspond qualitatively to observed lung 
cancer in occupational exposure" (Ex. 38-106-2, p. 21). Several other 
industry stakeholders disagree. In explaining the excess lung cancer 
mortality among pigment production workers, CPMA commented:

    [water-insoluble] Lead chromate pigments must be differentiated 
from [slightly soluble] zinc chromate corrosion inhibitor additives, 
which are consistently shown to be carcinogenic in various studies. 
When [water insoluble] lead chromate and [slightly soluble] zinc 
chromate exposures occur simultaneously, there appears to be a 
significant cancer hazard. However, when lead chromate pigments 
alone are the source of chromium exposure, a significant cancer 
response has never been found (Ex. 38-205, p. 91).

In explaining the excess lung cancer mortality among chromate 
production workers in the Gibb and Luippold cohorts, the Electric Power 
Research Institute states that:

    One important distinction is that workers of the historical 
chromate production industry were exposed to sparingly soluble forms 
of calcium chromate in the roast mix, which are recognized to have 
greater carcinogenic potential as compared to soluble forms of 
Cr(VI) based on animal implantation studies (Ex. 38-8, p. 12).

Deborah Proctor of Exponent also testified:

    Several studies of chromate production worker cohorts have 
demonstrated that the excess cancer risk is reduced when less lime 
is added to the roast mixture, reducing worker exposure to the 
sparingly soluble calcium chromate compounds" (Ex. 40-12-5).

    OSHA believes there is merit to the above comments that workplace 
exposure to slightly soluble Cr(VI) compounds may have contributed to 
the higher lung cancer mortality in both pigments workers producing 
mixed zinc and lead chromate pigments as well as
chromate production workers exposed to calcium chromate from high lime 
production processes in the 1930s and 1940s. Other factors, such as 
greater Cr(VI) exposure, probably also contributed to the higher lung 
cancer mortality observed in these cohorts. In any case, these 
epidemiological findings support the Boeing contention that the 
epidemiological findings are inconsistent with the results from animal 
intrabronchial implantation studies (Ex. 38-106-2, p. 26).
    Clearance, Retention, and Dissolution of Slightly Soluble Cr(VI) 
Compounds in the Lung--Boeing argues that animal experiments that 
examined the absorption, distribution and excretion of Cr(VI) compounds 
after intratracheal instillation of Cr(VI) compounds in rats do not 
show that highly soluble Cr(VI) is cleared more rapidly or retained in 
the lung for shorter periods than slightly soluble Cr(VI) compounds 
(Ex. 38-106-2, p. 18-19). The results of one study found that larger 
amounts of water-insoluble lead chromate were retained in the lungs of 
rats at both 30 minutes and at 50 days after instillation than for 
highly soluble sodium chromate or slightly soluble zinc chromate (Ex. 
35-56). Although the authors concluded that slightly soluble zinc 
chromate was more slowly absorbed from the lung than the highly soluble 
sodium chromate, the excretion and distribution of the absorbed 
chromium from the zinc and sodium chromate instillations was similar. 
Furthermore, there was little difference in the amounts of zinc and 
sodium chromate retained by the lung at the two extreme time points 
(e.g., 30 minutes and 50 days) measured in the study. OSHA agrees with 
Boeing that these findings indicate slower clearance and longer 
retention in the lung of the water insoluble lead chromate relative to 
highly soluble sodium chromate, but not in the case of the slightly 
soluble zinc chromate. Slower clearance and longer residence time in 
the lung will generally enhance carcinogenic potential assuming other 
dosimetric variables such as lung deposition, Cr(VI) concentration at 
the lung cell surface, and dissociation into chromate ion are 
unchanged.
    Boeing asserts that a study of strontium chromate dissociation from 
paint primer contradicts the notion that slightly soluble are more 
likely than highly soluble Cr(VI) compounds to concentrate and 
dissociate at the lung cell surface (Ex. 38-106-2, p. 25). This 
experimental research found that roughly 75 and 85 percent of strontium 
chromate contained in metal surface primer coating particles was 
solubilized in water after one and 24 hours, respectively (Ex. 31-2-1). 
The primer particles were generated using a high volume, low pressure 
spray gun according to manufacturer specifications, and collected in 
water impingers. The authors concluded that their study demonstrated 
that chromate dissociation from primer particles into the aqueous fluid 
lining lung cells would be modestly hindered relative to highly water 
soluble Cr(VI) aerosols.
    The slower dissociation of the slightly soluble Cr(VI) compound, 
strontium chromate, plausibly explains its higher carcinogenicity in 
animal implantation studies. The 'modest hindrance' allows the 
undissociated chromate to achieve higher concentrations at the surface 
of the lung cells facilitating chromate transport into the cell. The 
unhindered, instantaneous dispersion of highly water soluble chromates 
in aqueous fluid lining of the respiratory tract is less likely to 
achieve a high chromate concentration at the lung cell membrane. OSHA 
believes the results of the above study support, not contradict, that 
slightly soluble Cr(VI) may lead to higher chromium uptake into lung 
cells than highly soluble Cr(VI) compounds.
    In summary, slightly soluble Cr(VI) compounds have consistently 
caused higher lung tumor incidence in animal instillation studies 
specifically designed to examine comparative carcinogenic potency in 
the respiratory tract. The higher carcinogenic activity of slightly 
soluble Cr(VI) is consistent with cellular studies that indicate that 
chromate dissociation in close proximity to the lung cell surface may 
be a critical feature to efficient chromate ion uptake. This is 
probably best achieved by Cr(VI) compounds that have intermediate water 
solubility rather than by highly water-soluble Cr(VI) that rapidly 
dissolves and diffuses in the aqueous fluid layers lining the 
respiratory tract. The higher carcinogenicity of slightly soluble 
Cr(VI) may contribute, along with elevated Cr(VI) workplace exposures, 
to the greater lung cancer mortality in certain occupational cohorts 
exposed to both slightly soluble and other forms of Cr(VI). The vastly 
different study protocols employed in the few animal inhalation 
bioassays do not allow a valid comparison of lung tumor incidence 
between slightly soluble and highly soluble Cr(VI) compounds.
b. Summary of Cr(VI) Carcinogenicity
    After carefully considering all the epidemiological, animal and 
mechanistic evidence presented in the rulemaking record, OSHA regards 
all Cr(VI) compounds as agents able to induce carcinogenesis through a 
genotoxic mode of action. This position is consistent with findings of 
IARC, EPA, and ACGIH that classified Cr(VI) compounds as known or 
confirmed human carcinogens. Based on the above animal and experimental 
evidence, OSHA believes that slightly soluble Cr(VI) compounds are 
likely to exhibit a greater degree of carcinogenicity than highly water 
soluble or water insoluble Cr(VI) when the same dose is delivered to 
critical target cells in the respiratory tract of the exposed worker. 
In its evaluation of different Cr(VI) compounds, ACGIH recommended 
lower occupational exposure limits for the slightly soluble strontium 
chromate (TLV of 0.5 [mu]g/m\3\) and calcium chromate (TLV of 1 [mu]g/
m\3\) than either water insoluble (TLV of 10 [mu]g/m\3\) or water 
soluble (TLV of 50 [mu]g/m\3\) forms of Cr(VI) based on the animal 
instillation studies cited above. While these animal instillation 
studies are useful for hazard identification and qualitative 
determinations of relative potency, they cannot be used to determine a 
reliable quantitative estimate of risk for human workers breathing 
these chromates during occupational exposure. This was due to use of 
inadequate number of dose levels (e.g., single dose level) or a less 
appropriate route of administration (e.g., tracheal instillation).
    It is not clear from the animal or cellular studies whether the 
carcinogenic potency of water insoluble Cr(VI) compounds would be 
expected to be more or less than highly water soluble Cr(VI). However, 
it was found that a greater percentage of water insoluble lead chromate 
remains in the lungs of rats for longer periods than the highly water 
soluble sodium chromate when instilled intratracheally at similar doses 
(Ex. 35-56). Since water insoluble lead chromate can persist for long 
periods in the lung and increase intracellular levels of Cr and damage 
DNA in human lung cells at low doses (e.g., 0.1 [mu]g/cm\2\), OSHA 
believes that based on the scientific evidence discussed above it is 
reasonable to regard the water insoluble Cr(VI) to be of similar 
carcinogenic potency to highly soluble Cr(VI) compounds. No convincing 
scientific evidence was introduced into the record that shows lead 
chromate to be less carcinogenic than highly soluble chromate 
compounds.

C. Non-cancer Respiratory Effects

    The following sections describe the evidence from the literature on 
nasal irritation, nasal ulcerations, nasal perforations, asthma, and 
bronchitis following inhalation exposure to water
soluble Cr(VI) compounds. The evidence clearly demonstrates that 
workers can develop impairment to the respiratory system (nasal 
irritation, nasal ulceration, nasal perforation, and asthma) after 
workplace exposure to Cr(VI) compounds below the previous PEL.
    It is very clear from the evidence that workers may develop nasal 
irritation, nasal tissue ulcerations, and nasal septum perforations at 
occupational exposures level at or below the current PEL of 52 [mu]g/
m\3\. However, it is not clear what occupational exposure levels lead 
to the development of occupational asthma or bronchitis.
1. Nasal Irritation, Nasal Tissue Ulcerations and Nasal Septum 
Perforations
    Occupational exposure to Cr(VI) can lead to nasal tissue 
ulcerations and nasal septum perforations. The nasal septum separates 
the nostrils and is composed of a thin strip of cartilage. The nostril 
tissue consists of an overlying mucous membrane known as the mucosa. 
The initial lesion after Cr(VI) exposure is characterized by localized 
inflammation or a reddening of the affected mucosa, which can later 
lead to atrophy. This may progress to an ulceration of the mucosa layer 
upon continued exposure (Ex. 35-1; Ex. 7-3). If exposure is 
discontinued, the ulcer progression will stop and a scar may form. If 
the tissue damage is sufficiently severe, it can result in a 
perforation of the nasal septum, sometimes referred to chrome hole. 
Individuals with nasal perforations may experience a range of signs and 
symptoms, such as a whistling sound, bleeding, nasal discharge, and 
infection. Some individuals may experience no noticeable effects.
    Several cohort and cross-sectional studies have described nasal 
lesions from airborne exposure to Cr(VI) at various electroplating and 
chrome production facilities. Most of these studies have been reviewed 
by the Center for Disease Control's Agency for Toxic Substances and 
Disease Registry (ATSDR) toxicological profile for chromium (Ex. 35-
41). OSHA reviewed the studies summarized in the profile, conducted its 
own literature search, and evaluated studies and comments submitted to 
the rulemaking record. In its evaluation, OSHA took into consideration 
the exposure regimen and experimental conditions under which the 
studies were performed, including exposure levels, duration of 
exposure, number of animals, and the inclusion of appropriate control 
groups. Studies were not included if they did not contribute to the 
weight of evidence either because of inadequate documentation or 
because of poor quality. This section only covers some of the key 
studies and reviews. OSHA has also identified two case reports 
demonstrating the development of nasal irritation and nasal septum 
perforations, and these case reports are summarized as well. One case 
report shows how a worker can develop the nasal perforations from 
direct contact (i.e., touching the inner surface of the nose with 
contaminated fingers).
    Lindberg and Hedenstierna examined the respiratory symptoms and 
effects of 104 Swedish electroplaters (Ex. 9-126). Of the 104 
electroplaters, 43 were exposed to chromic acid by inhalation. The 
remaining 61 were exposed to a mixture of chromic acid and nitric acid, 
hydrochloric acid, boric acid, nickel, and copper salts. The workers 
were evaluated for respiratory symptoms, alterations in the condition 
of the nasal tissue, and lung function. All workers were asked to fill 
out a detailed questionnaire on their history of respiratory symptoms 
and function. Physicians performed inspections of the nasal passages of 
each worker. Workers were given a pulmonary function test to assess 
lung function. For those 43 workers exposed exclusively to chromic 
acid, the median exposure time was 2.5 years, ranging from 0.2 to 23.6 
years. The workers were divided into two groups, a low exposure group 
(19 workers exposed to eight-hour time weighted average levels below 2 
[mu]g/m\3\) and a high exposure group (24 workers exposed to eight-hour 
time weighted average levels above 2 [mu]g/m\3\). Personal air sampling 
was conducted on 11 workers for an entire week at stations close to the 
chrome baths to evaluate peak exposures and variations in exposure on 
different days over the week. Nineteen office employees who were not 
exposed to Cr(VI) were used as controls for nose and throat symptoms, 
and 119 auto mechanics (no car painters or welders) whose lung function 
had been evaluated using similar techniques to those used on Cr(VI) 
exposed workers were used as controls for lung function.
    The investigators reported nasal tissue ulcerations and septum 
perforations in a group of workers exposed to chromic acid as Cr(VI) at 
peak exposure ranging from 20 [mu]g/m\3\ to 46 [mu]g/m\3\. The 
prevalence of ulceration/perforation was statistically higher than the 
control group. Of the 14 individuals in the 20-46 [mu]g/m\3\ exposure 
group, 7 developed nasal ulcerations. In addition to nasal ulcerations, 
2 of the 7 also had nasal perforations. Three additional individuals in 
this group developed nasal perforations in the absence of ulcerations. 
None of the 14 workers in the 20-46 [mu]g/m\3\ exposure group were 
reported to have nasal tissue atrophy in the absence of the more 
serious ulceration or perforation.
    At average exposure levels from 2 [mu]g/m\3\ to 20 [mu]g/m\3\, half 
of the workers complained of "constantly running nose," "stuffy 
nose," or "there was a lot to blow out." (Authors do not provide 
details of each complaint). Nasal tissue atrophy, in the absence of 
ulcerations or perforations, was observed in 66 percent of 
occupationally exposed workers (8 of 12 subjects) at relatively low 
peak levels ranging from 2.5 [mu]g/m\3\ to 11 [mu]g/m\3\. No one 
exposed to levels below 1 [mu]g/m\3\ (time-weighted average, TWA) 
complained of respiratory symptoms or developed lesions.
    The authors also reported that in the exposed workers, both forced 
vital capacity and forced expiratory volume in one second were reduced 
by 0.2 L, when compared to controls. The forced mid-expiratory flow 
diminished by 0.4 L/second from Monday morning to Thursday afternoon in 
workers exposed to chromic acid as Cr(VI) at daily TWA average levels 
of 2 [mu]g/m\3\ or higher. The effects were small, not outside the 
normal range and transient. Workers recovered from the effects after 
two days. There was no difference between the control and exposed group 
after the weekend. The workers exposed to lower levels (2 [mu]g/m\3\ or 
lower, TWA) showed no significant changes.
    Kuo et al. evaluated nasal septum ulcerations and perforations in 
189 electroplaters in 11 electroplating factories (three factories used 
chromic acid, six factories used nickel-chromium, and two factories 
used zinc) in Taiwan (Ex. 35-10). Of the 189 workers, 26 used Cr(VI), 
129 used nickel-chromium, and 34 used zinc. The control group consisted 
of electroplaters who used nickel and zinc. All workers were asked to 
fill out a questionnaire and were given a nasal examination including a 
lung function test by a certified otolaryngologist. The authors 
determined that 30% of the workers (8/26) that used chromic acid 
developed nasal septum perforations and ulcerations and 38% (10/26) 
developed nasal septum ulcers. Using the Mantel Extension Test for 
Trends, the authors also found that chromium electroplaters had an 
increased likelihood of developing nasal ulcers and perforations 
compared to electroplating workers using nickel-chromium and zinc. 
Personal sampling of airborne Cr(VI) results indicated the highest 
levels (32 [mu]g/m\3\  35 [mu]g/m\3\, ranging from 0.1 
[mu]g/m\3\-119 [mu]g/m\3\) near the electroplating tanks of the Cr(VI) 
electroplating
factories (Ex. 35-11). Much lower personal sampling levels were 
reported in the "other areas in the manufacturing area" and in the 
"administrative area" (TWA 0.16  0.10 [mu]g/m\3\) of the 
Cr(VI) electroplating plant. The duration of sampling was not 
indicated. The lung function tests showed that Cr(VI) electroplaters 
had significantly lower forced vital capacity and forced expiratory 
volume when compared to other exposure groups.
    Cohen et al. examined respiratory symptoms of 37 electroplaters 
following inhalation exposure to chromic acid (Ex. 9-18). The mean 
length of employment for the 37 electroplaters was 26.9 months (range 
from 0.3 to 132 months). Fifteen workers employed in other parts of the 
plant were randomly chosen for the control group (mean length of 
employment was 26.1 months; range from 0.1 to 96). All workers were 
asked to fill out a questionnaire on their respiratory history and to 
provide details about their symptoms. An otolaryngologist then examined 
each individual's nasal passages and identified ulcerations and 
perforations. Air samples to measure Cr(VI) were collected for 
electroplaters. The air sampling results of chromic acid as Cr(VI) 
concentrations for electroplaters was a mean of 2.9 [mu]g/m\3\ (range 
from non-detectable to 9.1 [mu]g/m\3\). The authors found that 95% of 
the electroplaters developed pathologic changes in nasal mucosa. 
Thirty-five of the 37 workers who were employed for more than 1 year 
had nasal tissue damage. None of these workers reported any previous 
job experience involving Cr(VI) exposure. Four workers developed nasal 
perforations, 12 workers developed ulcerations and crusting of the 
septal mucosa, 11 workers developed discoloration of the septal mucosa, 
and eight workers developed shallow erosion of septal mucosa. The 
control group consisted of 15 workers who were not exposed to Cr(VI) at 
the plant. All but one had normal nasal mucosa. The one individual with 
an abnormal finding was discovered to have had a previous Cr(VI) 
exposure while working in a garment manufacturing operation as a fabric 
dyer for three years. In addition to airborne exposure, the authors 
observed employees frequently wiping their faces and picking their 
noses with contaminated hands and fingers. Many did not wear any 
protective gear, such as gloves, glasses, or coveralls.
    Lucas and Kramkowsi conducted a Health Hazard Evaluation (HHE) on 
11 chrome platers in an industrial electroplating facility (Ex. 3-84). 
The electroplaters worked for about 7.5 years on average. Physicians 
evaluated each worker for chrome hole scars, nasal septum ulceration, 
mucosa infection, nasal redness, perforated nasal septum, and wheezing. 
Seventeen air samples for Cr(VI) exposure were collected in the chrome 
area. Cr(VI) air concentrations ranged from 1 to 20 [mu]g/m\3\, with an 
average of 4 [mu]g/m\3\. In addition to airborne exposure, the authors 
observed workers being exposed to Cr(VI) by direct "hand to nose" 
contact, such as touching the nose with contaminated hands. Five 
workers had nasal mucosa that became infected, two workers had nasal 
septum ulcerations, two workers had atrophic scarring (author did not 
provide explanation), possibly indicative of presence of past 
ulcerations, and four workers had nasal septum perforations.
    Gomes evaluated 303 employees from 81 electroplating operations in 
Sao Paulo, Brazil (Ex. 9-31). Results showed that more than two-thirds 
of the workers had nasal septum ulcerations and perforations following 
exposure to chromic acid at levels greater than 100 [mu]g/m\3\, but 
less than 600 [mu]g/m\3\ (precise duration of exposure was not stated). 
These effects were observed within one year of employment.
    Lin et al. examined nasal septum perforations and ulcerations in 79 
electroplating workers from seven different chromium electroplating 
factories in Taipei, Taiwan (Ex.35-13). Results showed six cases of 
nasal septum perforations, four having scar formations, and 38 cases of 
nasal septum ulcerations following inhalation exposure to chromic acid. 
Air sampling near the electroplating tanks had the highest range of 
chromic acid as Cr(VI) (mean of 28 [mu]g/m\3\; range from 0.7 to 168.3 
[mu]g/m\3\). In addition to airborne exposures, the authors also 
observed direct "hand to nose" contact where workers placed 
contaminated fingers in their nose. The authors attributed the high 
number of cases to poor industrial hygiene practices in the facilities. 
Five of the seven factories did not have adequate ventilation systems 
in place. Workers did not wear any PPE, including respirators.
    Bloomfield and Blum evaluated nasal tissue damage and nasal septum 
perforations in 23 workers employed at six chromium electroplating 
plants (Ex. 9-13). They found that daily exposure to chromic acid as 
Cr(VI) at levels of 52 [mu]g/m\3\ or higher can lead to nasal tissue 
damage. Three workers developed nasal ulcerations, two workers had 
nasal perforations, nine workers had nose bleeds, and nine workers had 
inflamed mucosa.
    Kleinfeld and Rosso found that seven out of nine of chrome 
electroplaters had nasal septum ulcerations (Ex. 9-41). The nine 
workers were exposed to chromic acid as Cr(VI) by inhalation at levels 
ranging from 93 [mu]g/m\3\ to 728 [mu]g/m\3\. Duration of exposure 
varied from two weeks to one year. Nasal septum ulcerations were noted 
in some workers who had been employed for only one month.
    Royle, using questionnaire responses from 997 British 
electroplaters exposed to chromic acid, reported a significant increase 
in the prevalence of nasal ulcerations. The prevalence increased the 
longer the worker was exposed to chromic acid (e.g., from 14 cases with 
exposure less than one year to 62 cases with exposure over five years) 
(Ex. 7-50). In all but 2 cases, air samples revealed chromic acid 
concentrations of 0.03 mg/m\3\ (i.e., 30 [mu]g/m\3\).
    Gibb et al. reported nasal irritations, nasal septum bleeding, 
nasal septum ulcerations and perforations among a cohort of 2,350 
chrome production workers in a Baltimore plant (Ex. 31-22-12). A 
description of the cohort is provided in detail in the cancer health 
effects section V.B. of this preamble. The authors found that more than 
60% of the cohort had experienced nasal ulcerations and irritations, 
and that the workers developed these effects for the first time within 
the first three months of being hired (median). Gibb et al. found that 
the median annual exposure to Cr(VI) during first diagnosis of 
irritated and/or ulcerated nasal septum was 10 [mu]g/m\3\. About 17% of 
the cohort reported nasal perforations. Based on historical data, the 
authors believe that the nasal findings are attributable to Cr(VI) 
exposure.
    Gibb et al. also used a Proportional Hazard Model to evaluate the 
relationship between Cr(VI) exposure and the first occurrence of each 
of the clinical findings. Cr(VI) data was entered into the model as a 
time dependent variable. Other explanatory variables were calendar year 
of hire and age of hire. Results of the model indicated that airborne 
Cr(VI) exposure was associated with the occurrence of nasal septum 
ulceration (p = 0.0001). The lack of an association between airborne 
Cr(VI) exposure and nasal perforation and bleeding nasal septum may 
reflect the fact that Cr(VI) concentrations used in the model represent 
annual averages for the job, in which the worker was involved in at the 
time of the findings, rather than a short-term average. Annual averages 
do not factor in day-to-day fluctuations or extreme episodic 
occurrences. Also, the author believed that poor housekeeping
and hygiene practices may have contributed to these health effects as 
well as Cr(VI) air borne concentrations.
    Based on their hazard model, Gibb et al. estimated the relative 
risks for nasal septum ulcerations would increase 1.2 for each 52 [mu]g 
of Cr(VI)/m\3\ increase in Cr(VI) air levels. They found a reduction in 
the incidence of nasal findings in the later years. They found workers 
from the earlier years who did not wear any PPE had a greater risk of 
developing respiratory problems. They believe that the reduction in 
ulcerations was possibly due to an increased use of respirators and 
protective clothing and improved industrial hygiene practices at the 
facility.
    The U.S. Public Health Service conducted a study of 897 chrome 
production workers in seven chromate producing plants in the early 
1950s (Ex. 7-3). The findings of this study were used in part as 
justification for the current OSHA PEL. Workers were exposed by 
inhalation to various water soluble chromates and bichromate compounds. 
The total mean exposure to the workers was a TWA of 68 [mu]g/m\3\. Of 
the 897 workers, 57% (or 509 workers) were found to have nasal septum 
perforations. Nasal septum perforations were even observed in workers 
during their first year on the job.
    Case reports provide further evidence that airborne exposure and 
direct "hand to nose" contact of Cr(VI) compounds lead to the 
development of nasal irritation and nasal septum perforations.
    For example, a 70-year-old man developed nasal irritation, 
incrustation, and perforation after continuous daily exposure by 
inhalation to chromium trioxide (doses were not specified, but most 
likely quite high given the nature of his duties). This individual 
inhaled chromium trioxide daily by placing his face directly over an 
electroplating vessel. He worked in this capacity from 1934 to 1982. 
His symptoms continued to worsen after he stopped working. By 1991, he 
developed large perforations of the nasal septum and stenosis (or 
constriction) of both nostrils by incrustation (Ex. 35-8).
    Similarly, a 30-year-old female jigger (a worker who prepares the 
items prior to electroplating by attaching the items to be plated onto 
jigs or frames) developed nasal perforation in her septum following 
continuous exposure (doses in this case were not provided) to chromic 
acid mists. She worked adjacent to the automated Cr(VI) electroplating 
shop. She was also exposed to chromic acid from direct contact when she 
placed her contaminated fingers in her nose. Her hands became 
contaminated by handling wet components in the jigging and de-jigging 
processes (Ex. 35-24).
    Evidence of nasal septum perforations has also been demonstrated in 
experimental animals. Adachi exposed 23 C57BL mice to chromic acid by 
inhalation at concentrations of 1.81 mg Cr(VI)/m\3\ for 120 min per 
day, twice a week and 3.63 mg Cr(VI)/m\3\ for 30 minutes per day, two 
days per week for up to 12 months (Ex. 35-26). Three of the 23 mice 
developed nasal septum perforations in the 12 month exposure group.
    Adachi et al. also exposed 50 ICR female mice to chromic acid by 
inhalation at concentrations of 3.18 mg Cr(VI)/m\3\ for 30 minutes per 
day, two days per week for 18 months (Ex. 35-26-1). The authors used a 
miniaturized chromium electroplating system to mimic electroplating 
processes and exposures similar to working experience. Nasal septum 
perforations were found in six mice that were sacrificed after 10 
months of exposure. Of those mice that were sacrificed after 18 months 
of exposure, nasal septum perforations were found in three mice.
2. Occupational Asthma
    Occupational asthma is considered "a disease characterized by 
variable airflow limitation and/or airway hyperresponsiveness due to 
causes and conditions attributable to a particular occupational 
environment and not to stimuli encountered outside the workplace" (Ex. 
35-15). Asthma is a serious illness that can damage the lungs and in 
some cases be life threatening. The common symptoms associated with 
asthma include heavy coughing while exercising or when resting after 
exercising, shortness of breath, wheezing sound, and tightness of chest 
(Exs. 35-3; 35-6).
    Cr(VI) is considered to be an airway sensitizer. Airway sensitizers 
cause asthma through an immune response. The sensitizing agent 
initially causes production of specific antibodies that attach to cells 
in the airways. Subsequent exposure to the sensitizing agent, such as 
Cr(VI), can trigger an immune-mediated narrowing of the airways and 
onset of bronchial inflammation. All exposed workers do not become 
sensitized to Cr(VI) and the asthma only occurs in sensitized 
individuals. It is not clear what occupational exposure levels of 
Cr(VI) compounds lead to airway sensitization or the development of 
occupational asthma.
    The strongest evidence of occupational asthma has been demonstrated 
in four case reports. OSHA chose to focus on these four case reports 
because the data from other occupational studies do not exclusively 
implicate Cr(VI). The four case reports have the following in common: 
(1) The worker has a history of occupational exposure exclusively to 
Cr(VI); (2) a physician has confirmed a diagnosis that the worker has 
symptoms consistent with occupational asthma; and (3) the worker 
exhibits functional signs of air restriction (e.g., low forced 
expiratory volume in one second or low peak expiratory flow rate) upon 
bronchial challenge with Cr(VI) compounds. These case reports 
demonstrate, through challenge tests, that exposure to Cr(VI) compounds 
can cause asthmatic responses. The other general case reports below did 
not use challenge tests to confirm that Cr(VI) was responsible for the 
asthma; however, these reports came from workers similarly exposed to 
Cr(VI) such that Cr(VI) is likely to have been a contributing factor in 
the development of their asthmatic symptoms.
    DaReave reported the case of a 48-year-old cement floorer who 
developed asthma from inhaling airborne Cr(VI) (Ex. 35-7). This worker 
had been exposed to Cr(VI) as a result of performing cement flooring 
activities for more than 20 years. The worker complained of dyspnea, 
shortness of breath, and wheezing after work, especially after working 
in enclosed spaces. The Cr(VI) content in the cement was about 12 ppm. 
A bronchial challenge test with potassium dichromate produced a 50% 
decrease in forced expiratory volume in one second. The occupational 
physician concluded that the worker's asthmatic condition, triggered by 
exposure to Cr(VI) caused the worker to develop bronchial constriction.
    LeRoyer reported a case of a 28-year-old roofer who developed 
asthma from breathing dust while sawing material made of corrugated 
fiber cement containing Cr(VI) for nine years (Ex. 35-12). This worker 
demonstrated symptoms such as wheezing, shortness of breath, coughing, 
rhinitis, and headaches while working. Skin prick tests were all 
negative. Several inhalation challenges were performed by physicians 
and immediate asthmatic reactions were observed after nebulization of 
potassium dichromate. A reduction (by 20%) in the forced expiratory 
volume in one second after exposure to fiber cement dust was noted.
    Novey et al. reported a case of a 32-year-old electroplating worker 
who developed asthma from working with chromium sulfate and nickel 
salts (Ex. 35-16). He began experiencing coughs,
wheezing, and dyspnea within the first week of exposure. Separate 
inhalation challenge tests given by physicians using chromium sulfate 
and nickel salts resulted in positive reactions. The worker immediately 
had difficulty breathing and started wheezing. The challenges caused 
the forced expiratory volume in 1 second to decrease by 22% and the 
forced expiratory volume in 1 second/forced vital capacity ratio to 
decrease from 74.5% to 60.4%. The author believes the worker's 
bronchial asthma was induced from inhaling chromium sulfate and nickel 
salts. Similar findings were reported in a different individual by 
Sastre (Ex.35-20).
    Shirakawa and Morimoto reported a case of a 50-year-old worker who 
developed asthma while working at a metal-electroplating plant (Ex. 35-
21). Bronchial challenge by physicians produced positive results when 
using potassium bichromate, followed by a rapid recovery within 5 
minutes, when given no exposures. The worker's forced expiratory volume 
in one second dropped by 37% after inhalation of potassium bichromate. 
The individual immediately began wheezing, coughing with dyspnea, and 
recovered without treatment within five minutes. The author believes 
that the worker developed his asthma from inhaling potassium 
bichromate.
    In addition to the case reports confirming that Cr(VI) is 
responsible for the development of asthma using inhalation challenge 
tests, there are several other case reports of Cr(VI) exposed workers 
having symptoms consistent with asthma where the symptoms were never 
confirmed by using inhalation challenge tests.
    Lockman reported a case of a 41-year-old woman who was 
occupationally exposed to potassium dichromate during leather tanning 
(Ex. 35-14). The worker developed an occupational allergy to potassium 
dichromate. This allergy involved both contact dermatitis and asthma. 
The physicians considered other challenge tests using potassium 
dichromate as the test agent (i.e., peak expiratory flow rate, forced 
expiratory volume in 1 second and methacholine or bronchodilator 
challenge), but the subject changed jobs before the physicians could 
administer these tests. Once the subject changed jobs, all her symptoms 
disappeared. It was not confirmed whether the occupational exposure to 
Cr(VI) was the cause of the asthma.
    Williams reported a 23-year-old textile worker who was 
occupationally exposed to chromic acid. He worked near two tanks of 
chromic acid solutions (Ex. 35-23) and inhaled fumes while frequently 
walking through the room with the tanks. He developed both contact 
dermatitis and asthma. He believes the tank was poorly ventilated and 
was the source of the fumes. He stopped working at the textile firm on 
the advice of his physician. After leaving, his symptoms improved 
greatly. No inhalation bronchial challenge testing was conducted to 
confirm that chromic acid was causing his asthmatic attacks. However, 
as noted above, chromic acid exposure has been shown to lead to 
occupational asthma, and thus, chromic acid was likely to be a 
causative agent in the development of asthma.
    Park et al. reported a case of four workers who worked in various 
occupations involving exposure to either chromium sulfate or potassium 
dichromate (Ex. 35-18). Two worked in a metal electroplating factory, 
one worked at a cement manufacturer, and the other worked in 
construction. All four developed asthma. One individual had a positive 
response to a bronchial provocation test (with chromium sulfate as the 
test agent). This individual developed an immediate reaction, 
consisting of wheezing, coughing and dyspnea, upon being given chromium 
sulfate as the test agent. Peak expiratory flow rate decreased by about 
20%. His physician determined that exposure to chromium sulfate was 
contributing to his asthma condition. Two other individuals had 
positive reactions to prick skin tests with chromium sulfate as the 
test agent. Two had positive responses to patch tests using potassium 
dichromate as the testing challenge agent. Only one out of four 
underwent inhalation bronchial challenge testing (with a positive 
result to chromium sulfate) in this report.
3. Bronchitis
    In addition to nasal ulcerations, nasal septum perforations, and 
asthma, there is also limited evidence from reports in the literature 
of bronchitis associated with Cr(VI) exposure. It is not clear what 
occupational exposure levels of Cr(VI) compounds would lead to the 
development of bronchitis.
    Royle found that 28% (104/288) of British electroplaters developed 
bronchitis upon inhalation exposure to chromic acid, as compared to 23% 
(90/299) controls (Ex. 7-50). The workers were considered to have 
bronchitis if they had symptoms of persistent coughing and phlegm 
production. In all but two cases of bronchitis, air samples revealed 
chromic acid at levels of 0.03 mg/m\3\. Workers were asked to fill out 
questionnaires to assess respiratory problems. Self-reporting poses a 
problem in that the symptoms and respiratory health problems identified 
were not medically confirmed by physicians. Workers in this study 
believe they were developing bronchitis, but it is not clear from this 
study whether the development of bronchitis was confirmed by 
physicians. It is also difficult to assess the bronchitis health 
effects of chromic acid from this study because the study results for 
the exposed (28%) and control groups (23%) were similar.
    Alderson et al. reported 39 deaths of chromate production workers 
related to chronic bronchitis from three chromate producing factories 
(Bolton, Eaglescliffe, and Rutherglen) from 1947 to 1977 (Ex. 35-2). 
Neither the specific Cr(VI) compound nor the extent or frequency with 
which the workers were exposed were specified. However, workers at all 
three factories were exposed to sodium chromate, chromic acid, and 
calcium chromate at one time or another. The authors did not find an 
excess number of bronchitis related deaths at the Bolton and 
Eaglescliffe factories. At Rutherglen, there was an excess number of 
deaths (31) from chronic bronchitis with a ratio of observed/expected 
of 1.8 (p< 0.001). It is difficult to assess the respiratory health 
effects of Cr(VI) compounds from this study because there are no 
exposure data, there are no data on smoking habits, nor is it clear the 
extent, duration, and amount of specific Cr(VI) compound to which the 
workers were exposed during the study.
    While the evidence supports an association between bronchitis and 
Cr(VI) exposure is limited, studies in experimental animals demonstrate 
that Cr(VI) compounds can cause lung irritation, inflammation in the 
lungs, and possibly lung fibrosis at various exposure levels. Glaser et 
al. examined the effects of inhalation exposure of chromium (VI) on 
lung inflammation and alveolar macrophage function in rats (Ex. 31-18-
9). Twenty, 5-week-old male TNO-W-74 Wistar rats were exposed via 
inhalation to 25-200 [mu]g Cr(VI)/m3 as sodium dichromate 
for 28 days or 90 days for 22 hours per day, 7 days per week in 
inhalation chambers. Twenty, 5-week-old male TNO-W-74 Wistar rats also 
served as controls. All rats were killed at the end of the inhalation 
exposure period. The authors found increased lung weight in the 50-200 
[mu]g/m3 groups after the 90-day exposure period. They also 
found that 28-day exposure to levels of 25 and 50 [mu]g/m3 
resulted in "activated" alveolar macrophages with stimulated 
phagocytic activities. A more pronounced effect on the activation of
alveolar macrophages was seen during the 90-day exposure period of 25 
and 50 [mu]g/m3.
    Glaser et al. exposed 150 male, 8-week-old Wistar rats (10 rats per 
group) continuously by inhalation to aerosols of sodium dichromate at 
concentrations of 50, 100, 200, and 400 [mu]g Cr(VI)/m3 for 
22 hours per day, 7 days a week, for continuous exposure for 30 days or 
90 days in inhalation chambers (Ex. 31-18-11). Increased lung weight 
changes were noticeable even at levels as low as 50 and 100 [mu]g 
Cr(VI)/m3 following both 30 day and 90 day exposures. 
Significant accumulation of alveolar macrophages in the lungs was noted 
in all of the exposure groups. Lung fibrosis occurred in eight rats 
exposed to 100 [mu]g Cr(VI)/m3 or above for 30 days. Most 
lung fibrosis disappeared after the exposure period had ceased. At 50 
[mu]g Cr(VI)/m3 or higher for 30 days, a high incidence of 
hyperplasia was noted in the lung and respiratory tract. The total 
protein in bronchoalveolar lavage (BAL) fluid, albumin in BAL fluid, 
and lactate dehydrogenase in BAL fluid were significant at elevated 
levels of 200 and 400 [mu]g Cr(VI)/m3 in both the 30 day and 
90 day exposure groups (as compared to the control group). These 
responses are indicative of severe injury in the lungs of animals 
exposed to Cr(VI) dose levels of 200 [mu]g Cr(VI)/m3 and 
above. At levels of 50 and 100 [mu]g Cr(VI)/m3, the 
responses are indicative of mild inflammation in the lungs. The authors 
concluded that these results suggest that the severe inflammatory 
reaction may lead to more chronic and obstructive lesions in the lung.
4. Summary
    Overall, there is convincing evidence to indicate that Cr(VI) 
exposed workers can develop nasal irritation, nasal ulcerations, nasal 
perforations, and asthma. There is also some limited evidence that 
bronchitis may occur when workers are exposed to Cr(VI) compounds at 
high levels. Most of the studies involved exposure to water-soluble 
Cr(VI) compounds. It is very clear that workers may develop nasal 
irritations, nasal ulcerations, and nasal perforations at levels below 
the current PEL of 52 [mu]g/m3. However, it is not clear 
what occupational exposure levels lead to disorders like asthma and 
bronchitis.
    There are numerous studies in the literature showing nasal 
irritations, nasal perforations, and nasal ulcerations resulting from 
Cr(VI) inhalation exposure. It also appears that direct hand-to-nose 
contact (i.e., by touching inner nasal surfaces with contaminated 
fingers) can contribute to the incidence of nasal damage. Additionally, 
some studies show that workers developed these nasal health problems 
because they did not wear any PPE, including respiratory protection. 
Inadequate area ventilation and sanitation conditions (lack of 
cleaning, dusty environment) probably contributed to the adverse nasal 
effects.
    There are several well documented case reports in the literature 
describing occupational asthma specifically triggered by Cr(VI) in 
sensitized workers. All involved workers who frequently suffered 
symptoms typical of asthma (e.g. dyspnea, wheezing, coughing, etc.) 
while working in jobs involving airborne exposure to Cr(VI). In some of 
the reports, a physician diagnosed bronchial asthma triggered by Cr(VI) 
after specific bronchial challenge with a Cr(VI) aerosol produced 
characteristic symptoms and asthmatic airway responses. Several 
national and international bodies, such as the National Institute for 
Occupational Safety and Health, the World Health Organization's 
International Programme on Chemical Safety, and the United Kingdom 
Health and Safety Executive have recognized Cr(VI) as an airway 
sensitizer that can cause occupational asthma. Despite the widespread 
recognition of Cr(VI) as an airway sensitizer, OSHA is not aware of any 
well controlled occupational survey or epidemiological study that has 
found a significantly elevated prevalence of asthma among Cr(VI)-
exposed workers. The level of Cr(VI) in the workplace that triggers the 
asthmatic condition and the number of workers at risk are not known.
    The evidence that workers breathing Cr(VI) can develop respiratory 
disease that involve inflammation, such as asthma and bronchitis is 
supported by experimental animal studies. The 1985 and 1990 Glaser et 
al. studies show that animals experience irritation and inflammation of 
the lungs following repeated exposure by inhalation to water-soluble 
Cr(VI) at air concentrations near the previous PEL of 52 [mu]g/
m3.

D. Dermal Effects

    Occupational exposure to Cr(VI) is a well-established cause of 
adverse health effects of the skin. The effects are the result of two 
distinct processes: (1) Irritant reactions, such as skin ulcers and 
irritant contact dermatitis, and (2) delayed hypersensitivity 
(allergic) reactions. Some evidence also indicates that exposure to 
Cr(VI) compounds may cause conjunctivitis.
    The mildest skin reactions consist of erythema (redness), edema 
(swelling), papules (raised spots), vesicles (liquid spots), and 
scaling (Ex. 35-313, p. 295). The lesions are typically found on 
exposed areas of the skin, usually the hands and forearms (Exs. 9-9; 9-
25). These features are common to both irritant and allergic contact 
dermatitis, and it is generally not possible to determine the etiology 
of the condition based on histopathologic findings (Ex. 35-314). 
Allergic contact dermatitis can be diagnosed by other methods, such as 
patch testing (Ex. 35-321, p. 226). Patch testing involves the 
application of a suspected allergen to the skin, diluted in petrolatum 
or some other vehicle. The patch is removed after 48 hours and the skin 
examined at the site of application to determine if a reaction has 
occurred.
    Cr(VI) compounds can also have a corrosive, necrotizing effect on 
living tissue, forming ulcers, or "chrome holes" (Ex. 35-315). This 
effect is apparently due to the oxidizing properties of Cr(VI) 
compounds (Ex. 35-318, p. 623). Like dermatitis, chrome ulcers 
generally occur on exposed areas of the body, chiefly on the hands and 
forearms (Ex. 35-316). The lesions are initially painless, and are 
often ignored until the surface ulcerates with a crust which, if 
removed, leaves a crater two to five millimeters in diameter with a 
thickened, hardened border. The ulcers can penetrate deeply into tissue 
and become painful. Chrome ulcers may penetrate joints and cartilage 
(Ex. 35-317, p. 138). The lesions usually heal in several weeks if 
exposure to Cr(VI) ceases, leaving a flat, atrophic scar (Ex. 35-318, 
p.623). If exposure continues, chrome ulcers may persist for months 
(Ex. 7-3).
    It is generally believed that chrome ulcers do not occur on intact 
skin (Exs. 35-317, p. 138; 35-315; 35-25). Rather, they develop readily 
at the site of small cuts, abrasions, insect bites, or other injuries 
(Exs. 35-315; 35-318, p. 138). In experimental work on guinea pigs, 
Samitz and Epstein found that lesions were never produced on undamaged 
skin (Ex. 35-315). The degree of trauma, as well as the frequency and 
concentration of Cr(VI) application, was found to influence the 
severity of chrome ulcers.
    The development of chrome ulcers does not appear to be related to 
the sensitizing properties of Cr(VI). Edmundson provided patch tests to 
determine sensitivity to Cr(VI) in 56 workers who exhibited either 
chrome ulcers or scars (Ex. 9-23). A positive response to the patch 
test was found in only two of the workers examined.
    Parkhurst first identified Cr(VI) as a cause of allergic contact 
dermatitis in 1925 (Ex. 9-55). Cr(VI) has since been
confirmed as a potent allergen. Kligman (1966) used a maximization test 
(a skin test for screening possible contact allergens) to assess the 
skin sensitizing potential of Cr(VI) compounds (Ex. 35-327). Each of 
the 23 subjects was sensitized to potassium dichromate. On a scale of 
one to five, with five being the most potent allergen, Cr(VI) was 
graded as five (i.e., an extreme sensitizer). This finding was 
supported by a guinea pig maximization test, which assigned a grade of 
four to potassium chromate using the same scale (Ex. 35-328).
1. Prevalence of Dermal Effects
    Adverse skin effects from Cr(VI) exposure have been known since at 
least 1827, when Cumin described ulcers in two dyers and a chromate 
production worker (Ex. 35-317, p. 138). Since then, skin conditions 
resulting from Cr(VI) exposure have been noted in a wide range of 
occupations. Work with cement is regarded as the most common cause of 
Cr(VI)-induced dermatitis (Exs. 35-313, p. 295; 35-319; 35-320). Other 
types of work where Cr(VI)-related skin effects have been reported 
include chromate production, chrome plating, leather tanning, welding, 
motor vehicle assembly, manufacture of televisions and appliances, 
servicing of railroad locomotives, aircraft production, and printing 
(Exs. 31-22-12; 7-50; 9-31; 9-100; 9-63; 9-28; 9-95; 9-54; 35-329; 9-
97; 9-78; 9-9; 35-330). Some of the important studies on Cr(VI)-related 
dermal effects in workers are described below.
a. Cement Dermatitis
    Many workers develop cement dermatitis, including masons, tile 
setters, and cement workers (Ex. 35-318, p. 624). Cement, the basic 
ingredient of concrete, may contain several possible sources of 
chromium (Exs. 35-317, p.148; 9-17). Clay, gypsum, and chalk that serve 
as ingredients may contain traces of chromium. Ingredients may be 
crushed using chrome steel grinders that, with wear, contribute to the 
chromium content of the concrete. Refractory bricks in the kiln and ash 
residues from the burning of coal or oil to heat the kiln serve as 
additional sources. Trivalent chromium from these sources can be 
converted to Cr(VI) in the kiln (Ex. 35-317. p. 148).
    The prevalence of cement dermatitis in groups of workers with 
regular contact with wet cement has been reported to be from 8 to 45 
percent depending on the countries of origin, type of construction 
industry, and criteria used to diagnose dermatitis (Exs. 46-74, 9-131; 
35-317, 9-57, 40-10-10). Cement dermatitis can be caused by direct 
irritation of the skin, by sensitization to Cr(VI), or both (Ex. 35-
317, p. 147). The reported proportion of allergic and irritant contact 
dermatitis varies considerably depending on the information source. In 
a review of 16 different data sets, Burrows (1983) found that, on 
average, 80% of cement dermatitis cases were sensitized to Cr(VI) (Ex. 
35-317, p. 148). The studies were mostly conducted prior to 1970 on 
European construction workers. More recent occupational studies suggest 
that Cr(VI) allergy may make up a smaller proportion of all dermatitis 
in construction workers, depending on the Cr(VI) content of the cement. 
For example, examination of 1238 German and Austrian construction 
workers in dermatitis units found about half those with occupational 
dermatitis were skin sensitized to Cr(VI) (Ex. 40-10-10). Several other 
epidemiological investigations conducted in the 1980s and 1990s also 
reported that allergic contact dermatitis made up 50 percent or less of 
all dermatitis cases in various groups of construction workers exposed 
to wet cement (Ex. 46-74).
    Cement is alkaline, abrasive, and hydroscopic (water-absorbing), 
and it is likely that the irritant effect resulting from these 
properties interferes with the skin's defenses, permitting penetration 
and sensitization to take place more readily (Ex. 35-318, p. 624). Dry 
cement is considered relatively innocuous because it is not as alkaline 
as wet cement (Exs. 35-317, p. 147; 9-17). When water is mixed with 
cement the water liberates calcium hydroxide, causing a rise in pH (Ex. 
35-317, p. 147).
    Flyvholm et al. (1996) noted a correlation between the Cr(VI) 
concentration in the local cement and the frequency of allergic contact 
dermatitis (Ex. 35-326, p. 278). Because the Cr(VI) content depends 
partially upon the chromium concentration in raw materials, there is a 
great variability in the Cr(VI) content in cement from different 
geographical regions. In locations with low Cr(VI) content, the 
prevalence of Cr(VI)-induced allergic contact dermatitis was reported 
to be approximately one percent, while in regions with higher chromate 
concentrations the prevalence was reported to rise to between 9 to 11% 
of those exposed (Ex. 35-326, p. 278). For example, only one of 35 U.S. 
construction workers with confirmed cement dermatitis was reported to 
have a positive Cr(VI) patch test in a 1970 NIOSH study (Ex. 9-57). 
However, the same study revealed a low Cr(VI) content in 42 
representative cement samples from U.S. companies (e.g 80 percent of 
the samples with C(VI) <  2 [mu]g/g).
    The relationship between Cr(VI) content in cement and the 
prevalence of Cr(VI)-induced allergic contact dermatitis is supported 
by the findings of Avnstorp (1989) in a study of Danish workers who had 
daily contact with wet cement during the manufacture of pre-fabricated 
concrete products (Ex. 9-131). Beginning in September of 1981, low 
concentrations of ferrous sulfate were added to all cement sold in 
Denmark to reduce Cr(VI) to trivalent chromium. Two hundred and twenty 
seven workers were examined in 1987 for Cr(VI)-related skin effects. 
The findings from these examinations were compared to the results from 
190 workers in the same plants who were examined in 1981. The 
prevalence of hand eczema had declined from 11.7% to 4.4%, and the 
prevalence of Cr(VI) sensitization had declined from 10.5% to 2.6%. 
While the two-to four-fold drop in prevalence was statistically 
significant, the magnitude of the reduction may be overstated because 
the amount of exposure time was less in the 1987 than the 1981 group. 
There is also the possibility that other factors, in addition to 
ferrous sulfate, may have led to less dermal contact to Cr(VI), such as 
greater automation or less construction work. However, the study found 
no significant change in the frequency of irritant dermatitis.
    Another study also found lower prevalence of allergic contact 
dermatitis among Finish construction workers following the 1987 
decision to reduce Cr(VI) content of cement used in Finland to less 
than 2 ppm (Ex. 48-8). Ferrous sulfate was typically added to the 
cement to meet this requirement. There was a significantly decreased 
risk of allergic Cr(VI) contact dermatitis reported to the Finnish 
Occupational Disease Registry post-1987 as compared to pre-1987 
(OR=0.4, 95% CI: 0.2-0.7) indicating the occurrence of disease dropped 
one-third after use of the low Cr(VI) content cement. On the other 
hand, the occurrence of irritant dermatitis remained stable throughout 
the study period. Time of exposure was not a significant explanatory 
variable in the analysis. However, the findings may have been somewhat 
confounded by changes in diagnostic procedure over time. The Finnish 
study retested patients previously diagnosed with prior patch test 
protocols and found several false positives (i.e. false diagnosis of 
Cr(VI) allergy).
    In 2003, the Norwegian National Institute of Occupational Health 
sponsored an expert peer review of 24
key epidemiological investigations addressing; (1) whether exposure to 
wet cement containing water soluble Cr(VI) caused allergic contact 
dermatitis, and (2) whether there was a causal association between 
reduction of Cr(VI) in cement and reduction in the prevalence of the 
disease (Ex. 46-74). The panel of four experts concluded that, despite 
the documented limitations of each individual study, the collective 
evidence was consistent in supporting "fairly strong associations 
between Cr(VI) content in cement and the occurrence of allergic 
dermatitis * * * it seems unlikely that all these associations reported 
in the reviewed papers are due to systematic errors only" (Ex. 46-74, 
p. 42).
    Even though the Norwegian panel felt that the available evidence 
indicated a relationship between reduced Cr(VI) content of wet cement 
and lower occurrence of allergic dermatitis, they stated that the 
epidemiological literature was "not sufficient to conclude that there 
is a causal association" (Ex. 46-74, p. 42). This is somewhat 
different than the view expressed in a written June 2002 opinion by the 
Scientific Committee on Toxicity, Ecotoxicity and the Environment 
(CSTEE) to the European Commission, Directorate for General Health and 
Consumer Protection (Ex. 40-10-7). In responding to the question of 
whether it is scientifically justified to conclude that cement 
containing less than 2 ppm Cr(VI) content could substantially reduce 
the risk of skin sensitization, the CSTEE stated that "the available 
information clearly demonstrates that reduction of chromium VI in 
cement to less than 2 ppm * * * will reduce the prevalence of allergic 
contact eczema in workers" (Ex. 40-10-7, p. 5)
b. Dermatitis Associated With Cr(VI) From Sources Other Than Cement
    In 1953 the U.S. Public Health Service reported on hazards 
associated with the chromium-producing industry in the United States 
(Ex. 7-3). Workers were examined for skin effects from Cr(VI) exposure. 
Workers' eyes were also examined for possible effects from splashes of 
Cr(VI)-containing compounds that had been observed in the plants. Of 
the 897 workers examined, 451 had skin ulcers or scars of ulcers. 
Seventeen workers were reported to have skin lesions suggestive of 
chrome dermatitis. The authors noted that most plants provided adequate 
washing facilities, and had facilities for providing clean work 
clothes. A statistically significant increase in congestion of the 
conjunctiva was also reported in Cr(VI)-exposed workers when compared 
with non-exposed workers (38.7% vs. 25.8%).
    In the Baltimore, Maryland chromate production plant examined by 
Gibb et al. (2000), a substantial number of workers were reported to 
have experienced adverse skin effects (Ex. 31-22-12). The authors 
identified a cohort of 2,357 workers first employed at the plant 
between 1950 and 1974. Clinic and first aid records were examined to 
identify findings of skin conditions. These clinical findings were 
identified by a physician as a result of routine examinations or visits 
to the medical clinic by members of the cohort. Percentages of the 
cohort with various clinical findings were as follows:

Irritated skin: 15.1%
Dermatitis: 18.5%
Ulcerated skin: 31.6%
Conjunctivitis: 20.0%

    A number of factors make these results difficult to interpret. The 
reported findings are not specifically related to Cr(VI) exposure. They 
may have been the result of other workplace exposures, or non-workplace 
factors. The report also indicates the percentage of workers who were 
diagnosed with a condition during their tenure at the plant; however, 
no information is presented to indicate the expected incidence of these 
conditions in a population that is not exposed to Cr(VI).
    Measurements of Cr(VI) air concentrations by job title were used to 
estimate worker exposures. Based on these estimates, the authors used a 
proportional hazards model to find a statistically significant 
correlation (p=0.004) between ulcerated skin and airborne Cr(VI) 
exposure. Statistically significant correlations between year of hire 
and findings of ulcerated skin and dermatitis were also reported. 
Exposures to Cr(VI) in the plant had generally dropped over time. 
Median exposure to Cr(VI) at the time of occurrence for most of the 
findings was said to be about 10 [mu]g/m\3\ Cr(VI) (reported as 20 
[mu]g/m\3\ CrO3). It is unclear, however, what contribution 
airborne Cr(VI) exposures may have had to dermal effects. Direct dermal 
contact with Cr(VI) compounds in the plant may have been a contributing 
factor in the development of these conditions.
    Mean and median times on the job prior to initial diagnosis were 
also reported. The mean time prior to diagnosis of skin or eye effects 
ranged from 373 days for ulcerated skin to 719 days for irritated skin. 
Median times ranged from 110 days for ulcerated skin to 221 days for 
conjunctivitis. These times are notable because many workers in the 
plant stayed for only a short time. Over 40% worked for less than 90 
days. Because these short-term workers did not remain in the workplace 
for the length of time that was typically necessary for these effects 
to occur, the results of this study may underestimate the incidence 
that would occur with a more stable worker population.
    Lee and Goh (1988) examined the skin condition of 37 workers who 
maintained chrome plating baths and compared these workers with a group 
of 37 control subjects who worked in the same factories but were not 
exposed to Cr(VI) (Ex. 35-316). Mean duration of employment as a chrome 
plater was 8.1 (SD7.9) years. Fourteen (38%) of the chrome 
platers had some occupational skin condition; seven had chrome ulcers, 
six had contact dermatitis and one had both. A further 16 (43%) of the 
platers had scars suggestive of previous chrome ulcers. Among the 
control group, no members had ulcers or scars of ulcers, and three had 
dermatitis.
    Where ulcers or dermatitis were noted, patch tests were 
administered to determine sensitization to Cr(VI) and nickel. Of the 
seven workers with chrome ulcers, one was allergic to Cr(VI). Of the 
six workers with dermatitis, two were allergic to Cr(VI) and one to 
nickel. The worker with ulceration and dermatitis was not sensitized to 
either Cr(VI) or nickel. Although limited by a relatively small study 
population, this report clearly indicates that Cr(VI)-exposed workers 
face an increased risk of adverse skin effects. The fact that the 
majority of workers with dermatitis were not sensitized to Cr(VI) 
indicates that irritant factors play an important role in the 
development of dermatitis in chrome plating operations.
    Royle (1975) also investigated the occurrence of skin conditions 
among workers involved in chrome plating (Ex. 7-50). A questionnaire 
survey completed by 997 chrome platers revealed that 21.8% had 
experienced skin ulcers, and 24.6% had suffered from dermatitis. No 
information was presented to indicate the expected incidence in a 
comparable population that was not exposed to Cr(VI). Of the 54 plants 
involved in the study, 49 used nickel, another recognized cause of 
allergic contact dermatitis.
    The author examined the relationship between the incidence of these 
conditions and length of exposure. The plater population was divided 
into three groups: those with less than one year of Cr(VI) exposure, 
those with one to five years of Cr(VI) exposure, and those with over 
five years of Cr(VI) exposure. A statistically significant trend was 
found between length of Cr(VI) exposure and incidence of skin ulcers. The 
incidence of dermatitis, on the other hand, bore no relationship to 
length of exposure.
    In 1973, researchers from NIOSH reported on the results of a health 
hazard investigation of a chrome plating establishment (Ex. 3-5). In 
the plating area, airborne Cr(VI) concentrations ranged from less than 
0.71 to 9.12 [mu]g/m\3\ (mean 3.24 [mu]g/m\3\; SD=2.48 [mu]g/m\3\). Of 
the 37 exposed workers who received medical examinations, five were 
reported to have chrome-induced lesions on their hands. Hygiene and 
housekeeping practices in this facility were reportedly deficient, with 
the majority of workers not wearing gloves, not washing their hands 
before eating or leaving the plant, and consuming food and beverages in 
work areas.
    Gomes (1972) examined Cr(VI)-induced skin lesions among 
electroplaters in Sao Paulo, Brazil (Ex. 9-31). A clinical examination 
of 303 workers revealed 88 (28.8%) had skin lesions, while 175 (58.0%) 
had skin and mucus membrane lesions. A substantial number of employers 
(26.6%) also did not provide personal protective equipment to workers. 
The author attributed the high incidence of skin ulcers on the hands 
and arms to inadequate personal protective equipment, and lack of 
training for employees regarding hygiene practices.
    Fleeger and Deng (1990) reported on an outbreak of skin ulcerations 
among workers in a facility where enamel paints containing chromium 
were applied to kitchen range parts (Ex. 9-97). A ground coat of paint 
was applied to the parts, which were then placed on hooks and 
transported through a curing oven. In some cases, small parts were 
places on hooks before paint application. Tiny holes in the oven coils 
apparently resulted in improper curing of the paint, leaving sharp 
edges and a Cr(VI)-containing residue on the hooks. Most of the workers 
who handled the hooks reportedly did not wear gloves, because the 
gloves were said to reduce dexterity and decrease productivity. As a 
result, cuts from the sharp edges allowed the Cr(VI) to penetrate the 
skin, leading to ulcerations (Ex. 9-97).
2. Prognosis of Dermal Effects
    Cr(VI)-related dermatitis tends to become more severe and 
persistent with continuing exposure. Once established, the condition 
may persist even if occupational exposure ceases. Fregert followed up 
on cases of occupational contact dermatitis diagnosed over a 10-year 
period by a dermatology service in Sweden. Based on responses to 
questionnaires completed two to three years after treatment, only 7% of 
women and 10% of men with Cr(VI)-related allergic contact dermatitis 
were reported to be healed (Ex. 35-322). Burrows reviewed the condition 
of patients diagnosed with work-related dermatitis 10-13 years earlier. 
Only two of the 25 cases (8%) caused by exposure to cement had cleared 
(Ex. 35-323).
    Hogan et al. reviewed the literature regarding the prognosis of 
contact dermatitis, and reported that the majority of patients had 
persistent dermatitis (Ex. 35-324). It was reported that job changes 
did not usually lead to a significant improvement for most patients. 
The authors surveyed contact dermatitis experts around the world to 
explore their experience with the prognosis of patients suffering from 
occupational contact dermatitis of the hands. Seventy-eight percent of 
the 51 experts who responded to the survey indicated that chromate was 
one of the allergens associated with the worst possible prognosis.
    Halbert et al. reviewed the experience of 120 patients diagnosed 
with occupational chromate dermatitis over a 10-year period (Ex. 35-
320). The time between initial diagnosis and the review ranged from a 
minimum of six months to a maximum of nine years. Eighty-four (70%) of 
patients were reviewed two or more years after initial diagnosis, and 
40 (33%) after five years or more. In the majority of cases (78, or 
65%), the dermatitis was attributed to work with cement. For the study 
population as a whole, 76% had ongoing dermatitis at the time of the 
review.
    When the review was conducted, 62 (58%) patients were employed in 
the same occupation as when initially diagnosed. Fifty-five (89%) of 
these workers continued to suffer from dermatitis. Fifty-eight patients 
(48%) changed occupations after their initial diagnosis. Each of these 
individuals indicated that they had changed occupations because of 
their dermatitis. In spite of the change, dermatitis persisted in 40 
members of this group (69%).
    Lips et al. found a somewhat more favorable outcome among 88 
construction workers with occupational chromate dermatitis who were 
removed from Cr(VI) exposure (Ex. 35-325). Follow-up one to five years 
after removal indicated that 72% of the patients no longer had 
dermatitis. The authors speculated that this result might be due to 
strict avoidance of Cr(VI) contact. Nonetheless, the condition 
persisted in a substantial portion of the affected population.
3. Thresholds for Dermal Effects
    In a response to OSHA's RFI submitted on behalf of the Chrome 
Coalition, Exponent indicated that the findings of Fowler et al. (1999) 
and others provide evidence of a threshold for elicitation of allergic 
contact dermatitis (Ex. 31-18-1, p. 27). Exponent also stated that 
because chrome ulcers did not develop in the Fowler et al. study, 
"more aggressive" exposures appear to be necessary for the 
development of chrome ulcers.
    The Fowler et al. study involved the dermal exposure of 26 
individuals previously sensitized to Cr(VI) who were exposed to water 
containing 25 to 29 mg/L Cr(VI) as potassium dichromate (pH 9.4) (Ex. 
31-18-5). Subjects immersed one arm in the Cr(VI) solution, while the 
other arm was immersed in an alkaline buffer solution as a control. 
Exposure lasted for 30 minutes and was repeated on three consecutive 
days. Based on examination of the skin, the authors concluded that the 
skin response experienced by subjects was not consistent with either 
irritant or allergic contact dermatitis.
    The exposure scenario in the Fowler et al. study, however, does not 
take into account certain skin conditions often encountered in the 
workplace. While active dermatitis, scratches, and skin lesions served 
as criteria for excluding both initial and continuing participation in 
the study, it is reasonable to expect that individuals with these 
conditions will often continue to work. Cr(VI)-containing mixtures and 
compounds used in the workplace may also pose a greater challenge to 
the integrity of the skin than the solution used by Fowler et al. Wet 
cement, for example, may have a pH higher than 9.4, and may be capable 
of abrading or otherwise damaging the skin. As damaged skin is liable 
to make exposed workers more susceptible to Cr(VI)-induced skin 
effects, the suggested threshold is likely to be invalid. The absence 
of chrome ulcers in the Fowler et al. study is not unexpected, because 
subjects with "fissures or lesions" on the skin were excluded from 
the study (Ex. 31-18-5). As discussed earlier, chrome ulcers are not 
believed to occur on intact skin.
4. Conclusions
    OSHA believes that adverse dermal effects from exposure to Cr(VI), 
including irritant contact dermatitis, allergic contact dermatitis, and 
skin ulceration, have been firmly established. The available evidence 
is not sufficient to relate these effects to any given Cr(VI) air 
concentration. Rather, it appears that direct dermal contact with 
Cr(VI) is the most relevant factor in the development of dermatitis and 
ulcers. Based on the findings of Gibb et al. (Ex. 32-22-12) and U.S. 
Public Health Service (Ex. 7-3), OSHA believes that conjunctivitis may 
result from direct eye contact with Cr(VI).
    OSHA does not believe that the available evidence is sufficient to 
establish a threshold concentration of Cr(VI) below which dermal 
effects will not occur in the occupational environment. This finding is 
supported not only by the belief that the exposure scenario of Fowler 
et al. is not consistent with occupational exposures, but by experience 
in the workplace as well. As summarized by Flyvholm et al. (1996), 
numerous reports have indicated that allergic contact dermatitis occurs 
in cement workers exposed to Cr(VI) concentrations below the threshold 
suggested by Fowler et al. (1999). OSHA considers the evidence of 
Cr(VI)-induced allergic contact dermatitis in these workers to indicate 
that the threshold for elicitation of response suggested by Fowler et 
al. (1999) is not applicable to the occupational environment.

E. Other Health Effects

    OSHA has examined the possibility of health effect outcomes 
associated with Cr(VI) exposure in addition to such effects as lung 
cancer, nasal ulcerations and perforations, occupational asthma, and 
irritant and allergic contact dermatitis. Unlike the Cr(VI)-induced 
toxicities cited above, the data on other health effects do not 
definitively establish Cr(VI)-related impairments of health from 
occupational exposure at or below the previous OSHA PEL.
    There is some positive evidence that workplace inhalation of Cr(VI) 
results in gastritis and gastrointestinal ulcers, especially at high 
exposures (generally over OSHA's previous PEL) (Ex. 7-12). This is 
supported by ulcerations in the gastrointestinal tract of mice 
breathing high Cr(VI) concentration for long periods (Ex. 10-8). Other 
studies reported positive effects but significant information was not 
reported or the confounders made it difficult to draw positive 
conclusions (Ex. 3-84; Sassi 1956 as cited in Ex. 35-41). Other studies 
reported negative results (Exs. 7-14; 9-135).
    Likewise, several studies reported increases in renal proteins in 
the urine of chromate production workers and chrome platers (Exs. 35-
107; 5-45; 35-105; 5-57). The Cr(VI) air levels recorded in these 
workers were usually below the previous OSHA PEL (Exs. 35-107; 5-45). 
Workers with the highest urinary chromium levels tended to also have 
the largest elevations in renal markers (Ex. 35-107). One study 
reported no relationship between chromium in urine and renal function 
parameters, no relationship with age or with duration of exposure, and 
no relationship between the presence of chromium skin ulcers and 
chromium levels in urine or renal function parameters (Ex. 5-57). In 
most studies, the elevated renal protein levels were restricted to only 
one or two proteins out of several examined per study, generally 
exhibited small increases (Ex. 35-105) and the effects appeared to be 
reversible (Ex. 5-45). In addition, it has been stated that low 
molecular weight proteinuria can occur from other reasons and cannot by 
itself be considered evidence of chronic renal disease (Ex. 35-195). 
Other human inhalation studies reported no changes in renal markers 
(Exs. 7-27; 35-104). Animal inhalation studies did not report kidney 
damage (Exs. 9-135; 31-18-11; 10-11; 31-18-10; 10-10). Some studies 
with Cr(VI) administered by drinking water or gavage were positive for 
increases in renal markers as well as some cell and tissue damage (Exs. 
9-143; 11-10). However, it is not clear how to extrapolate such 
findings to workers exposed to Cr(VI) via inhalation. Well-designed 
studies of effects in humans via ingestion were not found.
    OSHA did not find information to clearly and sufficiently 
demonstrate that exposures to Cr(VI) result in significant impairment 
to the hepatic system. Two European studies, positive for an excess of 
deaths from cirrhosis of the liver and hepatobiliarity disorders, were 
not able to separate chromium exposures from exposures to the many 
other substances present in the workplace. The authors also could not 
rule out the role of alcohol use as a possible contributor to the 
disorder (Ex. 7-92; Sassi as cited in Ex. 35-41). Other studies did not 
report any hepatic abnormalities (Exs. 7-27; 10-11).
    The reproductive studies showed mixed results. Some positive 
reproductive effects occurred in some welding studies. However, it is 
not clear that Cr(VI) is the causative agent in these studies (Exs. 35-
109; 35-110; 35-108; 35-202; 35-203). Other positive studies were 
seriously lacking in information. Information was not given on 
exposures, the nature of the reproductive complications, or the women's 
tasks (Shmitova 1980, 1978 as cited in Ex. 35-41, p. 52). ATSDR states 
that because these studies were generally of poor quality and the 
results were poorly reported, no conclusions can be made on the 
potential for chromium to produce adverse reproductive effects in 
humans (Ex. 35-41, p. 52). In animal studies, where Cr(VI) was 
administered through drinking water or diet, positive developmental 
effects occurred in offspring (Exs. 9-142; 35-33; 35-34; 35-38). 
However, the doses administered in drinking water or given in the diet 
were high (i.e., 250, 500, and 750 ppm). Furthermore, strong studies 
showing reproductive or developmental effects in other situations where 
employees were working exclusively with Cr(VI) were not found. In fact, 
the National Toxicology Program (NTP) (Exs. 35-40; 35-42; 35-44) 
conducted an extensive multigenerational reproductive assessment by 
continuous breeding where the chromate was administered in the diet. 
The assessment yielded negative results (Exs. 35-40; 35-42; 35-44). 
Animal inhalation studies were also negative (Exs. 35-199; 9-135; 10-
10; Glaser 1984 as cited in Ex. 31-22-33;). Thus, it cannot be 
concluded that Cr(VI) is a reproductive toxin for normal working 
situations.

VI. Quantitative Risk Assessment

A. Introduction

    The Occupational Safety and Health (OSH) Act and some landmark 
court cases have led OSHA to rely on quantitative risk assessment, 
where possible, to support the risk determinations required to set a 
permissible exposure limit (PEL) for a toxic substance in standards 
under the OSH Act. Section 6(b)(5) of the Act states that "The 
Secretary [of Labor], in promulgating standards dealing with toxic 
materials or harmful agents under this subsection, shall set the 
standard which most adequately assures, to the extent feasible, on the 
basis of the best available evidence, that no employee will suffer 
material impairment of health or functional capacity even if such 
employee has regular exposure to the hazard dealt with by such standard 
for the period of his working life." (29 U.S.C. 651 et seq.)
    In a further interpretation of the risk requirements for OSHA 
standard setting, the United States Supreme Court, in the 1980 
"benzene" decision, (Industrial Union Department, AFL-CIO v. American 
Petroleum Institute, 448 U.S. 607 (1980)) ruled that the OSH Act 
requires that, prior to the issuance of a new standard, a determination 
must be made that there is a significant risk of material impairment of 
health at the existing PEL and that issuance of a new standard will 
significantly reduce or eliminate that risk. The Court stated that 
"before he can promulgate any
permanent health or safety standard, the Secretary is required to make 
a threshold finding that a place of employment is unsafe in the sense 
that significant risks are present and can be eliminated or lessened by 
a change in practices" [448 U.S. 642]. The Court also stated "that 
the Act does not limit the Secretary's power to require the elimination 
of significant risks" [488 U.S. 644]. While the Court indicated that 
the use of quantitative risk analysis was an appropriate means to 
establish significant risk, they made clear that "OSHA is not required 
to support its finding that a significant risk exists with anything 
approaching scientific certainty."
    The Court in the Cotton Dust case, (American Textile Manufacturers 
Institute v. Donovan, 452 U.S. 490 (1981)) found that Section 6(b)(5) 
of the OSH Act places benefits to worker health above all other 
considerations except those making attainment of the health benefits 
unachievable and, therefore, only feasibility analysis of OSHA health 
standards is required and not cost-benefit analysis. It reaffirmed its 
previous position in the "benzene" case, however, that a risk 
assessment is not only appropriate but should be used to identify 
significant health risk in workers and to determine if a proposed 
standard will achieve a reduction in that risk. Although the Court did 
not require OSHA to perform a quantitative risk assessment in every 
case, the Court implied, and OSHA as a matter of policy agrees, that 
assessments should be put into quantitative terms to the extent 
possible.
    The determining factor in the decision to perform a quantitative 
risk assessment is the availability of suitable data for such an 
assessment. As reviewed in section V.B. on Carcinogenic Effects, there 
are a substantial number of occupational cohort studies that reported 
excess lung cancer mortality in workers exposed to Cr(VI) in several 
industrial operations. Many of these found that workers exposed to 
higher levels of airborne Cr(VI) for a longer period of time had 
greater standardized mortality ratios (SMRs) for lung cancer.
    OSHA believes that two recently studied occupational cohorts by 
Gibb et al. (Ex. 31-22-11) and Luippold et al. (Ex. 33-10) have the 
strongest data sets on which to quantify lung cancer risk from 
cumulative Cr(VI) exposure (i.e., air concentration x exposure 
duration). A variety of exposure-response models were fit to these 
data, including linear relative risk, quadratic relative risk, log-
linear relative risk, additive risk, and Cox proportional hazards 
models. Using a linear relative risk model on these data to predict 
excess lifetime risk, OSHA estimated that the lung cancer risk from a 
45 year occupational exposure to Cr(VI) at an 8-hour TWA at the 
previous PEL of 52 [mu]g/m\3\ is 101 to 351 excess deaths per 1000. 
Quantitative lifetime risk estimates from a working lifetime exposure 
at several lower alternative PELs under consideration by the Agency 
were also estimated. The sections below discuss the selection of the 
appropriate data sets and risk models, the estimation of lung cancer 
risks based on the selected data sets and models, the uncertainty in 
the risk estimates, and the key issues that were raised in comments 
received during the public hearing process.
    A preliminary quantitative risk assessment was previously published 
in the Notice of Proposed Rulemaking (69 FR at 59306, 10/4/2004). This 
was peer-reviewed by three outside experts in the fields of 
occupational epidemiology and risk assessment. Their comments were 
discussed in the NPRM (69 FR at 59385-59388). They commented on the 
suitability of several occupational data sets for exposure-response 
analysis, the choice of exposure metric and risk model, the 
appropriateness of the risk estimates, and the characterization of key 
issues and uncertainties. The reviewers agreed that the soluble 
chromate production cohorts described by Gibb et al. and Luippold et 
al. provided the strongest data sets for quantitative risk assessment. 
They concurred that a linear model using cumulative exposure based on 
time-weighted average Cr(VI) air concentrations by job title and 
employment history was the most reasonable risk assessment approach. 
The experts showed less enthusiasm for average monthly Cr(VI) air 
concentrations as an appropriate exposure metric or for an exposure 
threshold below which there is no lung cancer risk. They found the 
range of excess lifetime lung cancer risks presented by OSHA to be 
sound and reasonable. They offered suggestions regarding issues such as 
the impact of cigarette smoking and the healthy worker effect on the 
assessment of risk. OSHA revised the preliminary quantitative risk 
assessment in several respects based on these peer review comments.
    In contrast to the more extensive occupational cohort data on 
Cr(VI) exposure-response, data from experimental animal studies are 
less suitable for quantitative risk assessment of lung cancer. Besides 
the obvious species difference, most of the animal studies administered 
Cr(VI) to the respiratory tract by less relevant routes, such as 
instillation or implantation. The few available inhalation studies in 
animals were limited by a combination of inadequate exposure levels, 
abbreviated durations, and small numbers of animals per dose group. 
Despite these limitations, the animal data do provide semi-quantitative 
information with regard to the relative carcinogenic potency of 
different Cr(VI) compounds. A more detailed discussion can be found in 
sections V.B.7 and V.B.9.
    The data that relate non-cancer health impairments, such as damage 
to the respiratory tract and skin, to Cr(VI) exposure are also not well 
suited for quantitative assessment. There are some data from cross-
sectional studies and worker surveys that group the prevalence and 
severity of nasal damage by contemporary time-weighted average (TWA) 
Cr(VI) air measurements. However, there are no studies that track 
either incidence or characterize exposure over time. Nasal damage is 
also more likely influenced by shorter-term peak exposures that have 
not been well characterized. While difficult to quantify, the data 
indicate that the risk of damage to the nasal mucosa will be 
significantly reduced by lowering the previous PEL, discussed further 
in section VII on Significance of Risk.
    There are even less suitable exposure-response data to assess risk 
for other Cr(VI)-induced impairments (e.g., mild renal damage, 
gastrointestinal ulceration). With the possible exception of 
respiratory tract effects (e.g., nasal damage, occupational asthma), 
the risk of non-cancer adverse effects that result from inhaling Cr(VI) 
are expected to be very low, except as a result of long-term regular 
airborne exposure around or above the previous PEL (52 [mu]g/m\3\). 
Since the non-cancer effects occur at relatively high Cr(VI) air 
concentrations, OSHA has concluded that lowering the PEL to reduce the 
risk of developing lung cancer over a working lifetime will also 
eliminate or reduce the risk of developing these other health 
impairments. As discussed in section V.E., adverse effects to the skin 
primarily result from dermal rather than airborne exposure.

B. Study Selection

    The more than 40 occupational cohort studies reviewed in Section 
VI.B on carcinogenic effects were evaluated to determine the adequacy 
of the exposure-response information for the quantitative assessment of 
lung cancer risk associated with Cr(VI) exposure. The key criteria were 
data that allowed for estimation of input variables,
specifically levels of exposure and duration of exposure (e.g., 
cumulative exposure in mg/m\3\-yr); observed numbers of cancers (deaths 
or incident cases) by exposure category; and expected (background) 
numbers of cancer deaths by exposure category.
    Additional criteria were applied to evaluate the strengths and 
weaknesses of the available epidemiological data sets. Studies needed 
to have well-defined cohorts with identifiable cases. Features such as 
cohort size and length of follow-up affect the ability of the studies 
to detect any possible effect of Cr(VI) exposure. Potential confounding 
of the responses due to other exposures was considered. Study 
evaluation also considered whether disease rates from an appropriate 
reference population were used to derive expected numbers of lung 
cancers. One of the most important factors in study evaluation was the 
ascertainment and use of exposure information (i.e., well-documented 
historical exposure data). Both level and duration of exposure are 
important in determining cumulative dose, and studies are often 
deficient with respect to the availability or use of such information.
    Two recently studied cohorts of chromate production workers, the 
Gibb cohort and the Luippold cohort, were found to be the strongest 
data sets for quantitative assessment (Exs. 31-22-11; 33-10). Of the 
various studies, these two had the most extensive and best documented 
Cr(VI) exposures spanning three or four decades. Both cohort studies 
characterized observed and expected lung cancer mortality and reported 
a statistically significant positive association between lung cancer 
risk and cumulative Cr(VI) exposure. For the remainder of this preamble 
the Gibb and Luippold cohorts are referred to as the "preferred 
cohorts", denoting that they are the cohorts used to derive OSHA's 
model of lung cancer risk from exposure to Cr(VI).
    Four other cohorts (Mancuso, Hayes et al., Gerin et al., and 
Alexander et al.) had less satisfactory data for quantitative 
assessments of lung cancer risk (Exs. 7-11; 23; 7-14; 7-120; 31-16-3). 
These cohorts include chromate production workers, stainless steel 
welders, and aerospace manufacturing workers. While the lung cancer 
response in these cohorts was stratified across multiple exposure 
groups, there were limitations to these data that affected their 
reliability for quantitative risk assessment. OSHA therefore did not 
consider them to be preferred cohorts (i.e., they were not used to 
derive OSHA's model of lung cancer risk from exposure to Cr(VI)). 
However, OSHA believes that quantitative analysis of these cohorts 
provides valuable information to the risk assessment, especially for 
the purpose of comparison with OSHA's risk model based on the preferred 
Gibb and Luippold cohorts. Analyses based on the Mancuso, Hayes et al., 
Gerin et al., and Alexander et al. cohorts, referred to as "additional 
cohorts" for the remainder of this preamble, were compared with the 
assessments based on the Gibb and Luippold cohorts. The strengths and 
weaknesses of all six cohorts as a basis for exposure-response analysis 
are discussed in more detail below.
1. Gibb Cohort
    The Gibb et al. study was a particularly strong study for 
quantitative risk assessment, especially in terms of cohort size and 
historical exposure data (Exs. 31-22-11; 33-11). Gibb et al. studied an 
updated cohort from the same Baltimore chromate production plant 
previously studied by Hayes et al. (see section VI.B.4). The cohort 
included 2357 male workers (white and non-white) first employed between 
1950 and 1974. Follow-up was through the end of 1992 for a total of 
70,736 person-years and an average length of 30 years per cohort 
member. Smoking status and amount smoked in packs per day at the start 
of employment was available for the majority of the cohort members.
    A significant advantage of the Gibb data was the availability of a 
large number of personal and area sampling measurements from a variety 
of locations and job titles which were collected over the years during 
which the cohort members were exposed (from 1950 to 1985, when the 
plant closed). Using these concentration estimates, a job exposure 
matrix was constructed giving annual average exposures by job title. 
Based on the job exposure matrix and work histories for the cohort 
members, Gibb et al. computed the person-years of observation, the 
observed numbers of lung cancer deaths, and the expected numbers of 
lung cancer deaths categorized by cumulative Cr(VI) exposure and age of 
death. They found that cumulative Cr(VI) exposure was a significant 
predictor of lung cancer risk over the exposure range of 0 to 2.76 
(meanSD = 0.702.75) mg/m\3\-yr. This included a 
greater than expected number of lung cancer deaths among relatively 
young workers. For example, chromate production workers between 40 and 
50 years of age with mean cumulative Cr(VI) exposure of 0.41 mg 
CrO3/m\3\-yr (equivalent to 0.21 mg Cr(VI)/m\3\-yr) were 
about four times more likely to die of lung cancer than a State of 
Maryland resident of similar age (Ex. 31-22-11, Table V).
    The data file containing the demographic, exposure, smoking, and 
mortality data for the individual cohort members was made available to 
OSHA (Ex. 295). These data were used in several reanalyses to produce 
several different statistical exposure-response models and to explore 
various issues raised in comments to OSHA, such as the use of linear 
and nonlinear exposure-response models, the difference between modern 
and historical levels of Cr(VI) exposure, and the impact of including 
or excluding short-term workers from the exposure-response analysis. 
The Agency's access to the dataset and to reanalyses of it performed by 
several different analysts has been a tremendous advantage in its 
consideration of these and other issues in the development of the final 
risk assessment.
2. Luippold Cohort
    The other well-documented exposure-response data set comes from a 
second cohort of chromate production workers. Luippold et al. studied a 
cohort of 482 predominantly white, male employees who started work 
between 1940 and 1972 at the same Painesville, Ohio plant studied 
earlier by Mancuso (Ex. 33-10) (see subsection VI.B.3). Mortality 
status was followed through 1997 for a total of 14,048 person-years. 
The average worker had 30 years of follow-up. Cr(VI) exposures for the 
Luippold cohort were based on 21 industrial hygiene surveys conducted 
at the plant between 1943 and 1971, yielding a total of more than 800 
area samples (Ex. 35-61). A job exposure matrix was computed for 22 
exposure areas for each month of plant operation starting in 1940 and, 
coupled with detailed work histories available for the cohort members, 
cumulative exposures were calculated for each person-year of 
observation. Luippold et al. found significant dose-related trends for 
lung cancer SMRs as a function of year of hire, duration of employment, 
and cumulative Cr(VI) exposure. Risk assessments on the Luippold et al. 
study data performed by Crump et al. had access to the individual data 
and, therefore, had the best basis for analysis of this cohort (Exs. 
31-18-1; 35-205; 35-58).
    While the Luippold cohort was smaller and less racially diverse 
than the Gibb cohort, the workforce contained fewer transient, short-
term employees. The Luippold cohort consisted entirely of workers 
employed over one year. Fifty-five percent worked
for more than five years. In comparison, 65 percent of the Gibb cohort 
worked for less than a year and 15 percent for more than five years at 
the Baltimore plant. There was less information about the smoking 
behavior (smoking status available for only 35 percent of members) of 
the Luippold cohort than the Gibb cohort.
    One aspect that the Luippold cohort had in common with the Gibb 
cohort was extensive and well-documented air monitoring of Cr(VI). The 
quality of exposure information for both the Gibb and Luippold cohorts 
was considerably better than that for the Mancuso, Hayes et al., Gerin 
et al., and Alexander et al. cohorts. The cumulative Cr(VI) exposures 
for the Luippold cohort, which ranged from 0.003 to 23 (mean< plus-
minus>SD = 1.582.50) mg Cr(VI)/m\3\-yr, were generally 
higher but overlapped those of the Gibb cohort. The use of individual 
work histories to define exposure categories and presentation of mean 
cumulative doses in the exposure groups provided a strong basis for a 
quantitative risk assessment. The higher cumulative exposure range and 
the longer work duration of the Luippold cohort serve to complement 
quantitative data available on the Gibb cohort.
3. Mancuso Cohort
    Mancuso (Ex. 7-11) studied the lung cancer incidence of an earlier 
cohort of 332 white male employees drawn from the same plant in 
Painesville, Ohio that was evaluated by the Luippold group. The Mancuso 
cohort was first employed at the facility between 1931 and 1937 and 
followed up through 1972, when the plant closed. Mancuso (Ex. 23) later 
extended the follow-up period through 1993, yielding a total of 12,881 
person-years of observation for an average length of 38.8 years and a 
total of 66 lung cancer deaths. Since the Mancuso workers were first 
employed in the 1930s and the Luippold workers were first employed 
after 1940, the two cohorts are completely different sets of 
individuals.
    A major limitation of the Mancuso study is the uncertainty of the 
exposure data. Mancuso relied exclusively on the air monitoring 
reported by Bourne and Yee (Ex. 7-98) conducted over a single short 
period of time during 1949. Bourne and Yee presented monitoring data as 
airborne insoluble chromium, airborne soluble chromium, and total 
airborne chromium by production department at the Painesville plant. 
The insoluble chromium was probably Cr(III) compounds with some 
slightly water-soluble and insoluble chromates. The soluble chromium 
was probably highly water-soluble Cr(VI). Mancuso (Exs. 7-11; 23) 
calculated cumulative exposures (mg/m\3\-yr) for each cohort member 
based on the 1949 mean chromium concentrations, by production 
department, under the assumption that those levels reflect exposures 
during the entire duration of employment for each cohort member, even 
though employment may have begun as early as 1931 and may have extended 
to 1972. Due to the lack of air measurements spanning the full period 
of worker exposure and the lack of adequate methodology to distinguish 
chromium valence states (i.e., Cr(VI) vs. Cr(III)), the exposure data 
associated with the Mancuso cohort were not as well characterized as 
data from the Luippold or Gibb cohorts.
    Mancuso (Exs. 7-11; 23)reported cumulative exposure-related 
increases in age-adjusted lung cancer death rates for soluble, 
insoluble, or total chromium. Within a particular range of exposures to 
insoluble chromium, lung cancer death rates also tended to increase 
with increasing total cumulative chromium. However, the study did not 
report whether these tendencies were statistically significant, nor did 
it report the extent to which exposures to soluble and insoluble 
chromium were correlated. Thus, it is possible that the apparent 
relationship between insoluble chromium (e.g., primarily Cr(III)) and 
lung cancer may have arisen because both insoluble chromium 
concentrations and lung cancer death rates were positively correlated 
with Cr(VI) concentrations. Further discussion with respect to 
quantitative risk estimation from the Mancuso cohort is provided in 
section VI.E.1 on additional risk assessments.
4. Hayes Cohort
    Hayes et al. (Ex. 7-14) studied a cohort of employees at the same 
chromate production site in Baltimore examined by Gibb et al. The Hayes 
cohort consisted of 2101 male workers who were first hired between 1945 
and 1974, excluding those employed for less than 90 days. The Gibb 
cohort had different but partially overlapping date criteria for first 
employment (1950-1974) and no 90 day exclusion. Hayes et al. reported 
SMRs for respiratory tract cancer based on workers grouped by time of 
hire, employment duration, and high or low exposure groups. Workers who 
had ever worked at an older plant facility and workers whose location 
of employment could not be determined were combined into a single 
exposure group referred to as "high or questionable" exposure. 
Workers known to have been employed exclusively at a newer renovated 
facility built in 1950 and 1951 were considered to have had "low" 
exposure. A dose-response was observed in the sense that higher SMRs 
for respiratory cancer were observed among long-term workers (workers 
who had worked for three or more years) than among short-term workers.
    Hayes et al. did not quantify occupational exposure to Cr(VI) at 
the time the cohort was studied, but Braver et al. (Ex. 7-17) later 
estimated average cumulative soluble chromium (presumed by the authors 
to be Cr(VI)) exposures for four subgroups of the Hayes cohort first 
employed between 1945 and 1959. The TWA Cr(VI) concentrations were 
determined from a total of 555 midget impinger air measurements that 
were collected at the older plant from 1945 to 1950. The cumulative 
exposures for the subgroups were estimated from the yearly average 
Cr(VI) exposure for the entire plant and the subgroups' average 
duration of employment rather than job-specific Cr(VI) concentrations 
and individual work histories. Such "group level" estimation of 
cumulative exposure is less appropriate than the estimation based on 
individual experiences as was done for the Gibb and Luippold cohorts.
    A more severe limitation of this study is that exposures attributed 
to many workers in the newly renovated facility at the Baltimore site 
throughout the 1950s were based on chromium measurements from an 
earlier period (i.e., 1949-1950) at an older facility. Samples 
collected at the new facility and reviewed by Gibb et al. (Exs. 25, 31-
22-12) show that the exposures in the new facility were substantially 
lower than assumed by Braver et al. Braver et al. (Ex. 7-17) discussed 
a number of other potential sources of uncertainty in the Cr(VI) 
exposure estimates, such as the possible conversion to Cr(III) during 
sample collection and the likelihood that samples may have been 
collected mainly in potential problem areas.
5. Gerin Cohort
    Gerin et al. (Ex. 7-120) developed a job exposure matrix that was 
used to estimate cumulative Cr(VI) exposures for male stainless steel 
welders who were part of the International Agency for Research on 
Cancer's (IARC) multi-center historical cohort study (Ex. 7-114). The 
IARC cohort included 11,092 welders. However, the number of cohort 
members who were stainless steel welders, for which Cr(VI) exposures 
were estimated, could not be determined from their report. Gerin et al. 
used occupational hygiene surveys reported in the published literature, 
including a limited amount of data collected from 8 of the 135 
companies that employed welders in the cohort, to estimate typical eight-hour 
TWA Cr(VI) breathing zone concentrations for various combinations of 
welding processes and base metal. The resulting exposure matrix was 
then combined with information about individual work history, including 
time and length of employment, type of welding, base metal welded, and 
information on typical ventilation status for each company (e.g., 
confined area, use of local exhaust ventilation, etc.) to estimate the 
cumulative Cr(VI) exposure. Individual work histories were not 
available for about 25 percent of the stainless steel welders. In these 
cases, information was assumed based on the average distribution of 
welding practices within the company. The lack of Cr(VI) air 
measurements from most of the companies in the study and the 
limitations in individual work practice information for this cohort 
raise questions concerning the accuracy of the exposure estimates.
    Gerin et al. reported no upward trend in lung cancer mortality 
across four cumulative Cr(VI) exposure categories for stainless steel 
welders, each accumulating between 7,000 and 10,000 person-years of 
observation. The welders were also known to be exposed to nickel, 
another potential lung carcinogen. Co-exposure to nickel may obscure or 
confound the Cr(VI) exposure-response relationship. As discussed 
further in Sections VI.E.3 and VI.G.4, exposure misclassification in 
this cohort may obscure an exposure-response relationship. This is the 
primary reason that the Gerin et al. cohort was not considered a 
preferred cohort (i.e., it was not used to derive OSHA's quantitative 
risk estimates), although a quantitative analysis of this cohort was 
performed for comparison with the preferred cohorts.
6. Alexander Cohort
    Alexander et al. (Ex. 31-16-3) conducted a retrospective cohort 
study of 2429 aerospace workers employed in jobs entailing chromate 
exposure (e.g., spray painting, sanding/polishing, chrome plating, 
etc.) between 1974 and 1994. The cohort included workers employed as 
early as 1940. Follow-up time was short, averaging 8.9 years per cohort 
member; in contrast, the Gibb and Luippold cohorts accumulated an 
average 30 or more years of follow-up. Long-term follow-up of cohort 
members is particularly important for determining the risk of lung 
cancer, which typically has an extended latency period of twenty years 
or more.
    Industrial hygiene data collected between 1974 and 1994 were used 
to classify jobs in categories of "high" exposure, "moderate" 
exposure, or "low" exposure to Cr(VI). The use of respiratory 
protection was accounted for when setting up the job exposure matrix. 
These exposure categories were assigned summary TWA concentrations and 
combined with individual job history records to estimate cumulative 
exposures for cohort members over time. As further discussed in section 
VI.E.4, it was not clear from the study whether exposures are expressed 
in units of Cr(VI) or chromate (CrO3). Exposures occurring 
before 1974 were assumed to be at TWA levels assigned to the interval 
from 1974 to 1985.
    Alexander et al. presented lung cancer incidence data for four 
cumulative chromate exposure categories based on worker duration and 
the three (high, moderate, low) exposure levels. Lung cancer incidence 
rates were determined using a local cancer registry, part of the 
National Cancer Institute (NCI) Surveillance Epidemiology and End 
Results (SEER) program. The authors reported no positive trend in lung 
cancer incidence with increasing Cr(VI) exposure. Limitations of this 
cohort study include the young age of the cohort members (median = 42) 
and lack of information on smoking. As discussed above, the follow-up 
time (average <  9 years) was probably too short to capture lung cancers 
resulting from Cr(VI) exposure. Finally, the available Cr(VI) air 
measurement data did not span the entire employment period of the 
cohort (e.g., no data for 1940 to 1974) and was heavily grouped into a 
relatively small number of "summary" TWA concentrations that may not 
have fully captured individual differences in workplace exposures to 
Cr(VI). For the above reasons, in particular the insufficient follow-up 
time for most cohort members, the Alexander cohort was not considered a 
preferred dataset for OSHA's quantitative risk analysis. However, a 
quantitative analysis of this cohort was performed for comparison with 
the preferred cohorts.
7. Studies Selected for the Quantitative Risk Assessment
    The epidemiologic database is quite extensive and contains several 
studies with exposure and response data that could potentially be used 
for quantitative risk assessment. OSHA considers certain studies to be 
better suited for quantitative assessment than others. The Gibb and 
Luippold cohorts are the preferred sources for quantitative risk 
assessment because they are large, have extensive follow-up, and have 
documentation of historical Cr(VI) exposure levels superior to the 
Mancuso, Hayes, Gerin and Alexander cohorts. In addition, analysts have 
had access to the individual job histories of cohort members and 
associated exposure matrices. OSHA's selection of the Gibb and Luippold 
cohorts as the best basis of exposure-response analysis for lung cancer 
associated with Cr(VI) exposure was supported by a variety of 
commenters, including for example NIOSH (Tr. 314; Ex. 40-10-2, p. 4), 
EPRI (Ex. 38-8, p.6), and Exponent (Ex. 38-215-2, p. 15). It was also 
supported by the three external peer reviewers who reviewed OSHA's 
preliminary risk assessment, Dr. Gaylor (Ex. 36-1-4-1, p. 24), Dr. 
Smith (Ex. 36-1-4-2 p. 28), and Dr. Hertz-Picciotto (Ex. 36-1-4-4, pp. 
41-42).
    The Mancuso cohort and the Hayes cohort were derived from workers 
at the same plants as Luippold and Gibb, respectively, but have 
limitations associated with the reporting of quantitative information 
and exposure estimates that make them less suitable for risk 
assessment. Similarly, the Gerin and Alexander cohorts are less 
suitable, due to limitations in exposure estimation and short follow-
up, respectively. For these reasons, OSHA did not rely upon the 
Mancuso, Hayes, Gerin, and Alexander cohorts to derive its exposure-
response model for the risk of lung cancer from Cr(VI).
    Although the Agency did not rely on the Mancuso, Hayes, Gerin, and 
Alexander studies to develop its exposure-response model, OSHA believes 
that evaluating risk among several different worker cohorts and 
examining similarities and differences between them adds to the overall 
completeness and quality of the assessment. The Agency therefore 
analyzed these datasets and compared the results with the preferred 
Gibb and Luippold cohorts. This comparative analysis is discussed in 
Section VI.E. In light of the extensive worker exposure-response data, 
there is little additional value in deriving quantitative risk 
estimates from tumor incidence results in rodents, especially 
considering the concerns with regard to route of exposure and study 
design.
    OSHA received a variety of public comments regarding the overall 
quality of the Gibb and Luippold cohorts and their suitability as the 
preferred cohorts in OSHA's quantitative risk analysis. Some commenters 
raised concerns about the possible impact of short-term workers in the 
Gibb cohort on the risk assessment (Tr. 123; Exs. 38-106, p. 10, 21; 
40-12-5, p. 9). The Gibb cohort's inclusion of many workers employed 
for short periods of time was cited as a
"serious flaw" by one commenter, who suggested that many lung cancers 
among short-term workers in the study were caused by unspecified other 
factors (Ex. 38-106, p. 10, p. 21). Another commenter stated that the 
Davies cohort of British chromate production workers "gives greater 
credence to the Painesville cohort as it showed that brief exposures 
(as seen in a large portion of the Baltimore cohort) did not have an 
increased risk of lung cancer" (Ex. 39-43, p. 1). However, separate 
analyses of the short-term (<  1 year employment) and longer-term ( 1 
year) Gibb cohort members indicated that restriction of the cohort to 
workers with tenures of at least one year did not substantially impact 
estimates of excess lung cancer mortality (Ex. 31-18-15-1 , p. 29). At 
the public hearing, Ms. Deborah Proctor of Exponent, Inc. stated that 
"the short term workers did not affect the results of the study" (Tr. 
1848). OSHA agrees with Ms. Proctor's conclusion, and does not believe 
that the inclusion of short term workers in the Gibb cohort is a source 
of substantial uncertainty in the Agency's risk estimates.
    Some commenters expressed concern that the Gibb study did not 
control for smoking (Exs. 38-218, pp. 20-21; 38-265, p. 28; 39-74, p. 
3). However, smoking status at the time of employment was ascertained 
for approximately 90% of the cohort (Ex. 35-435) and was used in 
statistical analyses by Gibb et al., Environ Inc., and Exponent Inc. to 
adjust for the effect of smoking on lung cancer in the cohort (Exs. 25; 
31-18-15-1; 35-435). NIOSH performed similar analyses using more 
detailed information on smoking level (packs per day) that was 
available for 70% of the cohort (Ex. 35-435, p.1100). OSHA believes 
that these analyses appropriately addressed the potential confounding 
effect of smoking in the Gibb cohort. Issues and analyses related to 
smoking are further discussed in Section VI.G.3.
    Other issues and uncertainties raised about the Gibb and Luippold 
cohorts include a lack of information necessary to estimate deposited 
dose of Cr(VI) for workers in either cohort and a concern that the 
Luippold exposure data were based on exposures to "airborne total 
soluble and insoluble chromium* * * rather than exposures to Cr(VI)" 
(Ex. 38-218, pp. 20-21). However, the exposure estimates for the 
Luippold (2003) cohort were recently developed by Proctor et al. using 
measurements of airborne Cr(VI), not the total chromium measurements 
used previously in Mancuso et al.'s analysis (Exs. 35-58, p. 1149; 35-
61). And, while it is true that the Gibb and Luippold (2003) datasets 
do not lend themselves to construction of deposited dose measures, the 
extensive Cr(VI) air monitoring data available on these cohorts are 
more than adequate for quantitative risk assessment. In the case of the 
Gibb cohort, the exposure dataset is extraordinarily comprehensive and 
well-documented (Tr. 709-710; Ex. 44-4, p.2), even "exquisite" 
according to one NIOSH expert (Tr. 312). Further discussion of the 
quality and reliability of the Gibb and Luippold (2003) exposure data 
and related comments appears in Section VI.G.1.
    OSHA received several comments regarding a new epidemiological 
study conducted by Environ, Inc. for the Industrial Health Foundation, 
Inc. of workers hired after the institution of process changes and 
industrial hygiene practices designed to limit exposure to Cr(VI) in 
two chromate production plants in the United States and two plants in 
Germany (Exs. 47-24-1; 47-27, pp. 15-16; 47-35-1, pp. 7-8). These 
commenters suggested that OSHA should use these cohorts to model risk 
of lung cancer from low exposures to Cr(VI). Unfortunately, the public 
did not have a chance to comment on this study because documents 
related to it were submitted to the docket after the time period when 
new information should have been submitted. However, OSHA reviewed the 
study and comments that were submitted to the docket. Based on the 
information submitted, the Agency does not believe that quantitative 
analysis of these studies would provide additional information on risk 
from low exposures to Cr(VI).
    A cohort analysis based on the U.S. plants is presented in an April 
2005 publication by Luippold et al. (Ex. 47-24-2). Luippold et al. 
studied a total of 617 workers with at least one year of employment, 
including 430 at a plant built in the early 1970s ("Plant 1") and 187 
hired after the 1980 institution of exposure-reducing process and work 
practice changes in a second plant ("Plant 2"). Workers were followed 
through 1998. Personal air-monitoring measures available from 1974 to 
1988 for the first plant and from 1981 to 1998 for the second plant 
indicated that exposure levels at both plants were low, with overall 
geometric mean concentrations below 1.5 [mu]g/m3 and area-
specific average personal air sampling values not exceeding 10 [mu]g/
m3 for most years (Ex. 47-24-2, p. 383). By the end of 
follow-up, which lasted an average of 20.1 years for workers at Plant 1 
and 10.1 years at Plant 2, 27 cohort members (4%) were deceased. There 
was a 41% deficit in all-cause mortality when compared to all-cause 
mortality from age-specific state reference rates, suggesting a strong 
healthy worker effect. Lung cancer was 16% lower than expected based on 
three observed vs. 3.59 expected cases, also using age-specific state 
reference rates (Ex. 47-24-2, p. 383). The authors concluded that 
"[t]he absence of an elevated lung cancer risk may be a favorable 
reflection of the postchange environment. However, longer follow-up 
allowing an appropriate latency for the entire cohort will be needed to 
confirm this conclusion" (Ex. 47-24-2, p. 381).
    OSHA agrees with the study authors that the follow-up in this study 
was not sufficiently long to allow potential Cr(VI)-related lung cancer 
deaths to occur among many cohort members. The mean times since first 
exposure of 10 and 20 years for Plant 1 and Plant 2 employees, 
respectively, suggest that most workers in the cohort may not have 
completed the " * * * typical latency period of 20 years or more" 
that Luippold et al. suggest is required for occupational lung cancer 
to emerge (Ex. 47-24-2, p. 384). Other important limitations of this 
study include the striking healthy worker effect on the SMR analysis, 
and the relatively young age of most workers at the end of follow-up 
(approximately 90% <  60 years old) (Ex. 47-24-2, p. 383). OSHA also 
agrees with the study authors' statements that " * * * the few lung 
cancer deaths in this cohort precluded * * * [analyses to] evaluate 
exposure-response relationships * * * " (Ex. 47-24-2, p. 384).
    Although OSHA's model predicts high excess lung cancer risk for 
highly exposed individuals (e.g., workers exposed for 45 years at the 
previous PEL of 52 [mu]g/m3), the model would predict much 
lower risks for workers with low exposures, as in the Luippold (2005) 
cohorts. To provide a point of comparison between the results of the 
Luippold et al. (2005) 'post-change' study and OSHA's risk model, the 
Agency used its risk model to generate an estimate of lung cancer risk 
for a population with exposure characteristics approximately similar to 
the 'post-change' cohorts described in Luippold et al. (2005). It 
should be noted that since this comparative analysis used year 2000 
U.S. reference rates were rather than the state-, race-, and gender-
specific historical reference mortality rates used by Luippold et al. 
(2005), this risk calculation provides only a rough estimate of 
expected excess lung cancer risk for the cohort. The derivation of 
OSHA's risk model (based on the preferred Gibb and Luippold
(2003) cohorts) is described in Sections VI.C.1 and VI.C.2.
    It is difficult to tell from the publication what the average level 
or duration of exposure was for the cohort. However, personal sampling 
data reported by Luippold et al. (2005) had annual geometric mean 8-
hour TWA concentrations "much less" than 1.5 [mu]g/m3 in 
most years (Ex. 47-24-2, p. 383). Most workers also probably had less 
than 20 years of exposure, given the average follow-up periods of 20 
and 10 years reported for the Luippold (2005) Plant 1 and Plant 2, 
respectively. OSHA assumed that workers had TWA exposures of 1.5 [mu]g/
m3 for 20 years, with the understanding that this assumption 
would lead to somewhat higher estimates of risk than OSHA s model would 
predict if the average exposure of the cohort was known. Using these 
assumptions, OSHA's model predicts a 2-9% excess lung cancer risk due 
to Cr(VI) exposure, or less than four cancers in the population the 
size and age of the Luippold 2005 cohort.
    Since this analysis used year 2000 U.S. reference rates rather than 
the state-, race-, and gender-specific historical reference mortality 
rates used by Luippold et al. (2005), this risk calculation provides 
only a rough estimate of the lung cancer risk that OSHA's model would 
predict for the cohort. Nevertheless, it illustrates that for a 
relatively young population with low exposures, OSHA's risk model 
(derived from the preferred Gibb and Luippold 2003 cohorts) predicts 
lung cancer risk similar to that observed in the low-exposure Luippold 
2005 cohort. The small number of lung cancer deaths observed in 
Luippold 2005 should not be considered inconsistent with the risk 
estimates derived using models developed by OSHA based on the Gibb and 
Luippold (2003) cohorts (Ex. 47-24-2, p. 383).
    Some commenters believed that analysis of the unpublished German 
cohorts would demonstrate that lung cancer risk was only increased at 
the highest Cr(VI) levels and, therefore, could form the basis for an 
exposure threshold (Exs. 47-24-1; 47-35-1). Although no data were 
provided to corroborate their comments, the Society of the Plastics 
Industry requested that OSHA obtain and evaluate the German study as 
"new and available evidence which may suggest a higher PEL than 
proposed" (Ex. 47-24-1, p. 4).
    Following the close of the comment period, OSHA gained access to a 
2002 final contract report by Applied Epidemiology Inc. prepared for 
the Industrial Health Foundation (Ex. 48-1-1; 48-1-2) and a 2005 
prepublication by ENVIRON Germany (Ex. 48-4). The 2002 report contained 
detailed cohort descriptions, exposure assessments, and mortality 
analyses of 'post-change' workers from the two German chromate 
production plants referred to above and two U.S. chromate production 
plants, one of which is plant 1 discussed in the 2005 study by Luippold 
et al. The mortality and multivariate analyses were performed on a 
single combined cohort from all four plants. The 2005 prepublication 
contained a more abbreviated description and analysis of a smaller 
cohort restricted to the two German plants only. The cohorts are 
referred to as 'post-change' because the study only selected workers 
employed after the participating plants switched from a high-lime to a 
no-lime (or very low lime facility, in the case of U.S. plant 1) 
chromate production process and implemented industrial hygiene 
improvements that considerably reduced Cr(VI) air levels in the 
workplace.
    The German cohort consisted of 901 post-change male workers from 
two chromate production plants employed for at least one year. 
Mortality experience of the cohort was evaluated through 1998. The 
study found elevated lung cancer mortality (SMR=1.48 95% CI: 0.93-2.25) 
when compared to the age- and calendar year-adjusted German national 
population rates (Ex. 48-4). The cohort lacked sufficient job history 
information and air monitoring data to develop an adequate job-exposure 
matrix required to estimate individual airborne exposures (Ex. 48-1-2). 
Instead, the researchers used the large amount of urinary chromium data 
from routine biomonitoring of plant employees to analyze lung cancer 
mortality using cumulative urinary chromium as an exposure surrogate, 
rather than the conventional cumulative Cr(VI) air concentrations. The 
study reported a statistically significant two-fold excess lung cancer 
mortality (SMR=2.09; 95% CI: 1.08-3.65; 12 observed lung cancer deaths) 
among workers in the highest cumulative exposure grouping (i.e. >200 
[mu]g Cr/L--yr). There was no increase in lung cancer mortality in the 
lower exposure groups, but the number of lung cancer deaths was small 
(i.e. < 5 deaths) and the confidence intervals were wide. Logistic 
regression modeling in the multi-plant cohort (i.e. German and U.S. 
plants combined) showed an increased risk of lung cancer in the high 
(OR=20.2; 95% CI: 6.2-65.4; 10 observed deaths) and intermediate 
(OR=4.9; 95% CI: 1.5-16.0; 9 deaths) cumulative exposure groups when 
compared to the low exposure group (Ex. 48-1-2, Table 18). The lung 
cancer risks remained unchanged when smoking status was controlled for 
in the model, indicating that the elevated risks were unlikely to be 
confounded by smoking in this study.
    OSHA does not believe that the results of the German study provide 
a basis on which to establish a threshold exposure below which no lung 
cancer risk exists. Like the U.S. post-change cohort (i.e., Luippold 
(2005) cohort) discussed above, small cohort size, few lung cancer 
cases (e.g., 10 deaths in the three lowest exposure groups combined) 
and limited follow-up (average 17 years) severely limit the power to 
detect small increases in risk that may be present with low cumulative 
exposures. The limited power of the study is reflected in the wide 
confidence intervals associated with the SMRs. For example, there is no 
apparent evidence of excess lung cancer (SMR=0.95; 95% CI: 0.26-2.44) 
in workers exposed to low cumulative urine chromium levels between 40-
100 [mu]g Cr/L--yr. However, the lack of precision in this estimate is 
such that a two-fold increase in lung cancer mortality can not be ruled 
out with a high degree of confidence. Although the study authors state 
that the data suggest a possible threshold effect, they acknowledge 
that "demonstrating a clear (and statistically significant) threshold 
response in epidemiological studies is difficult especially [where], as 
in this study, the number of available cases is relatively small, and 
the precise estimation of small risks requires large numbers" (Ex. 48-
4, p. 8). OSHA agrees that the number of lung cancer cases in the study 
is too small to clearly demonstrate a threshold response or precisely 
estimate small risks.
    OSHA has relied upon a larger, more robust cohort study for its 
risk assessment than the German cohort. In comparison, the Gibb cohort 
has about five times the person-years of observation (70736 vs. 14684) 
and number of lung cancer cases (122 vs. 22). The workers, on average, 
were followed longer (30 vs. 17 years) and a greater proportion of the 
cohort is deceased (36% vs. 14%). Limited air monitoring from the 
German plants indicate that average plant-wide airborne Cr(VI) roughly 
declined from about 35 [mu]g Cr(VI)/m\3\ in the mid 1970s to 5 [mu]g 
Cr(VI)/m\3\ in the 1990s (2002 report; Ex. 7-91). This overlaps the 
Cr(VI) air levels in the Baltimore plant studied by Gibb et al. (Ex. 
47-8). Furthermore, cumulative exposure estimates for members of the 
Gibb cohort were individually reconstructed
from job histories and Cr(VI) air monitoring data. These airborne 
Cr(VI) exposures are better suited than urinary chromium for evaluating 
occupational risk at the permissible exposure limits under 
consideration by OSHA. An appropriate conversion procedure that 
credibly predicts time-weighted average Cr(VI) air concentrations in 
the workplace from urinary chromium measurements is not evident and, 
thus, would undoubtedly generate additional uncertainty in the risk 
estimates. For the above reasons, OSHA believes the Gibb cohort 
provides a stronger dataset than the German cohort on which to assess 
the existence of a threshold exposure. This and other issues pertaining 
to the relationship between the cumulative exposure and lung cancer 
risk are further discussed in section VI.G.1.a.

C. Quantitative Risk Assessments Based on the Gibb Cohort

    Quantitative risk assessments were performed on the exposure-
response data from the Gibb cohort by three groups: Environ 
International (Exs. 33-15; 33-12) under contract with OSHA; the 
National Institute for Occupational Safety and Health (Ex. 33-13); and 
Exponent (Ex. 31-18-15-1) for the Chrome Coalition. All reported 
similar risks for Cr(VI) exposure over a working lifetime despite using 
somewhat different modeling approaches. The exposure-response data, 
risk models, statistical evaluation, and risk estimates reported by 
each group are discussed below.
1. Environ Risk Assessments
    In 2002, Environ International (Environ) prepared a quantitative 
analysis of the association between Cr(VI) exposure and lung cancer 
(Ex. 33-15) , which was described in detail in the Preamble to the 
Proposed Rule (69 FR at 59364-59365). After the completion of the 2002 
Environ analysis, individual data for the 2357 men in the Gibb et al. 
cohort became available. The new data included cumulative Cr(VI) 
exposure estimates, smoking information, date of birth, race, date of 
hire, date of termination, cause of death, and date of the end of 
follow-up for each individual (Ex. 35-295). The individual data allowed 
Environ to do quantitative risk assessments based on (1) redefined 
exposure categories, (2) alternate background reference rates for lung 
cancer mortality, and (3) Cox proportional hazards modeling (Ex. 33-
12). These are discussed below and in the 2003 Environ analysis (Ex. 
33-12).
    The 2003 Environ analysis presented two alternate groupings with 
ten cumulative Cr(VI) exposure groups each, six more than reported by 
Gibb et al. and used in the 2002 analysis. One alternative grouping was 
designed to divide the person-years of follow-up fairly evenly across 
groups. The other alternative allocated roughly the same number of 
observed lung cancers to each group. These two alternatives were 
designed to remedy the uneven distribution of observed and expected 
cases in the Gibb et al. categories, which may have caused parameter 
estimation problems due to the small number of cases in some groups. 
The new groupings assigned adequate numbers of observed and expected 
lung cancer cases to all groups and are presented in Table VI-1.
    Environ used a five-year lag to calculate cumulative exposure for 
both groupings. This means that at any point in time after exposure 
began, an individual's cumulative exposure would equal the product of 
chromate concentration and duration of exposure, summed over all jobs 
held up to five years prior to that point in time. An exposure lag is 
commonly used in exposure-response analysis for lung cancer since there 
is a long latency period between first exposure and the development of 
disease. Gibb et al. found that models using five- and ten-year lags 
provided better fit to the mortality data than lags of zero, two and 
twenty years (Ex. 31-22-11).
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    The 2003 Environ analysis also derived expected cases using lung 
cancer rates from alternative reference populations. In addition to the 
State of Maryland lung cancer rates that were used by Gibb et al., 
Environ used age- and race-specific rates from the city of Baltimore, 
where the plant was located. Baltimore may represent a more appropriate 
reference population because most of the cohort members
resided in Baltimore and Baltimore residents may be more similar to the 
cohort members than the Maryland or U.S. populations in their co-
exposures and lifestyle characteristics, especially smoking habits and 
urban-related risk factors. On the other hand, Baltimore may not be the 
more appropriate reference population if the higher lung cancer rates 
in the Baltimore population primarily reflect extensive exposure to 
industrial carcinogens. This could lead to underestimation of risk 
attributable to Cr(VI) exposure.
    The 2003 analysis used two externally standardized models, a 
relative risk model (model E1 below) and an additive risk model (model 
E2) defined as follows:

E1. Ni = C0 * Ei * (1 + C1Di + C2Di\2\)
E2. Ni = C0 * Ei + PYi * (C1Di + C2Di\2\)

where Ni is the predicted number of lung cancers in the i 
th group; PYi is the number of person-years for 
group i; Ei is the expected number of lung cancers in that 
group, based on the reference population; Di is the mean 
cumulative dose for that group; and C0, C1, and 
C2 are parameters to be estimated. Both models initially 
included quadratic exposure terms (C2Di\2\ ) as 
one way to test for nonlinearity in the exposure-response. Model E1 is 
a relative risk model, whereas Model E2 is an additive risk model. In 
the case of additive risk models, the exposure-related estimate of 
excess risk is the same regardless of the age- and race-specific 
background rate of lung cancer. For relative risk models, a dose term 
is multiplied by the appropriate background rate of lung cancer to 
derive an exposure-related estimate of risk, so that excess risk always 
depends on the background.
    Maximum likelihood techniques were used to estimate the parameters 
C0, C1, and C2. Likelihood ratio tests 
were used to determine which of the model parameters contributed 
significantly to the fit of the model. Parameters were sequentially 
added to the model, starting with C1, when they contributed 
significantly (p <  0.05) to improving the fit. Parameters that did not 
contribute significantly, including the quadratic exposure terms 
(C2Di\2\ ), were removed from the models.
    Two Cox proportional hazards models were also fit to the individual 
exposure-response data. The model forms were:

C1. h(t;z;D) = h0(t)*exp([beta]1z + 
[beta]2D)

C2. h(t;z;D) = h0(t)*[exp([beta]1z)][1 + 
[beta]2D]

where h is the hazard function, which expresses the age-specific rate 
of lung cancer among workers, as estimated by the model. In addition, t 
is age, z is a vector of possible explanatory variables other than 
cumulative dose, D is cumulative dose, h0(t) is the baseline 
hazard function (a function of age only), [beta]2 is the 
cumulative dose coefficient, and [beta]1 is a vector of 
coefficients for other possible explanatory variables--here, cigarette 
smoking status, race, and calendar year of death (Ex. 35-57). Cox 
modeling is an approach that uses the experience of the cohort to 
estimate an exposure-related effect, irrespective of an external 
reference population or exposure categorization. Because they are 
internally standardized, Cox models can sometimes eliminate concerns 
about choosing an appropriate reference population and may be 
advantageous when the characteristics of the cohort under study are not 
well matched against reference populations for which age-related 
background rates have been tabulated. Model C1 assumes the lung cancer 
response is nonlinear with cumulative Cr(VI) exposure, whereas C2 
assumes a linear lung cancer response with Cr(VI) exposure. For the Cox 
proportional hazards models, C1 and C2, the other possible explanatory 
variables considered were cigarette smoking status, race, and calendar 
year of death.
    The externally standardized models E1 and E2 provided a good fit to 
the data (p>=0.40). The choice of exposure grouping had little effect 
on the parameter estimates of either model E1 or E2. However, the 
choice of reference rates had some effect, notably on the 
"background" parameter, C0, which was included as a fitted 
parameter in the models to adjust for differences in background lung 
cancer rates between cohort members and the reference populations. For 
example, values of C0 greater than one "inflate" the base 
reference rates, reducing the magnitude of excess risks in the model. 
Such an adjustment was necessary for the Maryland reference population 
(the maximum likelihood estimate of C0 was significantly 
higher than one), but not for the Baltimore city reference population 
(C0 was not significantly different from one). This result 
suggests that the Maryland lung cancer rates may be lower than the 
cohort's background lung cancer rates, but the Baltimore city rates may 
adequately reflect the cohort background rates. The inclusion of the 
C0 parameter yielded a cumulative dose coefficient that 
reflected the effect of exposure and not the effect of differences in 
background rates, and was appropriate.
    The model results indicated a relatively consistent cumulative dose 
coefficient, regardless of reference population. The coefficient for 
cumulative dose in the models ranged from 2.87 to 3.48 per mg/m\3\-yr 
for the relative risk model, E1, and from 0.0061 to 0.0071 per mg/m\3\-
person-yr for the additive risk model, E2. These coefficients determine 
the slope of the linear cumulative Cr(VI) exposure-lung cancer response 
relationship. In no case did a quadratic model fit the data better than 
a linear model.
    Based on comparison of the models' AIC values, Environ indicated 
that the linear relative risk model E1 was preferred over the additive 
risk model E2. OSHA agrees with Environ's conclusion. The relative risk 
model is also preferred over an additive risk model because the 
background rate of lung cancer varies with age. It may not be 
appropriate to assume, as an additive model does, that increased lung 
cancer risk at age 25, where background risk is relatively low, would 
be the same (for the same cumulative dose) as at age 65, where 
background rates are much higher.
    The Cox proportional hazards models, C1 and C2, also fit the data 
well (although the fit was slightly better for model C2 than C1). 
Recall that for the Cox proportional hazards models, C1 and C2, the 
other possible explanatory variables considered were cigarette smoking 
status, race, and calendar year of death. For both models, addition of 
a term for smoking status significantly improved the fit of the models 
to the data (p< 0.00001). The experience with model C1 indicated that 
race (p=0.15) and year of death (p=0.4) were not significant 
contributors when cumulative dose and smoking status were included in 
the model. Based on results for model C1, race and year of death were 
not considered by Environ in the linear model C2. The cumulative dose 
coefficient, [beta]2, was 1.00 for model C1 and 2.68 for 
model C2. A more complete description of the models and variables can 
be found in the 2003 Environ analysis (Ex. 33-12, p. 10).
    Lifetable calculations were made of the number of extra lung 
cancers per 1000 workers exposed to Cr(VI) based on models E1, E2, C1, 
and C2, assuming a constant exposure from age 20 through a maximum of 
age 65. The lifetable accounted for both lung cancer risk and competing 
mortality through age 100. Rates of lung cancer and other mortality for 
the lifetable calculations were based, respectively, on 2000 U.S. lung 
cancer and all-cause mortality rates for both sexes and all races. In 
addition to the maximum likelihood estimates, 95% confidence intervals 
for the excess lifetime risk were derived. Details about the procedures 
used to estimate parameters, model fit, lifetable calculations, and 
confidence intervals are described in the 2003 Environ report (Ex. 33-12, p. 8-9).
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    Table VI-2 shows each model's predictions of excess lifetime lung 
cancer risk from a working lifetime of exposure to various Cr(VI) air 
levels. The estimates are very consistent regardless of model, exposure 
grouping, or reference population. The model that appears to generate 
results least similar to the others is C1, which yielded one of the 
higher risk estimates at 52 [mu]g/m3, but estimated the 
lowest risks for exposure levels of 10 [mu]g/m3 or lower. 
The change in magnitude, relative to the other models, is a result of 
the nonlinearity of this model. Confidence limits for all models, 
including C1, tend to overlap, suggesting a fair degree of statistical 
consistency.
2. National Institute for Occupational Safety and Health (NIOSH) Risk 
Assessment
    NIOSH (Ex. 33-13) developed a risk assessment from the Gibb cohort. 
The NIOSH analysis, like the 2003 Environ assessment, used the cohort 
individual data files to compute cumulative Cr(VI) exposure. However, 
NIOSH also explored some other exposure-related assumptions. For 
example, they performed the dose-response analysis with lag times in 
addition to the 5-year lag used by Environ. NIOSH also analyzed dose-
response using as many as 50 exposure categories, although their report 
presents data in five cumulative Cr(VI) exposure groupings.
    NIOSH incorporated information on the cohort smoking behavior in 
their quantitative assessments. They estimated (packs/day)-years of 
cumulative smoking for each individual in the cohort, using information 
from a questionnaire that was administered at the time of each cohort 
member's date of hire. To estimate cumulative smoking, NIOSH assumed 
that the cohort members maintained the level of smoking reported in the 
questionnaire from the age of 18 through the end of follow-up. 
Individuals with unknown smoking status were assigned a value equal to 
the average smoking level among all individuals with known smoking 
levels (presumably including non-smokers). Individuals who were known 
to smoke but for whom the amount was unknown were assigned a smoking 
level equal to the average of all smokers.
    NIOSH considered six different relative risk models, fit to the 
Gibb cohort data by Poisson regression methods. They did not consider 
additive risk models. The six relative risk models were externally 
standardized using age- and race-specific U.S. lung cancer rates. Their 
background coefficients, C0, explicitly included smoking, 
race, and age terms to adjust for differences between the cohort and 
the reference population. These models are described as follows:

NIOSH1a: Ni = C0 * Ei * exp(C1Di)
NIOSH1b: Ni = C0 * Ei * exp(C1Di\1/2\\)
NIOSH1c: Ni = C0 * Ei * exp(1 + C1Di + C2Di2)
NIOSH1d: Ni = C0 * Ei * (1 + Di)[alpha]
NIOSH1e: Ni = C0 * Ei * (1 + C1Di)
NIOSH1f: Ni = C0 * Ei * (1 + C1Di[alpha])

where the form of the equation has been modified to match the format 
used in the Environ reports. In addition, NIOSH fit Cox proportional 
hazard models (not presented) to the lung cancer mortality data using 
the individual cumulative Cr(VI) exposure estimates.
    NIOSH reported that the linear relative risk model 1e generally 
provided a superior fit to the exposure-response data when compared to 
the various log linear models, 1a-d. Allowing some non-linearity (e.g., 
model 1f) did not significantly improve the goodness-of-fit, therefore, 
they considered the linear relative risk model form 1e (analogous to 
the Environ model E1) to be the most appropriate for determining their 
lifetime risk calculations. A similar fit could be achieved with a log-
linear power model (model 1d) using log-transformed cumulative Cr(VI) 
and a piece-wise linear specification for the cumulative smoking term.
    The dose coefficient (C1) for the linear relative risk 
model 1e was estimated by NIOSH to be 1.444 per [mu]g CrO3/
m3-yr (Ex. 33-13, Table 4). If the exposures were converted 
to units of [mu]g Cr(VI)/m3-yr, the estimated cumulative 
dose coefficient would be 2.78 (95% CI: 1.04 to 5.44) per [mu]g/
m3-yr. This value is very close to the estimates derived in 
the Environ 2003 analysis (maximum likelihood estimates ranging from 
2.87 to 3.48 for model E1, depending on the exposure grouping and the 
reference population). Lifetime risk estimates based on the NIOSH-
estimated dose coefficient and the Environ lifetable method using 2000 
U.S. rates for lung cancer and all cause mortality are shown in Table 
VI-3. The values are very similar to the estimates predicted by the 
Environ 2003 analysis (Table VI-3). The small difference may be due to 
the NIOSH adjustment for smoking in the background coefficient. NIOSH 
found that excess lifetime risks for a 45-year occupational exposure to 
Cr(VI) predicted by the best-fitting power model gave very similar 
risks to the preferred linear relative risk model at TWA Cr(VI) 
concentrations between 0.52 and 52 [mu]g/m3 (Ex. 33-13, 
Table 5). Although NIOSH did not report the results, they stated that 
Cox modeling produced risk estimates similar to the Poisson regression. 
The consistency between Cox and Poisson regression modeling is 
discussed further in section VI.C.4.
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    NIOSH reported a significantly higher dose-response coefficient for 
nonwhite workers than for white workers. That is, nonwhite workers in 
the Gibb cohort are estimated to have a higher excess risk of lung 
cancer than white workers, given equal cumulative exposure to Cr(VI). 
In contrast, no significant race difference was found in the Cox 
proportional hazards analysis reported by 2003 Environ.

3. Exponent Risk Assessment
    In response to OSHA's Request For Information, Exponent prepared an 
analysis of lung cancer mortality from the Gibb cohort. Like the 2003 
Environ and NIOSH analyses, the Exponent analysis relied on the 
individual worker data. Exponent performed their dose-response analyses 
based on three different sets of exposure categories using two 
reference populations and 70,808 person-years of follow-up. A total of 
four analyses were completed, using (1) Maryland reference rates and 
the four Gibb et al. exposure categories; (2) Baltimore reference rates 
and the four Gibb et al. exposure categories; (3) Baltimore reference 
rates and six exposure groups defined by Exponent; and (4) Baltimore 
City reference rates and five exposure categories, obtained by removing 
the highest of the six groups defined by Exponent from the dose-
response analysis. A linear relative risk model without a background 
correction term (the term C0 used by Environ and NIOSH) was 
applied in all of these cases and cumulative exposures were lagged five 
years (as done by Environ and NIOSH). The analyses showed excess 
lifetime risk between 6 and 14 per 1000 for workers exposed to 1 [mu]g/
m\3\ Cr(VI) for 45 years.
    The analysis using Maryland reference lung cancer rates and the 
Gibb et al. four-category exposure grouping yielded an excess lifetime 
risk of 14 per 1000. This risk, which is higher than the excess 
lifetime risk estimates by Environ and NIOSH for the same occupational 
exposure, probably results from the absence of a background rate 
coefficient (C0) in Exponent's model. As reported in the 
Environ 2002 and 2003 analyses, the Maryland reference lung cancer 
rates require a background rate coefficient greater than 1 to achieve 
the best fit to the exposure-response data. The unadjusted Maryland 
rates probably underestimate the cohort's background lung cancer rate, 
leading to overestimation of the risk attributable to cumulative Cr(VI) 
exposure.
    The two analyses that used Baltimore reference rates and either 
Exponent's six-category exposure grouping or the Gibb et al. four-
category grouping both resulted in an excess lifetime unit risk of 9 
per 1000 for workers exposed to 1 [mu]g/m\3\ Cr(VI) for 45 years (Ex. 
31-18-15-1, p. 41). This risk is close to estimates reported by Environ 
using their relative risk model (E1) and Baltimore reference rates for 
the same occupational exposure (Table VI-2). The Environ analysis 
showed that, unlike the Maryland-standardized model discussed above, 
the Baltimore-standardized models had background rate coefficients very 
close to 1, the "default" value assumed by the Exponent relative risk 
model. This suggests that the Baltimore reference rates may represent 
the background lung cancer rate for this cohort more accurately than 
the Maryland reference rates.
    The lowest excess lifetime unit risk for workers exposed to 1 
[mu]g/m\3\ Cr(VI) for 45 years reported by Exponent, at 6 per 1000, was 
derived from the analysis that excluded the highest of Exponent's six 
exposure groups. While this risk value is close to the Environ and 
NIOSH unit risk estimates, the analysis merits some concern. Exponent 
eliminated the highest exposure group on the basis that most cumulative 
exposures in this group were higher than exposures usually found in 
current workplace conditions. However, eliminating this group could 
exclude possible long-term exposures (e.g., >15 years) below the 
previous OSHA PEL (52 [mu]g/m\3\ ) from the risk analysis. Moreover, no 
matter what current exposures might be, data on higher cumulative 
exposures are relevant for understanding the dose-response 
relationships.
    In addition, the Exponent six category cumulative exposure grouping 
may have led to an underestimate of the dose effect. The definition of 
Exponent's six exposure groups was not related to the distribution of 
cumulative exposure associated with individual person-years, but rather 
to the distribution of cumulative exposure among the workers at the end 
of their employment. This division does not result in either a uniform 
distribution of person-years or observed lung cancer cases among 
exposure categories. In fact, the six category exposure groupings of 
both person-years and observed lung cancers were very uneven, with a 
preponderance of both allocated to the lowest exposure group. This 
skewed distribution of person-years and observed cases puts most of the 
power for detecting significant differences from background cancer 
rates at low exposure levels, where these differences are expected to 
be small, and reduces the power to detect any significant differences 
from background at higher exposure concentrations.
4. Summary of Risk Assessments Based on the Gibb Cohort
    OSHA finds remarkable consistency among the risk estimates from the 
various quantitative analyses of the Gibb cohort. Both Environ and 
NIOSH determined that linear relative risk models generally provided a 
superior fit to the data when compared to other relative risk models, 
although the confidence intervals in the non-linear Cox model reported 
by Environ overlapped with the confidence intervals in their linear 
models. The Environ 2003 analysis further suggested that a linear 
additive risk model could adequately describe the observed dose-
response data. The risk estimates for NIOSH and Environ's best-fitting 
models were statistically consistent (compare Tables VI-2 and VI-3).
    The choice of reference population had little impact on the risk 
estimates. NIOSH used the entire U.S. population as the reference, but 
included adjustment terms for smoking, age and race in its models. The 
Environ 2003 analysis used both Maryland and Baltimore reference lung 
cancer rates, and included a generic background coefficient 
C0 to adjust for potential differences in background risk 
between the reference population and the worker cohort. This term was 
significant in the fitted model when Maryland rates were used for 
external standardization, but not when Baltimore rates were used. Since 
no adjustment in the model background term was required to better fit 
the exposure-response data using Baltimore City lung cancer rates, they 
may best represent the cohort's true background lung cancer incidence. 
OSHA considers the inclusion of such adjustment factors, whether 
specific to smoking, race, and age (as defined by NIOSH), or generic 
(as defined by Environ), to be appropriate and believes they contribute 
to accurate risk estimation by helping to correct for confounding risk 
factors. The Cox proportional hazard models, especially the linear Cox 
model, yielded risk estimates that were generally consistent with the 
externally standardized models.
    Finally, the number of exposure categories used in the analysis had 
little impact on the risk estimates. When an appropriate adjustment to 
the background rates was included, the four exposure groups originally 
defined by Gibb et al. and analyzed in the 2002 Environ report, the six 
exposure groups defined by Exponent, the two alternate sets of ten 
exposure categories as defined in the 2003 Environ analysis, and the 
fifty groups defined and aggregated by NIOSH all gave essentially the 
same risk estimates. The robustness of the results to various 
categorizations of cumulative exposure adds credence to the risk 
projections.
    Having reviewed the analyses described in this section, OSHA finds 
that the best estimates of excess lung cancer risk to workers exposed 
to the previous PEL (52 [mu]g Cr(VI)/m3) for a
working lifetime are about 300 to 400 per thousand based on data from 
the Gibb cohort. The best estimates of excess lung cancer risks to 
workers exposed to other TWA exposure concentrations are presented in 
Table VI-2. These estimates are consistent with predictions from 
Environ, NIOSH and Exponent models that applied linear relative and 
additive risk models based on the full range of cumulative Cr(VI) 
exposures experienced by the Gibb cohort and used appropriate 
adjustment terms for the background lung cancer mortality rates.

D. Quantitative Risk Assessments Based on the Luippold Cohort

    As discussed earlier, Luippold et al. (Exs. 35-204; 33-10) provided 
information about the cohort of workers employed in a chromate 
production plant in Painesville, Ohio. Follow-up for the 482 members of 
the Luippold cohort started in 1940 and lasted through 1997, with 
accumulation of person-years for any individual starting one year after 
the beginning of his first exposure. There were 14,048 total person-
years of follow-up for the cohort. The person-years were then divided 
into five exposure groups that had approximately equal numbers of 
expected lung cancers in each group. Ohio reference rates were used to 
compute expected numbers of deaths. White male rates were used because 
the number of women was small (4 out of 482) and race was known to be 
white for 241 of 257 members of the cohort who died and for whom death 
certificates were available. The 1960-64 Ohio rates (the earliest 
available) were assumed to hold for the time period from 1940 to 1960. 
Rates from 1990-94 were assumed to hold for the period after 1994. For 
years between 1960 and 1990, rates from the corresponding five-year 
summary were used. There were significant trends for lung cancer SMR as 
a function of year of hire, duration of employment, and cumulative 
Cr(VI) exposure. The cohort had a significantly increased SMR for lung 
cancer deaths of 241 (95% C.I. 180 to 317).

Click here to view table VI-4

    Environ conducted a risk assessment based on the cumulative Cr(VI) 
exposure-lung cancer mortality data from Luippold et al. and presented 
in Table VI-4 (Ex. 33-15). Cumulative Cr(VI) exposures were categorized 
into five groups with about four expected lung cancer deaths in each 
group. In the absence of information to the contrary, Environ assumed 
Luippold et al. did not employ any lag time in determining the 
cumulative exposures. The calculated
and expected numbers of lung cancers were derived from Ohio reference 
rates. Environ applied the relative and additive risk models, E1 and 
E2, to the data in Table VI-4.
    Linear relative and additive risk models fit the Luippold cohort 
data adequately (p>=0.25). The final models did not include the 
quadratic exposure coefficient, C2, or the background rate 
parameter, C0, as they did not significantly improve the fit 
of the models. The maximum likelihood estimates for the Cr(VI) 
exposure-related parameter, C1, of the linear relative and 
additive risk models were 0.88 per mg/m3-yr and 0.0014 per 
mg/m3-person-yr, respectively. The C1 estimates 
based on the Luippold cohort data were about 2.5-fold lower than the 
parameter estimates based on the Gibb cohort data. The excess lifetime 
risk estimate calculated by Environ for a 45-year working-lifetime 
exposure to 1 [mu]g Cr(VI)/m3 (e.g., the unit risk) for both 
models was 2.2 per 1000 workers (95% confidence intervals from 1.3 to 
3.5 per 1000 for the relative risk model and 1.2 to 3.4 per 1000 for 
the additive risk model) using a lifetable analysis with 1998 U.S. 
mortality reference rates. These risks were 2.5 to 3-fold lower than 
the projected unit risks based on the Gibb data set for equivalent 
cumulative Cr(VI) exposures.
    Crump et al. (Exs. 33-15; 35-58; 31-18) also performed an exposure-
response analysis from the Painesville data. In a Poisson regression 
analysis, cumulative exposures were grouped into ten exposure 
categories with approximately two expected lung cancer deaths in each 
group. The observed and expected lung cancer deaths by Cr(VI) exposure 
category are shown in Table VI-5. Ohio reference rates were used in 
calculating the expected lung cancer deaths and cumulative exposures 
were lagged five years.

Click here to view table VI-5

    The Crump et al. analysis used the same linear relative risk and 
additive risk models as Environ on the individual data categorized into 
the ten cumulative exposure groups (Ex. 35-58). Tests for systematic 
departure from
linearity were non-significant for both models (p>=0.11). The 
cumulative dose coefficient determined by the maximum likelihood method 
was 0.79 (95% CI: 0.47 to 1.19) per mg/m3-yr for the 
relative risk model and 0.0016 (95% CI: 0.00098 to 0.0024) per mg/
m3-person-yr for the additive risk model, respectively. The 
authors noted that application of the linear models to five and seven 
exposure groups resulted in no significant difference in dose 
coefficients, although the results were not presented. The exposure 
coefficients reported by Crump et al. were very similar to those 
obtained by Environ above, although different exposure groups were used 
and Crump et al. used a five-year lag for the cumulative exposure 
calculation. The authors noted that the linear models did not fit the 
exposure data grouped into ten categories very well (goodness-of-fit 
p< =0.01) but fit the data much better with seven exposure groups 
(p>0.3), replacing the many lower exposure categories where there were 
few observed and expected cancers with more stable exposure groupings 
with greater numbers of cancers. The reduction in number of exposure 
groups did not substantially change the fitted exposure coefficients.
    The maximum likelihood estimate for the cumulative exposure 
coefficient using the linear Cox regression model C2 was 0.66 (90% CI: 
0.11 to 1.21), which was similar to the linear [Poisson regression] 
relative risk model. When the Cox analysis was restricted to the 197 
workers with known smoking status and a smoking variable in the model, 
the dose coefficient for Cr(VI) was nearly identical to the estimate 
without controlling for smoking. This led the authors to conclude that 
"the available smoking data did not suggest that exposure to Cr(VI) 
was confounded with smoking in this cohort, or that failure to control 
for smoking had an appreciable effect upon the estimated carcinogenic 
potency of Cr(VI)" (Ex. 35-58, p. 1156).
    Given the similarity in results, OSHA believes it is reasonable to 
use the exposure coefficients reported by Crump et al. based on their 
groupings of the individual cumulative exposure data to estimate excess 
lifetime risk from the Luippold cohort. Table VI-6 presents the excess 
risk for a working lifetime exposure to various TWA Cr(VI) levels as 
predicted by Crump et al.'s relative and additive risk models using a 
lifetable analysis with 2000 U.S. rates for all causes and lung cancer 
mortality. The resulting maximum likelihood estimates indicate that 
working lifetime exposures to the previous Cr(VI) PEL would result in 
excess lifetime lung cancer risks around 100 per 1000 (95% C.I. approx. 
60-150). The risk estimates based on the Luippold cohort are lower than 
the risk estimates based on the Gibb cohort, as discussed further in 
section VI.F.
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E. Quantitative Risk Assessments Based on the Mancuso, Hayes, Gerin, 
and Alexander Cohorts

    In addition to the preferred data sets analyzed above, there are 
four other cohorts with available data sets for estimation of 
additional lifetime risk of lung cancer. These are the Mancuso cohort, 
the Hayes cohort, the Gerin cohort, and the Alexander cohort. Environ 
did exposure-response analysis for all but the Hayes cohort (Ex. 33-
15). Several years earlier, the K.S. Crump Division did quantitative 
assessments on data from the Mancuso and Hayes cohort, under contract 
with OSHA (Ex.13-5). The U.S. EPA developed quantitative risk 
assessments from the Mancuso cohort data for its Integrated Risk 
Information System (Exs. 19-1; 35-52). The California EPA (Ex. 35-54), 
Public Citizen Health Research Group (Ex. 1), and the U.S. Air Force 
Armstrong Laboratory (AFAL) for the Department of Defense (Ex. 35-51) 
performed assessments from the Mancuso data using the 1984 U.S. EPA 
risk estimates as their starting point. The U.S. EPA also published a 
risk assessment based on the Hayes cohort data (Ex. 7-102). Until the 
cohort studies of Gibb et al. and Luippold et al. became available, 
these earlier assessments provided the most current projected cancer 
risks from airborne exposure to Cr(VI). The previous risk assessments 
were extensively described in the NPRM sections VI.E.1 and VI.E.2 (69 
FR at 59375-59378). While the risk estimates from Mancuso, Hayes, 
Gerin, and Alexander data sets are associated with a greater degree of 
uncertainty, it is nevertheless valuable to compare them to the risk 
estimates from the higher quality Gibb and Luippold data sets in order 
to determine if serious discrepancies exist between them. OSHA believes 
evaluating consistency in risk among several worker cohorts adds to the 
overall quality of the assessment.
    The Mancuso and Luippold cohorts each worked at the Painesville 
plant but the worker populations did not overlap due to different 
selection criteria. Exposure estimates were also based on different 
industrial hygiene surveys. The Hayes and Gibb cohorts both worked at 
the Baltimore plant. Even though Cr(VI) exposures were reconstructed 
from monitoring data measured at different facilities resulting in 
significantly different exposure-response functions (see section VI.F), 
there was some overlap in the two study populations. As a result, the 
projected risks from these data sets can not strictly be viewed as 
independent estimates. The Gerin and Alexander cohorts were not 
chromate production workers and are completely independent from the 
Gibb and Luippold data sets. The quantitative assessment of the four 
data sets and comparison with the risk assessments based on the Gibb 
and Luippold cohorts are discussed below.
1. Mancuso Cohort
    As described in subsection VII.B.3, the Mancuso cohort was 
initially defined in 1975 and updated in 1997. The cohort members were 
hired between 1931 and 1937 and worked at the same Painesville facility 
as the Luippold cohort workers. However, there was no overlap between 
the two cohorts since all Luippold cohort workers were hired after 
1939. The quantitative risk assessment by Environ used data reported in 
the 1997 update (Ex. 23, Table XII) in which lung cancer deaths and 
person-years of follow-up were classified into four groups of 
cumulative exposure to soluble chromium, assumed to represent Cr(VI) 
(Ex. 33-15). The mortality data and person-years were further broken 
down by age of death in five year increments starting with age interval 
40 to 44 years and going up to >75 years. No expected numbers of lung 
cancers were computed, either for the cohort as a whole or for specific 
groups of person-years. Environ applied an indirect method based on the 
recorded median age and year of entry into the cohort to estimate age 
information necessary to derive expected numbers of age- and calendar 
year-adjusted lung cancers deaths required to complete the risk 
assessment.
    Observed and expected lung cancer deaths by age and cumulative 
exposure (mg/m\3\-yr) are presented in Table 3 of the 2002 Environ 
report (Ex. 33-15, p. 39). The mean cumulative exposures to soluble 
Cr(VI) were assumed to be equal to the midpoints of the tabulated 
ranges. No lag was used for calculating the cumulative exposures. 
Environ applied externally standardized risk models to these data, 
similar to those described in section VI.C.1 but using an age-related 
parameter, as discussed in the 2002 report (Ex. 33-15, p. 39). The 
externally-standardized linear relative risk model with an age-
dependent exposure term provided a superior fit over the other models.
    The predicted excess risk of lung cancer from a 45-year working 
lifetime of exposure to Cr(VI) at the previous OSHA PEL using the best-
fitting linear relative risk model is 293 per 1000 workers (95% C.I. 
188 to 403). The maximum likelihood estimate from working lifetime 
exposure to new PEL of 5.0 [mu]g/m\3\ Cr(VI) is 34 per 1000 workers 
(95% C.I. 20 to 52 per 1000). These estimates are close to those 
predicted from the Gibb cohort but are higher than predicted from the 
Luippold cohort.
    There are uncertainties associated with both the exposure estimates 
and the estimates of expected numbers of lung cancer deaths for the 
1997 Mancuso data set. The estimates of exposure were derived from a 
single set of measurements obtained in 1949 (Ex. 7-98). Although little 
prior air monitoring data were available, it is thought that the 1949 
air levels probably understate the Cr(VI) concentrations in the plant 
during some of the 1930s and much of the 1940s when chromate production 
was high to support the war. The sampling methodology used by Bourne 
and Yee only measured soluble Cr(VI), but it is believed that the 
chromate production process employed at the Painesville plant in these 
early years yielded slightly soluble and insoluble Cr(VI) compounds 
that would not be fully accounted for in the sampling results (Ex. 35-
61). This would imply that risks would be overestimated by use of 
concentration estimates that were biased low. However, it is possible 
that the 1949 measurements did not underestimate the Cr(VI) air levels 
in the early 1930s prior to the high production years. Some older 
cohort members were also undoubtedly exposed to less Cr(VI) in the 
1950s than measured in 1949 survey.
    Another uncertainty in the risk assessment for the Mancuso cohort 
is associated with the post-hoc estimation of expected numbers of lung 
cancer deaths. The expected lung cancers were derived based on 
approximate summaries of the ages and assumed start times of the cohort 
members. Several assumptions were dictated by reliance on the published 
groupings of results (e.g., ages at entry, calendar year of entry, age 
at end of follow-up, etc.) as well as by the particular choices for 
reference mortality rates (e.g., U.S. rates, in particular years close 
to the approximated time at which the person-years were accrued). Since 
the validity of these assumptions could not be tested, the estimates of 
expected numbers of lung cancer deaths are uncertain.
    There is also a potential healthy worker survivor effect in the 
Mancuso cohort. The cohort was identified as workers first hired in the 
1930s based on employment records surveyed in the late 1940s (Ex. 2-
16). The historical company files in this time period were
believed to be sparse and more likely to only identify employees still 
working at the plant in the 1940s (Ex. 33-10). If there was a sizable 
number of unidentified short-term workers who were hired but left the 
plant in the 1930s or who died before 1940 (i.e. prior to systematic 
death registration), then there may have been a selection bias (i.e., 
healthy worker survivor effect) toward longer-term, healthier 
individuals (Ex. 35-60). Since the mortality of these long-term 
"survivors" is often more strongly represented in the higher 
cumulative exposures, it can negatively confound the exposure-response 
and lead to an underestimation of risk, particularly to shorter-term 
workers (Ex. 35-63). This may be an issue with the Mancuso cohort, 
although the magnitude of the potential underestimation is unclear.
    Earlier quantitative risk assessments by the K.S. Crump Division, 
EPA, and others were done on cohort data presented in the 1975 Mancuso 
report (Ex. 7-11). These assessments did not have access to the 20 
additional years of follow-up nor did they have age-grouped lung cancer 
mortality stratified by cumulative soluble chromium (presumed Cr(VI)) 
exposure), which was presented later in the 1997 update. Instead, age-
grouped lung cancer mortality was stratified by cumulative exposure to 
total chromium that included not only carcinogenic Cr(VI) but 
substantial amounts of non-carcinogenic Cr(III). OSHA believes that the 
Environ quantitative risk assessment is the most credible analysis from 
the Mancuso cohort. It relied on the updated cohort mortality data and 
cumulative exposure estimates derived directly from air measurements of 
soluble chromium.
2. Hayes Cohort
    The K.S. Crump Division (Ex. 13-5) assessed risk based on the 
exposure-response data reported in Table IV by Braver et al. (Ex. 7-17) 
for the cohort studied by Hayes et al. (Ex. 7-14). The Hayes cohort 
overlapped with the Gibb cohort. The Hayes cohort included 734 members, 
not part of the Gibb cohort, who worked at an older facility from 1945 
to 1950 but did not work at the newer production facility built in 
August 1950. The Hayes cohort excluded 990 members of the Gibb cohort 
who worked less than 90 days in the new production facility after 
August 1950. As noted in section VI.B.4, Braver et al. derived a single 
cumulative soluble Cr(VI) exposure estimate for each of four subcohorts 
of chromate production workers categorized by duration of employment 
and year of hire by Hayes et al. Thus, exposures were not determined 
for individual workers using a more comprehensive job exposure matrix 
procedure, as was done for the Gibb and Luippold cohorts. In addition, 
the exposures were estimated from air monitoring conducted only during 
the first five of the fifteen years the plant was in operation. Unlike 
the Mancuso cohort, Hayes et al. did not stratify the observed lung 
cancer deaths by age group. The expected number of lung cancer deaths 
for each subcohort was based on the mortality statistics from 
Baltimore.
    The K.S. Crump Division applied the externally standardized linear 
relative risk approach to fit the exposure-response data (Ex. 13-5). 
The maximum likelihood estimate for the dose coefficient (e.g., 
projected linear slope of the Cr(VI) exposure-response curve) was 0.75 
per mg Cr(VI)/m\3\-yr with a 90% confidence bound of between 0.45 and 
1.1 per mg Cr(VI)/m\3\-yr. These confidence bounds are consistent with 
the dose coefficient estimate obtained from modeling the Luippold 
cohort data (0.83, 95% CI: 0.55 to 1.2) but lower than that from the 
Gibb cohort data (3.5, 95% CI: 1.5 to 6.0). The linear relative risk 
model fit the Hayes cohort data well (p=0.50). The K.S. Crump Division 
predicted the excess risk from occupational exposure to Cr(VI) for a 45 
year working lifetime at the previous OSHA PEL (52 [mu]g/m\3\) to be 88 
lung cancer cases per 1000 workers (95% CI: 61 to 141). Predicted 
excess risk at the new PEL of 5 [mu]g/m\3\ is about 9 excess lung 
cancer deaths per 1000 (95% CI: 6.1 to 16) for the same duration of 
occupational exposure. These estimates are somewhat lower than the 
corresponding estimates based on the Gibb cohort data, probably because 
of the rather high average soluble Cr(VI) level (218 [mu]g/m\3\) 
assumed by Braver et al. for plant workers throughout the 1950s. If 
these assumed air levels led to an overestimate of worker exposure, the 
resulting risks would be underestimated.
3. Gerin Cohort
    Environ (Ex. 33-15) did a quantitative assessment of the observed 
and expected lung cancer deaths in stainless steel welders classified 
into four cumulative Cr(VI) exposure groups reported in Tables 2 and 3 
of Gerin et al. (Ex. 7-120). The lung cancer data came from a large 
combined multi-center welding study in which a statistically 
significant excess lung cancer risk was observed for the whole cohort 
and non-statistically significant elevated lung cancer mortality was 
found for the stainless steel welder subcohorts (Ex. 7-114). A positive 
relationship with time since first exposure was also observed for the 
stainless steel welders (the type of welding with the highest exposure 
to Cr(VI)) but not with duration of employment.
    The exposure-response data from the Gerin study was only presented 
for those stainless steel welders with at least five years employment. 
Workers were divided into "ever stainless steel welders" and 
"predominantly stainless steel welders" groups. The latter group were 
persons known to have had extended time welding stainless steel only or 
to have been employed by a company that predominantly worked stainless 
steel. As stated in section VI.B.5, the cumulative exposure estimates 
were not based on Cr(VI) air levels specifically measured in the cohort 
workers, and therefore are subject to greater uncertainty than exposure 
estimates from the chromate production cohort studies. Environ 
restricted their analysis to the "ever stainless steel welders" since 
that subcohort had the greater number of eligible subjects and person-
years of follow-up, especially in the important lower cumulative 
exposure ranges. The person-years, observed numbers of lung cancers, 
and expected numbers of lung cancers were computed starting 20 years 
after the start of employment. Gerin et al. provided exposure-response 
data on welders with individual work histories (about two-thirds of the 
workers) as well as the entire subcohort. Regardless of the subcohort 
examined, there was no obvious indication of a Cr(VI) exposure-related 
effect on lung cancer mortality. A plausible explanation for this 
apparent lack of exposure-response is the potentially severe exposure 
misclassification resulting from the use of exposure estimates based on 
the welding literature (rather than exposure measurements at the plants 
used in the study, which were not available to the authors).
    Environ used externally standardized models to fit the data (Ex. 
33-15). They assumed that the cumulative Cr(VI) exposure for the 
workers was at the midpoint of the reported range. A value of 2.5 mg/
m\3\-yr was assumed for the highest exposure group (e.g., >0.5 mg/m\3\-
yr), since Gerin et al. cited it as the mean value for the group, which 
they noted to also include the "predominantly stainless steel 
welders". All models fit the data adequately (p>0.28) with exposure 
coefficients considerably lower than for the Gibb or Luippold cohorts 
(Ex. 33-15, Table 6). In fact, the 95% confidence intervals for the 
exposure coefficients overlapped 0, which would be expected when there 
is no exposure-related trend.
    Based on the best fitting model, a linear relative risk model (Ex. 
33-15, Table 9, p. 44), the projected excess risk of lung cancer from a 
working lifetime exposure to Cr(VI) at the previous PEL was 46 (95% CI: 
0 to 130) cases per 1000 workers. The 95 percent confidence interval 
around the maximum likelihood estimate reflects the statistical 
uncertainty associated with risk estimates from the Gerin cohort.
    Following the publication of the proposed rule, OSHA received 
comments from Exponent (on behalf of a group of steel industry 
representatives) stating that it is not appropriate to model exposure-
response for this cohort because there was not a statistically 
significant trend in lung cancer risk with estimated exposure, and risk 
of lung cancer did not increase monotonically with estimated exposure 
(Ex. 38-233-4, pp. 7-8). OSHA disagrees. Because the best-fitting model 
tested by Environ fit the Gerin data adequately, OSHA believes that it 
is reasonable to generate risk estimates based on this model for 
comparison with the risk estimates based on the Gibb and Luippold 
cohorts. This allows OSHA to quantitatively assess the consistency 
between its preferred estimates and risk estimates derived from the 
Gerin cohort.
    In post-hearing comments, Dr. Herman Gibb expressed support for 
OSHA's approach. Dr. Gibb stated:

    The epidemiologic studies of welders * * * conducted to date 
have been limited in their ability to evaluate a lung cancer risk. 
It is conceivable that differences in exposure * * * between [this 
industry] and the chromate production industry could lead to 
differences in cancer risk. Because there aren't adequate data with 
which to evaluate these differences, it is appropriate to compare 
the upper bounds [on risk] derived from the Gerin et al. * * * 
[study] with those predicted from the chromate production workers to 
determine if they are consistent.

    OSHA agrees with Exponent that the results of the Gerin et al. 
study were different from those of the Luippold (2003) and Gibb 
cohorts, in that a statistically significant exposure-response 
relationship and a monotonically increasing lung cancer risk with 
exposure were not found in Gerin. Also, the maximum likelihood risk 
estimates based on the Gerin cohort were somewhat lower than those 
based on the Gibb and Luippold cohorts. However, OSHA believes the 
lower risk estimates from the Gerin cohort may be explained by the 
strong potential for bias due to Cr(VI) exposure misclassification and 
possibly by the presence of co-exposures, as discussed in sections 
VI.B.5 and VI.G.4. Part of the difference may also relate to 
statistical uncertainty; note that the 95% confidence intervals (shown 
in Table VI-7) overlap the lower end of OSHA's range based on the 
preferred Gibb and Luippold (2003) studies.
4. Alexander Cohort
    Environ (Ex. 33-15) did a quantitative assessment of the observed 
and expected lung cancer incidence among aerospace workers exposed to 
Cr(VI) classified into four cumulative chromate exposure groups, 
reported in Table 4 of Alexander et al. (Ex. 31-16-3). The authors 
stated that they derived "estimates of exposure to chromium [VI]" 
based on the TWA measurements, but later on referred to "the index of 
cumulative total chromate exposure (italics added) reported as [mu]g/
m\3\ chromate TWA-years" (Ex. 31-16-3, p. 1254). Alexander et al. 
grouped the lung cancer data by cumulative exposure with and without a 
ten year lag period. They found no statistically significant elevation 
in lung cancer incidence among the chromate-exposed workers or clear 
trend with cumulative chromate exposure.
    For their analysis, Environ assumed that the cumulative exposures 
were expressed in [mu]g/m\3\-yr of Cr(VI), rather than chromate 
(CrO4-2) or chromic acid (CrO3). 
Environ used an externally standardized linear relative risk model to 
fit the unlagged data (Ex. 33-15). An additive risk model could not be 
applied because person-years of observation were not reported by 
Alexander et al. Environ assumed that workers were exposed to a 
cumulative Cr(VI) exposure at the midpoint of the reported ranges. For 
the open-ended high exposure category, Environ assumed a cumulative 
exposure 1.5 times greater than the lower limit of 0.18 mg/m\3\-yr. The 
model fit the data poorly (p=0.04) and the exposure coefficient was 
considered to be 0 since positive values did not significantly improve 
the fit. Given the lack of a positive trend between lung cancer 
incidence and cumulative Cr(VI) exposure for this cohort, these results 
are not surprising.
    Following the publication of the proposed rule, OSHA received 
comments from Exponent (on behalf of the Aerospace Industries 
Association) stating that the Agency should not apply a linear model to 
the Alexander et al. study to derive risk estimates for comparison with 
the estimates based on the Gibb and Luippold (2003) cohorts (Ex. 38-
215-2, p. 10). Due to the poor fit of Environ's exposure-response model 
to the Alexander cohort data, OSHA agrees with Exponent in this matter. 
Risk estimates based on Alexander et al. are therefore not presented in 
this risk assessment.
    OSHA believes that there are several possible reasons for the lack 
of a positive association between Cr(VI) exposure and lung cancer 
incidence in this cohort. First, follow-up time was extremely short, 
averaging 8.9 years per cohort member. Long-term follow-up of cohort 
members is particularly important for determining the risk of lung 
cancer, which typically has an extended latency period of roughly 20 
years or more. One would not necessarily expect to see excess lung 
cancer or an exposure-response relationship among workers who had been 
followed less than 20 years since their first exposure to Cr(VI), as 
most exposure-related cancers would not yet have appeared. Other 
possible reasons that an exposure-response relationship was not 
observed in the Alexander cohort include the young age of the cohort 
members (median 42 years at end of follow-up), which also suggests that 
occupational lung cancers may not yet have appeared among many cohort 
members. The estimation of cumulative Cr(VI) exposure was also 
problematic, drawing on air measurement data that did not span the 
entire employment period of the cohort (there were no data for 1940 to 
1974) and were heavily grouped into a relatively small number of 
"summary" TWA concentrations that did not capture individual 
differences in workplace exposures to Cr(VI).

F. Summary of Risk Estimates Based on Gibb, Luippold, and Additional 
Cohorts

    OSHA believes that the best estimates of excess lifetime lung 
cancer risks are derived from the Gibb and Luippold cohorts. Due to 
their large size and long follow-up, these two cohorts accumulated a 
substantial number of lung cancer deaths that were extensively examined 
by several different analyses using a variety of statistical 
approaches. Cohort exposures were reconstructed from air measurements 
and job histories over three or four decades. The linear relative risk 
model fit the Gibb and Luippold data sets well. It adequately fit 
several epidemiological data sets used for comparative analysis. 
Environ and NIOSH explored a variety of nonlinear dose-response forms, 
but none provided a statistically significant improvement over the 
linear relative risk model.
    The maximum likelihood estimates from a linear relative risk model 
fit to the Gibb data are three- to five-fold higher than estimates 
based on the Luippold data at equivalent cumulative
Cr(VI) exposures and the confidence limits around the projected risks 
from the two data sets do not overlap. This indicates that the maximum 
likelihood estimates derived from one data set are unlikely to describe 
the lung cancer mortality observed in the other data set. Despite this 
statistical inconsistency between the risk estimates, the differences 
between them are not unreasonably great given the potential 
uncertainties involved in estimating cancer risk from the data (see 
section VI.G). Since the analyses based on these two cohorts are each 
of high quality and their projected risks are reasonably close (well 
within an order of magnitude), OSHA believes the excess lifetime risk 
of lung cancer from occupational exposure to Cr(VI) is best represented 
by the range of risks that lie between maximum likelihood estimates of 
the Gibb and Luippold data sets.

Click here to view table VI-7

BILLING CODE 4510-26-C

    OSHA's best estimates of excess lung cancer cases from a 45-year 
working lifetime exposure to Cr(VI) are presented in Table VI-7. As 
previously discussed, several acceptable assessments of the Gibb data 
set were performed, with similar results. The 2003 Environ model E1, 
applying the Baltimore City reference population and ten exposure 
categories based on a roughly equal number of person-years per group, 
was selected to represent the range of best risk estimates derived from 
the Gibb cohort, in part because this assessment employed an approach 
most consistent with the exposure grouping applied in the Luippold 
analysis (see Table VI-6). To characterize the statistical uncertainty 
of OSHA's risk estimates, Table VI-7 also presents the 95% confidence 
limits associated with the maximum likelihood risk estimates from the 
Gibb cohort and the Luippold cohort.
    OSHA finds that the most likely lifetime excess risk at the 
previous PEL of 52 [mu]g/m\3\ Cr(VI) lies between 101 per 1000 and 351 
per 1000, as shown in Table VI-7. That is, OSHA predicts that between 
101 and 351 of 1000 workers occupationally exposed for 45 years at the 
previous PEL would develop lung cancer as a result of their exposure. 
The wider range of 62 per 1000 (lower 95% confidence bound, Luippold 
cohort) to 493 per 1000 (upper 95% confidence bound, Gibb cohort) 
illustrates the range of risks considered statistically plausible based 
on these cohorts, and thus represents the statistical uncertainty in 
the estimates of lung cancer risk. This range of risks decreases 
roughly proportionally with exposure, as illustrated by the risk 
estimates shown in Table VI-7 for working lifetime exposures at various 
levels at and below the previous PEL.
    The risk estimates for the Mancuso, Hayes, and Gerin data sets are 
also presented in Table VI-7. (As discussed previously, risk estimates 
were not derived from the Alexander data set.) The exposure-response 
data from these cohorts are not as strong as those from the two 
featured cohorts. OSHA believes that the supplemental assessments for 
the Mancuso and Hayes cohorts support the range of projected excess 
lung cancer risks from the Gibb and Luippold cohorts. This is 
illustrated by the maximum likelihood estimates and 95% confidence 
intervals shown in Table VI-7. The risk estimates and 95% confidence 
interval based on the Hayes cohort are similar to those based on the 
Luippold cohort, while the estimates based on the Mancuso cohort are 
more similar to those based on the Gibb cohort. Also, OSHA's range of 
best risk estimates based on the two primary cohorts for a given 
occupational Cr(VI) exposure overlap the 95 percent confidence limits 
for the Mancuso, Hayes, and Gerin cohorts. This indicates that the 
Agency's range of best estimates is statistically consistent with the 
risks calculated by Environ from any of these data sets, including the 
Gerin cohort where the lung cancers did not show a clear positive trend 
with cumulative Cr(VI) exposure.
    Several commenters remarked on OSHA's use of both the Gibb cohort 
and the Luippold cohort to define a preliminary range of risk estimates 
associated with a working lifetime of exposure at the previous and 
alternative PELs. Some suggested that OSHA should instead rely 
exclusively on the Gibb study, due to its superior size, smoking data, 
completeness of follow-up, and exposure information (Tr. 709-710, 769; 
Exs. 40-18-1, pp. 2-3; 47-23, p. 3; 47-28, pp. 4-5). Others suggested 
that OSHA should devise a weighting scheme to derive risk estimates 
based on both studies but with greater weight assigned to the Gibb 
cohort (Tr. 709-710, 769, Exs. 40-18-1, pp. 2-3; 47-23, p. 3), arguing 
that "the use of the maximum likelihood estimate from the Luippold 
study as the lower bound of OSHA's risk estimates * * * has the effect 
of making a higher Permissible Exposure Limit (PEL) appear acceptable" 
(Ex. 40-18-1, p. 3). OSHA disagrees with this line of reasoning. OSHA 
believes that including all studies that provide a strong basis to 
model the relationship between Cr(VI) and lung cancer, as the Luippold 
study does, provides useful information and adds depth to the Agency's 
risk assessment. OSHA agrees that in some cases derivation of risk 
estimates based on a weighting scheme is an appropriate approach when 
differences between the results of the two or more studies are believed 
to primarily reflect sources of uncertainty or error in the underlying 
studies. A weighting scheme might then be used to reflect the degree of 
confidence in their respective results. However, the Gibb and Luippold 
cohorts were known to be quite different populations, and the 
difference between the risk estimates based on the two cohorts could 
partly reflect variability in exposure-response. In this case, OSHA's 
use of a range of risk defined by the two studies is appropriate for 
the purpose of determining significance of risk at the previous PEL and 
the alternative PELs that the Agency considered.
    Another commenter suggested that OSHA should derive a "single 
'best' risk estimate [taking] into account all of the six quantitative 
risk estimates" identified by OSHA as featured or supporting risk 
assessments in the preamble to the proposed rule, consisting of the 
Gibb and Luippold cohorts as well as studies by Mancuso (Ex. 7-11), 
Hayes (Ex. 7-14), Gerin (Ex. 7-120), and Alexander (Ex. 31-16-3) (Ex. 
38-265, p. 76). The commenter, Mr. Stuart Sessions of Environomics, 
Inc., proposed that OSHA should use a weighted average of risk 
estimates derived from all six studies, weighting the Gibb and Luippold studies 
more heavily than the remaining four "admittedly weaker studies" (Ex. 
38-265, p. 78). During the public hearing, however, he stated that OSHA 
may reasonably choose not to include some studies in the development of 
its quantitative risk model based on certain criteria or qualifications 
related to the principles of sound epidemiology and risk assessment 
(Tr. 2484-2485). Mr. Sessions agreed with OSHA that sufficient length 
of follow-up (>=20 years) is a critical qualification for a cohort to 
provide an adequate basis for lung cancer risk assessment, admitting 
that "if we are dealing with [a] long latency sort of effect and if 
you only follow them for a few years it wouldn't be showing up with 
anywhere near the frequency that you would need to get a statistically 
significant excess risk" (Tr. 2485). This criterion supports OSHA's 
decision to exclude the Alexander study as a primary data set for risk 
assessment, due in part to the inadequate length of follow-up on the 
cohort (average 8.9 years).
    Mr. Sessions also agreed that the quality and comprehensiveness of 
the exposure information for a study could be a deciding factor in 
whether it should be used for OSHA's risk estimates (Tr. 2485-2487). As 
discussed in the preamble to the proposed rule, significant uncertainty 
in the exposure estimates for the Mancuso and Gerin studies was a 
primary reason they were not used in the derivation of OSHA's 
preliminary risk estimates (69 FR at 59362-3). Mancuso relied 
exclusively on the air monitoring reported by Bourne and Yee (Ex. 7-98) 
conducted over a single short period of time during 1949 to calculate 
cumulative exposures for each cohort member, although the cohort 
definition and follow-up period allowed inclusion of workers employed 
as early as 1931 and as late as 1972. In the public hearing, Mr. 
Sessions indicated that reliance on exposure data from a single year 
would not necessarily "disqualify" a study from inclusion in the 
weighted risk estimate he proposed, if "for some reason the exposure 
hasn't changed much over the period of exposure" (Tr. 2486). However, 
the Mancuso study provides no evidence that exposures in the 
Painesville plant were stable over the period of exposure. To the 
contrary, Mancuso stated that:

    The tremendous progressive increase in production in the 
succeeding years from zero could have brought about a concomitant 
increase in the dust concentrations to 1949 that could have exceeded 
the level of the first years of operation. The company instituted 
control measures after the 1949 study which markedly reduced the 
exposure (Ex. 7-11, p. 4).

    In the Gerin et al. study, cohort members' Cr(VI) exposures were 
estimated based on total fume levels and fume composition figures from 
"occupational hygiene literature and and welding products 
manufacturers' literature readily available at the time of the study", 
supplemented by "[a] limited amount of industrial hygiene measurements 
taken in the mid 1970s in eight of the [135] companies" from which the 
cohort was drawn (Ex. 7-120, p. S24). Thus, cumulative exposure 
estimates for workers in this cohort were generally not based on data 
collected in their particular job or company. Gerin et al. explained 
that the resulting "global average" exposure estimates "obscure a 
number of between-plant and within-plant variations in specific factors 
which affect exposure levels and would dilute a dose-response 
relationship", including type of activity, * * * special processes, 
arcing time, voltage and current characteristics, welder position, use 
of special electrodes or rods, presence of primer paints and background 
fumes coming from other activities (Ex. 7-120, p. S25).
    Commenting on the available welding epidemiology, NIOSH emphasized 
that wide variation in exposure conditions across employers may exist, 
and should be a consideration in multi-employer studies (Ex. 47-19, p. 
6). Gerin et al. recommended refinement and validation of their 
exposure estimates using "more complete and more recent quantitative 
data" and accounting for variability within and between plants, but 
did not report any such validation for their exposure-response 
analysis. OSHA believes that the exposure misclassification in the 
Gerin study could be substantial. It is therefore difficult to place a 
high degree of confidence in its results, and it should not be used to 
derive the Agency's quantitative risk estimates. Comments received from 
Dr. Herman Gibb support OSHA's conclusion. He stated that epidemiologic 
studies of welders conducted to date do not include adequate data with 
which to evaluate lung cancer risk (Ex. 47-8, p. 2).
    Finally, Mr. Sessions agreed with OSHA that it is best to rely on 
"independent studies on different cohorts of workers", rather than 
including the results of two or more overlapping cohorts in the 
weighted average he proposed (Tr. 2487). As discussed in the preamble 
to the proposed rule, the Hayes et al. and Gibb et al. cohorts were 
drawn from the same Baltimore chromate production plant (FR 69 at 
59362). The workers in the subcohort of Hayes et al. analyzed by Braver 
were first hired between 1945 and 1959; the Gibb cohort included 
workers first hired between 1950 and 1974. Due to the substantial 
overlap between the two cohorts, it is not appropriate to use the 
results of the Hayes as well as the Gibb cohort in a weighted average 
calculation (as proposed by Mr. Sessions).
    Having carefully reviewed the various comments discussed above, 
OSHA finds that its selection of the Gibb and Luippold cohorts to 
derive a range of quantitative risk estimates is the most appropriate 
approach for the Cr(VI) risk assessment. Support for this approach was 
expressed by NIOSH, which stated that "the strength is in looking at 
[the Gibb and Luippold studies] together * * * appreciating the 
strengths of each" (Tr. 313). Several commenters voiced general 
agreement with OSHA's study selection, even while disagreeing with 
OSHA's application of these studies' results to specific industries. 
Said one commenter, "[w]e concur with the selection of the two focus 
cohorts (Luippold et al. 2003 and Gibb et al. 2000) as the best data 
available upon which to base an estimate of the exposure-response 
relationship between occupational exposure to Cr(VI) and an increased 
lung cancer risk" (38-8, p. 6); and another, "[i]t is clear that the 
data from the two featured cohorts, Gibb et al. (2000) and Luippold et 
al. (2003), offer the best information upon which to quantify the risk 
due to Cr(VI) exposure and an increased risk of lung cancer" (Ex. 38-
215-2, p. 16). Comments regarding the suitability of the Gibb and 
Luippold cohorts as a basis for risk estimates in specific industries 
will be addressed in later sections.

G. Issues and Uncertainties

    The risk estimates presented in the previous sections include 
confidence limits that reflect statistical uncertainty. This 
statistical uncertainty concerns the limits of precision for 
statistical inference, given assumptions about the input parameters and 
risk models (e.g., exposure estimates, observed lung cancer cases, 
expected lung cancer cases, linear dose-response). However, there are 
uncertainties with regard to the above input and assumptions, not so 
easily quantified, that may lead to underestimation or overestimation 
of risk. Some of these uncertainties are discussed below.

1. Uncertainty With Regard to Worker Exposure to Cr(VI)
    The uncertainty that may have the greatest impact on risk estimates 
relates to the assessment of worker exposure. Even for the Gibb cohort, 
whose exposures were estimated from roughly 70,000 air measurements 
over a 35-year period, the calculation of cumulative exposure is 
inherently uncertain. The methods used to measure airborne Cr(VI) did 
not characterize particle size that determines deposition in the 
respiratory tract (see section V.A). Workers typically differ from one 
another with respect to working habits and they may have worked in 
different areas in relation to where samples are taken. Inter-
individual (and intra-facility) variability in cumulative exposure can 
only be characterized to a limited degree, even with extensive 
measurement. The impact of such variability is likely less for 
estimates of long-term average exposures when there were more extensive 
measurements in the Gibb and Luippold cohorts in the 1960s through 
1980s, but could affect the reliability of estimates in the 1940s and 
1950s when air monitoring was done less frequently. Exposure estimates 
that rely on annual average air concentrations are also less likely to 
reliably characterize the Cr(VI) exposure to workers who are employed 
for short periods of time. This may be particularly true for the Gibb 
cohort in which a sizable fraction of cohort members were employed for 
only a few months.
    Like many retrospective cohort studies, the frequency and methods 
used to monitor Cr(VI) concentrations may also be a source of 
uncertainty in reconstructing past exposures to the Gibb and Luippold 
cohorts. Exposures to the Gibb cohort in the Baltimore plant from 1950 
until 1961 were determined based on periodic collection of samples of 
airborne dust using high volume sampling pumps and impingers that were 
held in the breathing zone of the worker for relatively short periods 
of time (e.g., tens of minutes) (Ex. 31-22-11). The use of high volume 
sampling with impingers to collect Cr(VI) samples may have 
underestimated exposure since the accuracy of these devices depended on 
an air flow low enough to ensure efficient Cr(VI) capture, the absence 
of agents capable of reducing Cr(VI) to Cr(III), the proper storage of 
the collected samples, and the ability of short-term collections to 
accurately represent full-shift worker exposures. Further, impingers 
would not adequately capture any insoluble forms of Cr(VI) present, 
although other survey methods indicated minimal levels of insoluble 
Cr(VI) were produced at the Baltimore facility (Ex. 13-18-14).
    In the 1960s, the Baltimore plant expanded its Cr(VI) air 
monitoring program beyond periodic high volume sampling to include 
extensive area monitoring in 27 exposure zones around the facility. 
Multiple short-term samples were collected (e.g., twelve one-hour or 
eight three-hour samples) on cellulose tape for an entire 24 hour 
period and analyzed for Cr(VI). Studies have shown that Cr(VI) can be 
reduced to Cr(III) on cellulose filters under certain circumstances so 
there is potential for underestimation of Cr(VI) using this collection 
method (Ex. 7-1, p. 370). Monitoring was conducted prior to 1971, but 
the results were misplaced and were not accessible to Gibb et al. The 
area monitoring was supplemented by routine full-shift personal 
monitoring of workers starting in 1977. The 24-hour area sampling 
supplemented with personal monitoring was continued until plant closure 
in 1985.
    Some of the same uncertainties exist in reconstructing exposures 
from the Luippold cohort. Exposure monitoring from operations at the 
Painesville plant in the 1940s and early 1950s was sparse and consisted 
of industrial hygiene surveys conducted by various groups (Ex. 35-61). 
The United States Public Health Service (USPHS) conducted two 
industrial hygiene surveys (1943 and 1951), as did the Metropolitan 
Life Insurance Company (1945 and 1948). The Ohio Department of Health 
(ODH) conducted surveys in 1949 and 1950. The most detailed exposure 
information was available in annual surveys conducted by the Diamond 
Alkali Company (DAC) from 1955 to 1971. Exponent chose not to consider 
the ODH data in their analysis since the airborne Cr(VI) concentrations 
reported in these surveys were considerably lower than values measured 
at later dates by DAC. Excluding the ODH survey data in the exposure 
reconstruction process may have led to higher worker exposure estimates 
and lower predicted lung cancer risks.
    There were uncertainties associated with the early Cr(VI) exposure 
estimates for the Painesville cohort. Like the monitoring in the 
Baltimore plant, Cr(VI) exposure levels were determined from periodic 
short-term, high volume sampling with impingers that may have 
underestimated exposures (Ex. 35-61). Since the Painesville plant 
employed a "high-lime" roasting process to produce soluble Cr(VI) 
from chromite ore, a significant amount of slightly soluble and 
insoluble Cr(VI) was formed. It was estimated that up to approximately 
20 percent of the airborne Cr(VI) was in the less soluble form in some 
areas of the plant prior to 1950 (Ex. 35-61). The impingers were 
unlikely to have captured this less soluble Cr(VI) so some reported 
Cr(VI) air concentrations may have been underestimated for this reason.
    The annual air monitoring program at the Painesville plant was 
upgraded in 1966 in order to evaluate a full 24 hour period (Ex. 35-
61). Unlike the continuous monitoring at the Baltimore plant, twelve 
area air samples from sites throughout the plant were collected for 
only 35 minutes every two hours using two in-series midget impingers 
containing water. The more frequent monitoring using the in-series 
impinger procedure may be an improvement over previous high-volume 
sampling and is believed to be less susceptible to Cr(VI) reduction 
than cellulose filters. While the impinger collection method at the 
Painesville plant may have reduced one source of potential exposure 
uncertainty, another source of potential uncertainty was introduced by 
failure to collect air samples for more than 40 percent of the work 
period. Also, personal monitoring of workers was not conducted at any 
time.
    Concerns about the accuracy of the Gibb and Luippold exposure data 
were expressed in comments following the publication of the proposed 
rule. Several commenters suggested that exposures of workers in both 
the Gibb and Luippold (2003) cohorts may have been underestimated, 
resulting in systematic overestimation of risk in the analyses based on 
these cohorts (Exs. 38-231, pp. 19-20; 38-233, p. 82; 39-74, p. 2; 47-
27, p. 15; 47-27-3, p. 1). In particular, the possibility was raised 
that exposure measurements taken with the RAC sampler commonly used in 
the 1960s may have resulted in lower reported Cr(VI) levels as a result 
of reduction of Cr(VI) on the sample strip. Concerns were also raised 
that situations of exceptionally high exposure may not have been 
captured by the sampling plans at the Baltimore and Painesville plants 
and that Cr(VI) concentrations in workers' breathing zones would have 
been generally higher than concentrations measured in general area 
samples taken in the two plants (Exs. 38-231, p. 19; 40-12-1, p. 2). 
One commenter noted that "the exposure values identified in both the 
Painesville and Baltimore studies are consistently lower than those 
reported for a similar time period by alternative sources (Braver et 
al. 1985; PHS 1953)" (Exs. 38-231, p. 19; 40-12-1, p. 2). It was also 
suggested that impinger samples used to estimate exposures in the 
Painesville plant and the impinger and RAC samples used between 1950 and 1985 in 
the Baltimore plant did not efficiently capture particles smaller than 
1 [mu]m in diameter, which were believed to have constituted a 
substantial fraction of particles generated during the chromite ore 
roasting process, and thus led to an underestimate of exposures (Ex. 
47-27-3, pp. 1-4).
    In his written testimony for the public hearing, Dr. Herman Gibb 
addressed concerns about the type of samples on which the Gibb cohort 
exposure estimates were based. Dr. Gibb stated, "[a] comparison of the 
area and personal samples [collected during 1978-1985] found 
essentially no difference for approximately two-thirds of the job 
titles with a sufficient number of samples to make this comparison." 
An adjustment was made for the remaining job titles, in which the area 
samples were found to underestimate the breathing zone exposure, so 
that the potential for underestimation of exposures based on general 
area samples " * * * was accounted for and corrected * * * " in the 
Gibb cohort exposure estimates (Ex. 44-4, pp. 5-6). Dr. Gibb also noted 
that the publications claimed by commenters to have reported 
consistently higher levels of exposure than those specified by the 
authors of the Gibb et al. and Luippold et al. studies, in fact did not 
report exposures in sufficient detail to provide a meaningful 
comparison. In particular, Dr. Gibb said that the Public Health Service 
(PHS) publication did not report plant-specific exposure levels, and 
that Braver et al. did not report the locations or sampling strategies 
used (Ex. 44-4, pp. 5-6).
    OSHA agrees with Dr. Gibb that the use of RAC general area samples 
in the Baltimore plant are unlikely to have caused substantial error in 
risk estimates based on the Gibb cohort. A similar comparison and 
adjustment between area and personal samples could not be performed for 
the Luippold et al. cohort, for which only area samples were available. 
The fact that most general area samples were similar to personal 
breathing zone samples in the Gibb cohort does not support the 
contention that reduction on the RAC sample strip or small particle 
capture issues would have caused substantial error in OSHA's risk 
estimates. Speculation regarding unusually high exposures that may not 
have been accounted for in sampling at the Baltimore and Painesville 
plants raises an uncertainty common to many epidemiological studies and 
quantitative risk analysis, but does not provide evidence that 
occasional high exposures would have substantially affected the results 
of this risk assessment.
    OSHA received comments from the Small Business Administration's 
Office of Advocacy and others suggesting that, in addition to water-
soluble sodium dichromate, sodium chromate, potassium dichromate, and 
chromic acid, some members of the Gibb and Luippold cohorts may have 
been exposed to less soluble compounds such as calcium chromate (Tr. 
1825, Exs. 38-7, p. 4; 38-8, p. 12; 40-12-5, p. 5). These less soluble 
compounds are believed to be more carcinogenic than Cr(VI) compounds 
that are water-soluble or water-insoluble (e.g. lead chromate). The 
Painesville plant used a high-lime process to roast chromite ore, which 
is known to form calcium chromate and lesser amounts of other less 
water-soluble Cr(VI) compounds (Ex. 35-61). The 1953 USPHS survey 
estimated that approximately 20 percent of the total Cr(VI) in the 
roasting residue at the Painesville plant consisted of the less water-
soluble chromates (Ex. 2-14). The high lime roasting process is no 
longer used in the production of chromate compounds.
    Proctor et al. estimated that a portion of the Luippold cohort 
prior to 1950 were probably exposed to the less water-soluble Cr(VI) 
compounds due to the use of a high-lime roasting process, but that it 
would amount to less than 20 percent of their total Cr(VI) exposure 
(Ex. 35-61). The Painesville plant subsequently reduced and eliminated 
exposure to Cr(VI) roasting residue through improvements in the 
production process. A small proportion of workers in the Special 
Products Division of the Baltimore plant may have been exposed to less 
water-soluble Cr(VI) compounds during the occasional production of 
these compounds over the years. However, the high-lime process believed 
to generate less soluble compounds at the Painesville plant was not 
used at the Baltimore plant, and the 1953 USPHS survey detected minimal 
levels of less soluble Cr(VI) at this facility (Braver et al. 1985, Ex. 
7-17).
    OSHA agrees that some workers in the Luippold 2003 cohort 
(Painesville plant) and perhaps in the Gibb cohort (Baltimore plant) 
may have been exposed to minor amounts of calcium chromate and other 
less-soluble Cr(VI) compounds. However, these exposures would have been 
limited for most workers due to the nature of the production process 
and controls that were instituted after the early production period at 
the Painesville plant. The primary operation at the plants in 
Painesville and Baltimore was the production of the water-soluble 
sodium dichromate from which other primarily water-soluble chromates 
such as sodium chromate, potassium dichromate, and chromic acid could 
be made (Exs. 7-14; 35-61). Therefore, the Gibb and Luippold cohorts 
were principally exposed to water-soluble Cr(VI). Risk of lung cancer 
in these cohorts is therefore likely to reflect exposure to sodium 
chromate and sodium dichromate, rather than calcium chromate.
    The results of the recent German post-change cohort showed that 
excess lung cancer mortality occurred among chromate-exposed workers in 
plants exclusively using a no-lime production process (Ex. 48-4). Like 
the Gibb cohort, the German cohort was exposed to average full-shift 
Cr(VI) exposures well below the previous PEL of 52 [mu]g/m\3\ but 
without the possible contribution from the more carcinogenic calcium 
chromate (Exs. 48-1-2; Ex. 7-91). OSHA believes the elevated lung 
cancer mortality in these post-change workers are further evidence that 
occupational exposure to the less carcinogenic water-soluble Cr(VI) 
present a lung cancer risk.
    In their post-hearing brief, the Aerospace Industries Association 
of America (AIA) stated:

    OSHA's quantitative risk estimates are based on exposure 
estimates derived from impinger and RAC samplers in the Painesville 
and Baltimore chromate production plants. It is likely that these 
devices substantially underestimated airborne levels of Cr(VI), 
especially considering that particles were typically < 1 [mu]m. If 
exposure in these studies were underestimated, the risk per unit 
exposure was overestimated, and the risk estimates provided in the 
proposed rule overstate lung cancer risks (Ex. 47-29-2, p. 4).

AIA supports its statements by citing a study by Spanne et al. (Ex. 48-
2) that found very low collection efficiencies (e.g. < 20 percent) of 
submicron particles (i.e. < 1 [mu]m) using midget impingers. OSHA does 
not dispute that liquid impinger devices, primarily used to measure 
Cr(VI) air levels at the Painesville plant, are less effective at 
collecting small submicron particles. However, OSHA does not believe 
AIA has adequately demonstrated that the majority of Cr(VI) particles 
generated during soluble chromate production are submicron in size. 
This issue is further discussed in preamble section VI.G.4.a. Briefly, 
the AIA evidence is principally based on a particle size distribution 
from two airborne dust samples collected at the Painesville plant by an 
outdated sampling device under conditions that essentially excludes 
particles >5 [mu]m (Ex. 47-29-2, Figure 4).
OSHA believes it is more likely that Cr(VI) production workers in the 
Gibb and Luippold cohorts were exposed to Cr(VI) mass as respirable 
dust (i.e. < 10 [mu]m) mostly over 1 [mu]m in size. The Spanne et al. 
study found that the impinger efficiency for particles greater than 2 
[mu]m is above 80 percent. Cr(VI) exposure not only occurs during 
roasting of chromite ore, where the smallest particles are probably 
generated, but also during the leaching of water-soluble Cr(VI) and 
packaging sodium dichromate crystals where particle sizes are likely 
larger. Based on this information, OSHA does not have reason to believe 
that the impinger device would substantially underestimate Cr(VI) 
exposures during the chromate production process or lead to a serious 
overprediction of risk.
    The RAC samplers employed at the Baltimore plant collected airborne 
particles on filter media, not liquid media. AIA provided no data on 
the submicron particle size efficiency of these devices. For reasons 
explained earlier in this section, OSHA finds it unlikely that use of 
the RAC samplers led to substantial error in worker exposure estimates 
for the Gibb cohort.
    In summary, uncertainties associated with the exposure estimates 
are a primary source of uncertainty in any assessment of risk. However, 
the cumulative Cr(VI) exposure estimates derived from the Luippold 
(2003) and Gibb cohorts are much more extensive than usually available 
for a cancer cohort and are more than adequate as a basis for 
quantitative risk assessment. OSHA does not believe the potential 
inaccuracies in the exposure assessment for the Gibb and Luippold 
(2003) cohorts are large enough to result in serious overprediction or 
underprediction of risk.
2. Model Uncertainty, Exposure Threshold, and Dose Rate Effects
    The models used to fit the observed data may also introduce 
uncertainty into the quantitative predictions of risk. In the Preamble 
to the Proposed Rule, OSHA solicited comments on whether the linear 
relative risk model is the most appropriate approach on which to 
estimate risk associated with occupational exposure to Cr(VI) (FR 69 at 
59307). OSHA expressed particular interest in whether there is 
convincing scientific evidence of a non-linear exposure-response 
relationship and, if so, whether there are sufficient data to develop a 
non-linear model that would provide more reliable risk estimates than 
the linear approach that was used in the preliminary risk assessment.
    OSHA received a variety of comments regarding the uncertainties 
associated with using the risk model based on the Gibb and Luippold 
cohorts to predict risk to individuals exposed over a working lifetime 
to low levels of Cr(VI). OSHA's model assumes that the risk associated 
with a cumulative exposure resulting from long-term, low-level exposure 
is similar to the risk associated with the same cumulative exposure 
from briefer exposures to higher concentrations, and that a linear 
relative risk model adequately describes the cumulative exposure-
response relationship. These assumptions are common in cancer risk 
assessment, and are based on scientifically accepted models of 
genotoxic carcinogenesis. However, OSHA received comments from the 
Small Business Administation's Office of Advocacy and others that 
questioned the Agency's reliance on these assumptions in the case of 
Cr(VI) (see e.g. Exs. 38-7, p. 2; 38-231, p. 18; 39-74, p. 2; 40-12-1, 
p. 2; 38-106, p. 10, p. 23; 38-185, p. 4; 38-233, p. 87; 38-265-1, pp. 
27-29; 43-2, pp. 2-3). Some comments suggested that a nonlinear or 
threshold exposure-response model is an appropriate approach to 
estimate lung cancer risk from Cr(VI) exposures. Evidence cited in 
support of this approach rely on: (1) The lack of a statistically 
significant increased lung cancer risk for workers exposed below a 
cumulative Cr(VI) exposure of 1.0 mg/m\3\=yr (e.g., roughly equivalent 
to 20 [mu]g/m\3\ TWA for a 45 year working lifetime) and below "a 
highest reported eight hour average" Cr(VI) concentration of 52 [mu]g/
m\3\; (2) the lack of observed lung tumors at lower dose levels in rats 
chronically exposed to Cr(VI) by inhalation and repeated intratracheal 
installations; and (3) the existence of physiological defense 
mechanisms within the lung, such as extracellular reduction of Cr(VI) 
to Cr(III) and repair of DNA damage. These commenters argue that the 
evidence suggests a sublinear nonlinearity or threshold in exposure-
response at exposures in the range of interest to OSHA.
    The Small Business Administration's Office of Advocacy and several 
other commenters stated that OSHA's risk model may overestimate the 
risk to individuals exposed for a working lifetime at "low" 
concentrations (Exs. 38-7, p. 2; 38-231, p. 18; 39-74, p. 2; 40-12-1, 
p. 2) or at concentrations as high as 20-23 [mu]g/m\3\ (Exs. 38-7, p. 
6; 38-106, p. 10, p. 23; 38-185, p. 4; 38-233, p. 87; 38-265-1, pp. 27-
29; 43-2, pp. 2-3), due to possible nonlinear features in the exposure-
response relationship for Cr(VI). These comments cited various 
published analyses of the Luippold and Gibb cohorts, including the 
Luippold et al. 2003 publication (Exs. 38-106, p. 10, p. 22; 38-233-4, 
p. 17), the Proctor et al. 2004 publication (Ex. 38-233-4, p. 17), the 
Crump et al. 2003 publication (Exs. 38-106, p. 22; 38-265-1, p. 27), 
and an analysis conducted by Exponent on behalf of chromium industry 
representatives (Ex. 31-18-15-1). The following discussion considers 
each of these analyses, as well as the overall weight of evidence with 
respect to cancer risk from low exposure to Cr(VI).
a. Linearity of the Relationship Between Lung Cancer Risk and 
Cumulative Exposure
    In the Luippold et al. 2003 publication (Ex. 33-10) and the Proctor 
et al. 2004 publication (Ex. 38-216-10), the authors reported observed 
and expected lung cancer deaths for five categories of cumulative 
exposure. Lung cancer mortality was significantly elevated in 
categories above 1.05 mg/m3-yr Cr(VI) (p < 0.05), and was 
non-significantly elevated in the category spanning 0.20-0.48 mg/
m3-yr (8 observed lung cancer deaths vs. 4.4 expected), with 
a slight deficit in lung cancer mortality for the first and third 
categories (3 observed vs. 4.5 expected below 0.2 mg/m3-yr, 4 observed 
vs. 4.4 expected at 0.48-1.04 mg/m3-yr) (Ex. 33-10, p. 455). 
This analysis is cited by commenters who suggest that the lack of a 
significantly elevated lung cancer risk in the range below 1.05 mg/
m3-yr may reflect the existence of a threshold or other 
nonlinearity in the exposure-response for Cr(VI), and that OSHA's use 
of a linear relative risk model in the preliminary risk assessment may 
not be appropriate (Exs. 38-106, pp. 10-11; 38-233-4, p. 18). OSHA 
received similar comments citing the Crump et al. (2003) publication, 
in which the authors found a "consistently significant" trend of 
increasing risk with increasing cumulative exposure for categories of 
exposure above 1 mg/m3-yr (Ex. 35-58, p. 1157). The Exponent 
analysis of the Gibb et al. cohort was also cited, which found that 
lung cancer SMRs were not significantly elevated for workers with 
cumulative exposures below 0.42 mg/m3-yrs Cr(VI) when 
Baltimore reference rates and a six-category exposure grouping were 
used (Ex. 31-18-15-1, Table 6).
    Some commenters have interpreted these analyses to indicate 
uncertainty about the exposure-response relationship at low exposure 
levels. Others have asserted that "[c]redible health experts assessing 
the same data as OSHA have concluded that 23 [mu]g/m3 is a protective 
workplace standard (Ex. 38-185, p. 4) or that "[t]he Crump study 
concluded that 23 [mu]g/m3 would be a standard that is 
protective of workers health" (Ex. 47-35-1, p. 5). Contrary to these 
assertions, it should be noted that the Gibb et al., Luippold et al., 
and Crump et al. publications do not include any statements concluding 
that 23 [mu]g/m3 or any other exposure level is protective 
against occupational lung cancer. OSHA has reviewed these analyses to 
determine whether they provide sufficient evidence to support the use 
of a nonlinear or threshold-based exposure-response model for the 
Cr(VI) risk assessment, and whether they support the assertion that a 
PEL higher than that proposed would protect workers against a 
significant risk of lung cancer.
    In discussing their results, Luippold et al. reported that 
evaluation of a linear dose-response model using a chi-squared test 
showed no significant departure from linearity and concluded that the 
data are consistent with a linear dose-response model. They noted that 
the results were also consistent with threshold or nonlinear effects at 
low cumulative exposures, as they observed substantial increases in 
cumulative exposure levels above approximately 1 mg/m3-yrs 
(Ex. 33-10, p. 456). Ms. Deborah Proctor, lead author of the Proctor et 
al. (2004) publication, confirmed these conclusions at the public 
hearing, stating her belief that nonlinearities may exist but that the 
data were also consistent with a linear dose response (Tr. 1845). The 
authors of the Crump et al. 2003 publication (Ex. 35-58), in which 
trend analyses were used to examine the exposure-response relationship 
for cumulative exposure, stated that the data were " * * * neutral 
with respect to these competing hypotheses" (Ex. 35-58, pp. 1159-
1160). Crump et al. concluded that their study of the Luippold cohort 
" * * * had limited power to detect increases [in lung cancer risk] at 
these low exposure levels" (Ex. 35-58, p. 1147). OSHA agrees with 
Crump et al.'s conclusion that their study could not detect the 
relatively small increases in risk that would be expected at low 
exposures. With approximately 3000 person-years of observation time and 
4.5 expected lung cancers in each of the three cumulative exposure 
categories lower than 0.19 mg/m3-yrs Cr(VI) (Ex. 33-10, p. 
455), analyses of the Luippold cohort cannot effectively discriminate 
between alternative risk models for cumulative exposures that a worker 
would accrue from a 45-year working lifetime of occupational exposure 
at relatively low exposures (e.g., 0.045-0.225 mg/m3-yrs 
Cr(VI), corresponding to a working lifetime of exposure at 1-5 [mu]g 
Cr(VI)/m3).
    The Exponent reanalysis of the Gibb cohort found that lung cancer 
rates associated with exposures around 0.045 mg/m3-yrs 
Cr(VI) and below were not significantly elevated in some analyses (Ex. 
31-18-15-1, Table 6 p. 26). However, OSHA believes that this result is 
likely due to the limited power of the study to detect small increases 
in risk, rather than a threshold or nonlinearity in exposure-response. 
In written testimony, Dr. Gibb explained that "[l]ack of a 
statistically elevated lung cancer risk at lower exposures does not 
imply that a threshold of response exists. As exposure decreases, so 
does the statistical power of a given sample size to detect a 
significantly elevated risk" (Ex. 44-4, p. 6). Exponent's analyses 
found (non-significant) elevated risks for all exposure groups above 
approximately 0.1 mg/m3-yrs, equivalent to 45 years of 
occupational exposure at about 2.25 [mu]g/m3 Cr(VI) (Ex. 31-
18-15-1, p. 20, Table 3). Furthermore, Gibb et al.'s SMR analysis based 
on exposure quartiles found statistically significantly elevated lung 
cancer risks among workers with cumulative exposures well below the 
equivalent of 45 years at the proposed PEL of 1 [mu]g/m3. As 
Dr. Gibb commented at the hearing, the proposed PEL " * * * is within 
the range of observation [of the studies] * * * In a sense, you don't 
even need risk models" to show that workers exposed to cumulative 
exposures equivalent to a working lifetime of exposure at or above the 
proposed PEL have excess risk of lung cancer as a result of their 
occupational exposure to Cr(VI)" (Tr. 121-122).
    Furthermore, Robert Park of NIOSH reminded OSHA that "[a]nalysts 
of both the Painesville and the Baltimore cohorts * * * did test for 
deviation or departure from linearity in the exposure response and 
found no significant effect. If there was a large threshold, you would 
expect to see some deviance there" (Tr. 350-351). Post-hearing 
comments from NIOSH indicated that further analysis of the Gibb data 
provided no significant improvement in fit for nonlinear and threshold 
models compared to the linear relative risk model (Ex. 47-19, p. 7). 
Based on this evidence and on the previously discussed findings that 
(1) linear relative risk models fit both the Gibb and Luippold data 
sets adequately, and (2) the wide variety of nonlinear models tested by 
various analysts failed to fit the available data better than the 
linear model, OSHA believes that a linear risk model is appropriate and 
that there is not convincing evidence to support the use of a threshold 
or nonlinear exposure-response model, or to conclude that OSHA's risk 
assessment has seriously overestimated risk at low exposures.
b. The Cumulative Exposure Metric and Dose-Rate Effects on Risk
    The Small Business Administration's Office of Advocacy and several 
other commenters questioned OSHA's reliance in the preliminary risk 
assessment on models using cumulative exposure to estimate excess risk 
of lung cancer, suggesting that cumulative exposures attained from 
exposure to high concentrations of Cr(VI) for relatively short periods 
of time, as for some individuals in the Gibb and Luippold cohorts, may 
cause greater excess risk than equivalent cumulative exposures attained 
from long-term exposure to low concentrations of Cr(VI) (Exs. 38-7, pp. 
3-4, 38-215-2, pp. 17-18; 38-231, p. 18; 38-233, p. 82; 38-265-1, p. 
27; 39-74, p. 2, 40-12-1, p. 2, 43-2, p. 2, 47-27, p. 14; 47-27-3, p. 
1). This assertion implies that OSHA's risk assessment overestimates 
risk from exposures at or near the proposed PEL due to a threshold or 
dose-rate effect in exposure intensity. One commenter stated that 
"[a]pplication of a linear model estimating lung cancer risk from 
high-level expsoures . . . to very low-level exposure using the 
exposure metric of cumulative dose will inevitably overestimate risk 
estimates in the proposed PEL" (Ex. 47-27-3, p. 1). Comments on this 
subject have cited analyses by Proctor et al. (2004) (Ex. 38-233-4, p. 
17), Crump et al. (2003) (Exs. 38-106, p. 22; 38-265-1, p. 27), 
Exponent (Ex. 31-18-15-1, pp. 31-34) and NIOSH (Ex. 47-19-1, p. 7); a 
new study by Luippold et al. on workers exposed to relatively low 
concentrations of Cr(VI) (Ex. 47-24-2); and mechanistic and animal 
studies examining the potential for dose-rate effects in Cr(VI)-related 
health effects (Exs. 31-18-7; 31-18-8; 11-7).
    Of the two featured cohorts in OSHA's preliminary risk assessment, 
the Gibb cohort is better suited to assess risk from exposure 
concentrations below the previous PEL of 52 [mu]g Cr(VI)/m\3\. Contrary 
to some characterizations of the cohort's exposures as too high to 
provide useful information about risk under modern workplace conditions 
(See e.g. Exs. 38-106, p. 21; 38-233, p. 82; 38-265-1, p. 28), most 
members of the Gibb cohort had relatively low exposures, with 
42[percnt] of the cohort members having a median annual average exposure
value below 10 [mu]g/m\3\ Cr(VI), 69[percnt] below 20 [mu]g/m\3\, and 91[percnt] below the 
previous PEL (Ex. 35-295). In addition, Dr. Gibb indicated that 
exposures in general were lower than suggested by some commenters (Tr. 
1856, Ex. 38-215-2, p. 17). For example, about half of the total time 
that workers were exposed was estimated to be below 14 [mu]g/m\3\ 
Cr(VI) from 1960-1985 (Ex. 47-8, p. 1).
    Exponent calculated SMRs for six groups of workers in the Gibb 
cohort, classified according to the level of their highest average 
annual exposure estimates. They found that only the group of workers 
whose highest exposure estimates were above approximately 95 [mu]g/m\3\ 
Cr(VI) had statistically significantly elevated lung cancer risk when 
Baltimore reference rates were used (Ex. 31-18-15-1, p. 33). Exponent's 
results are presented in Table VI-8 below, adapted from Table 10 in 
their report (Ex. 31-18-15-1, p. 33).

Click here to view table VI-8

    OSHA does not believe that Exponent's analysis of the Gibb data 
provides convincing evidence of a threshold in exposure-response. While 
the lower-exposure groups do not have statistically significantly 
elevated lung cancer risk (p > 0.05) when compared with a Baltimore 
reference population, the SMRs for all groups above 3.7 [mu]g/
m3 are consistently elevated. Moreover, the increased risk 
approaches statistical significance, especially for those subgroups 
with higher power (Groups 2 and 3). This can be seen by the lower 95% 
confidence bound on the SMR for these groups, which is only slightly 
below 1. The analysis suggests a lack of power to detect excess risk in 
Groups 2-5, rather than a lack of excess risk at these exposure levels.
    Analyses of the Luippold cohort by Crump et al. (Ex. 35-58) and 
Proctor et al. (Ex. 38-216-10) used exposure estimates they called 
"highest average monthly exposure" to explore the effects of exposure 
intensity on lung cancer risk. They reported that lung cancer risk was 
elevated only for individuals with exposure estimates higher than the 
previous PEL of 52 [mu]g/m3 Cr(VI). Crump et al. 
additionally found "statistically significant evidence of a dose-
related increase in the relative risk of lung cancer mortality" only 
for groups above four times the previous PEL, using a series of Poisson 
regressions modeling the increase in risk across the first two 
subgroups and with the successive addition of higher-exposed subgroups 
(Ex. 35-58, p. 1154).
    As with the Gibb data, OSHA does not believe that the subgroup of 
workers exposed at low levels is large enough to provide convincing 
evidence of a threshold in exposure-response. In the Crump et al. and 
Proctor et al. analyses, the groups for which no statistically 
significant elevation or dose-related trends in lung cancer risk were 
observed are quite small by the standards of cancer epidemiology (e.g., 
the Luippold cohort had only about 100 workers below the previous PEL 
and about 40 workers within 1-3 times the previous PEL). Crump et al. 
emphasized that " * * * this study had limited power to detect 
increases [in lung cancer risk] at these low exposure levels" (Ex. 35-
58, p. 1147). The authors did not conclude that their results indicate 
a threshold. They stated that their cancer potency estimates based on a 
linear relative risk model using the cumulative exposure metric " * * 
* are comparable to those developed by U.S. regulatory agencies and 
should be useful for assessing the potential cancer hazard associated 
with inhaled Cr(VI)" (Ex. 35-58, p. 1147).
    OSHA discussed the Exponent, Crump et al. and Luippold et al. SMR 
analyses of the Gibb and Luippold cohorts in the preamble to the 
proposed rule, stating that the lack of a statistically significant 
result for a subset of the entire cohort should not be construed to 
imply a threshold (69 FR at 59382). During the hearing, Robert Park of 
NIOSH expressed agreement with OSHA's preliminary interpretation, 
adding that:

    [W]e think that any interpretation of threshold in these studies 
is basically a statistical artifact * * * It is important I think to 
understand that any true linear or even just monotonic exposure 
response that doesn't have a threshold will exhibit a threshold by 
the methods that they used. If you stratify the exposure metric fine 
enough and look at the lower levels, they will be statistically 
insignificant in any finite study * * * telling you nothing about 
whether or not in fact there is a threshold (Tr. 351).

    To further explore the effects of highly exposed individuals on 
OSHA's risk model, The Chrome Coalition suggested that OSHA should base 
its exposure-response model on a subcohort of workers excluding those 
who were exposed to " * * * an extraordinary exposure level for some 
extended period of time* * * ", e.g., estimated exposures greater than 
the previous PEL for more than one year (Ex. 38-231, p. 21). The Chrome 
Coalition stated,

    We are not aware of any study that has performed this type of 
analysis but we believe that it should be a way of better estimating 
the risk for exposures in the range that OSHA is considering for the 
PEL (Ex. 38-231, p. 21).

To gauge the potential utility of such an analysis, OSHA examined the 
subset of the Gibb cohort that was exposed for more than 365 days and 
had average annual exposure estimates above the previous PEL of 52 
[mu]g/m3 Cr(VI). The Agency found that the subcohort 
includes only 82 such individuals, of whom 37 were reported as deceased 
at the end of follow-up and five had died of lung cancer. In a cohort 
of 2357 workers with 122 lung cancers out of 855 deaths, it is unlikely that 
exclusion of a group this size would impact the results of a regression 
analysis significantly, especially as the proportion of mortality 
attributable to lung cancer is similar in the highly-exposed subgroup 
and the overall cohort (5/37 0.135, 122/855 [cong] 0.143). The great 
majority of the Gibb cohort members did not have the 'extraordinary' 
exposure levels implied by the Chrome Coalition. As discussed 
previously, most had relatively low exposures averaging less than 20 
[mu]g/m3.
    As discussed in their post-hearing comments, NIOSH performed 
regression analyses designed to detect threshold or dose-rate effects 
in the exposure-response relationship for the Gibb dataset (Ex. 47-19-
1, p. 7). NIOSH reported that "[t]he best fitting models had no 
threshold for exposure intensity and the study had sufficient power to 
rule out thresholds as large as 30 [mu]g/m\3\ CrO3 (15.6 
[mu]g/m\3\ Cr(VI) * * * " and that there was no statistically 
significant departure from dose-rate linearity when powers of annual 
average exposure values were used to predict lung cancer risk (Ex. 47-
19-1, p. 7). This indicates that a threshold of approximately 20 [mu]g/
m\3\ Cr(VI) suggested in some industry comments is not consistent with 
the Gibb cohort data. Based on these and other analyses described in 
their post-hearing comments, NIOSH concluded that:

    [E]xamination of non-linear features of the hexavalent chromium-
lung cancer response supports the use of the traditional (lagged) 
"cumulative exposure paradigm * * * ": that is, linear exposure-
response with no threshold (Ex. 47-19-1, p. 7).

    OSHA recognizes that, like most epidemiologic studies, neither the 
Luippold nor the Gibb cohort provides ideal information with which to 
identify a threshold or detect nonlinearities in the relationship 
between Cr(VI) exposure and lung cancer risk, and that it is important 
to consider other sources of information about the exposure-response 
relationship at very low levels of Cr(VI) exposure. The Agency agrees 
with Dr. Gibb's belief that " * * * arguments for a 'threshold' should 
not be based on statistical arguments but rather on a biological 
understanding of the disease process" (Ex. 44-4, p. 7) and Crump et 
al.'s statement that " * * * one needs to consider supporting data 
from mechanistic and animal studies" in order to determine the 
appropriateness of assuming that a threshold (or, presumably, other 
nonlinearity) in exposure-response exists (Ex. 35-58, p. 1159). 
Experimental and mechanistic evidence and related comments relevant to 
the issue of threshold and dose-rate effects are reviewed in the 
following discussion.
    c. Animal and Mechanistic Evidence Regarding Nonlinearities in 
Cr(VI) Exposure-Response
    In the NPRM, OSHA analyzed several animal and mechanistic studies 
and did not find convincing evidence of a threshold concentration in 
the range of interest (i.e. 0.25 to 52 [mu]g/m\3\). However, the Agency 
recognized that evidence of dose rate effects in an animal instillation 
study and the existence of extracellular reduction, DNA repair, and 
other molecular pathways within the lung that protect against Cr(VI)-
induced respiratory tract carcinogenesis could potentially introduce 
nonlinearities in Cr(VI) exposure-cancer response. OSHA solicited 
comment on the scientific evidence for a non-linear exposure-response 
relationship in the occupational exposure range of interest and whether 
there was sufficient data to develop a non-linear model that would 
provide more reliable risk estimates than the linear approach used in 
the preliminary risk assessment (69 FR at 59307).
    Some commenters believed the scientific evidence from animal 
intratracheal instillation and inhalation of Cr(VI) compounds showed 
that a linear risk model based on lung cancers observed in the Gibb and 
Luippold cohorts seriously overpredicts lung cancer risk to workers 
exposed at the proposed PEL (Exs. 38-216-1; 38-233-4; 38-231). The 
research cited in support of this presumed non-linear response was the 
intratracheal instillation study of Steinhoff et al. and the inhalation 
study of Glaser et al. (Exs. 11-7; 10-11). For example, Elementis 
Chromium states that:

    Considering either the Steinhoff or Glaser studies, a calculated 
risk based on the effect frequency at the highest daily exposure 
would be considerably greater than that calculated from the next 
lower daily exposure. We believe that the same effect occurs when 
humans are exposed to Cr(VI) and consideration of this should be 
taken when estimating risk at very low exposure levels based on 
effects at much higher exposure levels (Ex. 38-216-1, p. 4).

    Despite the different mode of Cr(VI) administration and dosing 
schemes, the Steinhoff and Glaser studies both feature dose levels at 
which there was no observed incidence of lung tumors. The Steinhoff 
study found no significant lung tumor incidence in rats intratracheally 
administered highly soluble sodium dichromate at 87 [mu]g Cr(VI)/kg or 
less regardless of whether the dose was received five times a week or 
once a week for 30 months. However, rats administered a higher dose of 
437 [mu]g Cr(VI)/kg of sodium dichromate or a similar amount of the 
slightly soluble calcium chromate once a week developed significant 
increases (about 17 percent incidence) in lung tumors. The study 
documented a 'dose rate effect' since the same total dose administered 
more frequently (i.e. five times weekly) at a five-fold lower dose 
level (i.e. 87 [mu]g Cr(VI)/kg) did not increase lung tumor incidence 
in the highly soluble sodium dichromate-treated rats. The Glaser 
inhalation study reported no lung tumors in rats inhaling 50 [mu]g 
Cr(VI)/m\3\ of sodium dichromate or lower Cr(VI) concentrations for 22 
hours/day, 7 days a week. However, the next highest dose level of 100 
[mu]g Cr(VI)/m\3\ produced a 15 percent lung tumor incidence (i.e. 3 of 
19 rats). Both studies are more fully described in Section V.B.7.a.
    The apparent lack of lung tumors at lower Cr(VI) dose levels is 
interpreted by the commenters to be evidence of a non-linear exposure-
response relationship and, possibly, an exposure threshold below which 
there is no risk of lung cancer.
    In written testimony, Dr. Harvey Clewell of ENVIRON Health Science 
Institute addressed whether the Steinhoff, Glaser and other animal 
studies provided evidence of a threshold for Cr(VI) induced lung 
carcinogenicity (Ex. 44-5). He stated that the argument for the 
existence of a threshold rests on two faulty premises:

    (1) Failure to detect an increased incidence of tumors from a 
given exposure indicates there is no carcinogenic activity at that 
exposure, and
    (2) Nonlinearities in dose response imply a threshold below 
which there is no carcinogenic activity (Ex. 44-5, p. 13).

In terms of the first premise, Dr. Clewell states:

    The ability to detect an effect depends on the power of the 
study design. A statistically-based No Observed Adverse Effect Level 
(NOAEL) in a toxicity study does not necessarily mean there is no 
risk of adverse effect. For example, it has been estimated that a 
typical animal study can actually be associated with the presence of 
an effect in as many as 10% to 30% of the animals. Thus the failure 
to observe a statistically significant increase in tumor incidence 
at a particular exposure does not rule out the presence of a 
substantial carcinogenic effect at that exposure (Ex. 44-5, p. 13-
14).

Dr. Clewell also addressed the second premise as it applies to the 
Steinhoff instillation study as follows:

    It has been suggested, for example, that the results of the 
Steinhoff study suggest that dose rate is an important factor in the 
carcinogenic potency of chrome (VI), and therefore, there must be a 
threshold. But these data, while they do provide an indication of a 
dose rate effect * * * they don't provide information about where and 
whether a threshold or even a non-linearity occurs, and to what extent 
it does occur at lower concentrations (Tr. 158-159).

    OSHA agrees with Dr. Clewell that the absence of observed lung 
tumor incidence at a given exposure (i.e. a NOAEL) in an animal study 
should not be interpreted as evidence of a threshold effect. This is 
especially true for clearly genotoxic carcinogens, such as Cr(VI), 
where it is considered scientifically reasonable to expect some small, 
but finite, probability that a very few molecules may damage DNA in a 
single cell and eventally develop into a tumor. For this reason, it is 
not appropriate to regard the lack of tumors in the Steinhoff or Glaser 
studies as evidence for an exposure-response threshold.
    Exponent, in a technical memorandum prepared for an ad hoc group of 
steel manufacturers, raises the possibility that the lung tumor 
responses in the Steinhoff and Glaser studies were the result of damage 
to lung tissue from excessive levels of Cr(VI). Exponent suggests that 
lower Cr(VI) exposures that do not cause 'respiratory irritation' are 
unlikely to lead an excess lung cancer risk (Ex. 38-233-4). Exponent 
went on to summarize:
    In examining the weight of scientific evidence, for exposure 
concentrations below the level which causes irritation, lung cancer 
has not been reported. Not surprisingly, Cr(VI)-induced respiratory 
irritation is an important characteristic of Cr(VI)-induced 
carcinogenicity in both humans and animals * * * Based on the 
information reviewed herein, it appears that the no effect level for 
non-neoplastic respiratory irritation and lung cancer from 
occupational exposure to Cr(VI) is approximately 20 [mu]g/m\3\. Thus 
establishing a PEL of 1 [mu]g/m\3\ to protect against an excess lung 
cancer risk is unnecessarily conservative (Ex. 38-233-4, p. 24).

    In support of the above hypothesis, Exponent points out that only 
the highest Cr(VI) dose level (i.e. 437 [mu]g Cr(VI)/kg) of sodium 
dichromate employed in the Steinhoff study resulted in significant lung 
tumor incidence. Tracheal instillation of this dose once a week 
severely damaged the lungs leading to emphysematous lesions and 
pulmonary fibrosis in the Cr(VI)-exposed rats. Lower Cr(VI) dose levels 
(i.e. 87 [mu]g Cr(VI)/kg or less) of the highly water-soluble sodium 
dichromate that caused minimal lung damage did not result in 
significant tumor incidence. However, the study also showed that a 
relatively low dose (i.e. 81 [mu]g Cr(VI)/kg) of slightly soluble 
calcium chromate repeatedly instilled (i.e. five times a week) in the 
trachea of rats caused significant lung tumor incidence (about 7.5 
percent) in the absence of lung tissue damage. This finding is 
noteworthy because it indicates that tissue damage is not an essential 
requirement for Cr(VI)-induced respiratory tract carcinogenesis. The 
same instilled dose of the slightly soluble calcium chromate would be 
expected to provide a more persistent and greater source of Cr(VI) in 
proximity to target cells within the lung than would the highly water-
soluble sodium dichromate. This suggests that the internal dose of 
Cr(VI) at the tissue site, rather than degree of damage, may be the 
critical factor determining lung cancer risk from low-level Cr(VI) 
exposures.
    Exponent applies similar logic to the results of the Glaser 
inhalation study of sodium dichromate in rats. Exponent states:

    In all experimental groups (i.e. 25, 50, and 100 [mu]g Cr(VI)/
m\3\), inflammation effects were observed, but at 100 [mu]g Cr(VI)/
m\3\ [the high dose group with significant lung tumor incidence], 
effects were more severe, as expected (Ex. 38-233-4, p. 22).

This assessment contrasts with that of the study authors who remarked:

    In this inhalation study, in which male Wistar rats were 
continuously exposed for 18 months to both water soluble sodium 
dichromate and slightly soluble chromium oxide mixture aerosols, no 
clinical signs of irritation were obvious * * * For the whole time 
of the study no significant effects were found from routine 
hematology and clinico-chemical examinations in all rats exposed to 
sodium dichromate aerosol (Ex. 10-11, p. 229).

The rats in the Glaser carcinogenicity study developed a focalized form 
of lung inflammation only evident from microscopic examination. This 
mild response should not be considered equivalent to the widespread 
bronchiolar fibrosis, collapsed/distorted alveolar spaces and severe 
damage found upon macroscopic examination of rat lungs instilled with 
the high dose (437 [mu]g Cr(VI)/kg) of sodium dichromate in the 
Steinhoff study. The non-neoplastic lung pathology (e.g. accumulation 
of pigmentized macrophages) described following inhalation of sodium 
dichromate at all air concentrations of Cr(VI) in the Glaser study are 
more in line with the non-neoplastic responses seen in the lungs of 
rats intratracheally instilled with lower dose levels of sodium 
dichromate (i.e. 87 [mu]g Cr(VI)/kg or less) that did not cause tumor 
incidence in the Steinhoff study. OSHA finds no evidence that severe 
pulmonary inflammation occurred following inhalation of 100 [mu]g 
Cr(VI)/m\3\ in the Glaser carcinogenicity study or that the lung tumors 
observed in these rats were the result of 'respiratory irritation'. Dr. 
Clewell also testified that lung damage or chronic inflammation is not 
a necessary and essential condition for C(VI) carcinogenesis in the 
Glaser study:

    I didn't find any evidence that it [lung damage and chronic 
inflammation] was necessary and essential. In particular, I think 
the Glaser study was pretty good in demonstrating that there were 
effects where they saw no evidence of irritation, or any clinical 
signs of those kinds of processes (Tr. 192).

    Subsequent shorter 30-day and 90-day inhalation exposures with 
sodium dichromate in rats were undertaken by the Glaser group to better 
understand the non-neoplastic changes of the lung (Ex. 31-18-11). The 
investigation found a transitory dose-related inflammatory response in 
the lungs at exposures of 50 [mu]g Cr(VI)/m\3\ and above following the 
30 day inhalation. This initial inflammatory response did not persist 
during the 90 day exposure study except at the very highest dose levels 
(i.e. 200 and 400 [mu]g Cr(VI)/m\3\). Significant increases in 
biomarkers for lung tissue damage (such as albumin and lactate 
dehydrogenase (LDH) in bronchioalveolar lavage fluid (BALF) as well as 
bronchioalveolar hyperplasia) also persisted through 90 days at these 
higher Cr(VI) air levels, especially 400 [mu]g Cr(VI)/m\3\. The study 
authors considered the transient 30-day responses to represent 
adaptive, rather than persistent pathological, responses to Cr(VI) 
challenge. A dose-related elevation in lung weights due to 
histiocytosis (i.e. accumulation of lung macrophages) was seen in all 
Cr(VI)-administered rats at both time periods. The macrophage 
accumulation is also likely to be an adaptive response that reflects 
lung clearance of inhaled Cr(VI). These study results are more fully 
described in section V.C.3.
    OSHA believes that Cr(VI)-induced carcinogenesis may be influenced 
not only by the total Cr(VI) dose retained in the respiratory tract but 
also by the rate at which the dose is administered. Exponent is correct 
that one possible explanation for the dose rate effect observed in the 
Steinhoff study may be the widespread, severe damage to the lung caused 
by the immediate instillation of a high Cr(VI) dose to the respiratory 
tract repeated weekly for 30 months. It is biologically plausible that 
the prolonged cell proliferation in response to the tissue injury would 
enhance tumor development and progression compared to the same total Cr(VI)
instilled more frequently at smaller dose levels that do not cause widespread 
damage to the respiratory tract. This is consistent with the opinion of Dr. Clewell 
who testified that:

    I would not say that it [respiratory tract irritation, lung 
damage, or chronic inflammation] is necessary and sufficient, but 
rather it exacerbates an underlying process. If there is a 
carcinogenic process, then increased cell proliferation secondary to 
irritation is going to put mitogenic pressure on the cells, and this 
will cause more likelihood of a transformation (Tr. 192).

    OSHA notes that increased lung tumor incidence was observed in 
animals instilled with lower dose levels of calcium chromate in the 
Steinhoff study and after inhalation of sodium dichromate in the Glaser 
study. These Cr(VI) exposures did not trigger extensive lung damage and 
OSHA believes it unlikely that the lung tumor response from these 
treatments was secondary to 'respiratory irritation' as suggested by 
Exponent. The more thorough investigation by the Glaser group did not 
find substantive evidence of persistent tissue damage until rats 
inhaled Cr(VI) at doses two- to four-fold higher than the Cr(VI) dose 
found to elevate lung tumor incidence in the their animal cancer 
bioassay.
    Exponent goes on to estimate a NOAEL (no observable adverse effect 
level) for lung histopathology in the Steinhoff study. They chose the 
lowest dose level (i.e. 3.8 [mu]g Cr(VI)/kg) in the study as their 
NOAEL based on the minimal accumulation of macrophages found in the 
lungs instilled with this dose of sodium dichromate five times weekly 
(Ex. 38-233-4, p. 21). Exponent calculates that this lung dose is 
roughly equivalent to the daily dose inhaled by a worker exposed to 27 
[mu]g Cr(VI)/m\3\ using standard reference values (e.g. 70 kg human 
inhaling 10 m\3\/day over a daily 8 hour work shift). Exponent 
considers this calculated Cr(VI) air level as a threshold below which 
no lung cancer risk is expected in exposed workers.
    However, Steinhoff et al. instilled Cr(VI) compounds directly on 
the trachea rather than introducing the test compound by inhalation, 
and was only able to characterize a significant dose rate effect at one 
cumulative dose level. For these reasons, OSHA considers the data 
inadequate to reliably determine the human exposures where this 
potential dose transition might occur and to confidently predict the 
magnitude of the resulting non-linearity. NIOSH presents a similar view 
in their post-hearing comments:

    NIOSH disagrees with Dr. Barnhardt's analysis [Ex. 38-216-1] and 
supports OSHA's view that the Steinhoff et al. [1986] rat study 
found a dose-rate effect in rats under the specified experimental 
conditions, that this effect may have implications for human 
exposure and that the data are insufficient to use in a human risk 
assessment for Cr(VI) * * * The study clearly demonstrates that, 
within the constraints of the experimental design, a dose rate 
effect was observed. This may be an important consideration for 
humans exposed to high levels of Cr(VI). However, quantitative 
extrapolation of that information to the human exposure scenario is 
difficult (Ex. 47-19-1, p. 8).

    Exponent also relies on a case investigation of the benchmark dose 
methodology applied to the pulmonary biomarker data measured in the 90-
day Glaser study (Ex. 40-10-2-8). In this instance, the benchmark doses 
represent the 95 percent lower confidence bound on the Cr(VI) air level 
corresponding a 10 percent increase relative to unexposed controls for 
a chosen biomarker (e.g. BALF total protein, albumin, or LDH). The 
inhaled animal doses were adjusted to reflect human inhalation and 
deposition in the respiratory tract as well as continuous environmental 
exposure (e.g. 24 hours/day, 7 days/week) rather than an occupational 
exposure pattern (e.g. 8 hours/day, 5 days/week). The benchmark doses 
were reported to range from 34 to 140 [mu]g Cr(VI)/m\3\.
    Exponent concludes that "these [benchmark] values are akin to a 
no-observed-adverse-effect level NOAEL in humans to which uncertainty 
factors are added to calculate an RfC [i.e. Reference Concentration 
below which adverse effects will not occur in most individuals]" and 
"taken as a whole, the studies of Glaser et al. suggest that both non-
neoplastic tissue damage and carcinogenicity are not observed among 
rats exposed to Cr(VI) at exposure concentrations below 25 [mu]g/m\3\" 
(Ex. 38-233-4, p. 22). Since the Exponent premise is that Cr(VI)-
induced lung cancer only occurs as a secondary response to 
histopathological changes in the respiratory tract, the suggested 25 
[mu]g Cr(VI)/m\3\ is essentially being viewed as a threshold 
concentration below which lung cancer is presumed not to occur.
    In his written testimony, Dr. Clewell indicated that the tumor data 
from the Glaser cancer bioassay was more appropriately analyzed using 
linear, no threshold exposure-response model rather than the benchmark 
uncertainty factor approach that presumes the existence of threshold 
exposure-response.

    The bioassay of Glaser et al. provides an example of a related 
difficulty of interpreting data from carcinogenicity studies. The 
tumor outcome appears to be nonlinear (0/18, 0/18, and 3/19 at 
0.025, 0.05, and 0.1 mg Cr/m\3\). However, although the outcomes are 
restricted to be whole numbers (of animals), they should not be 
evaluated as such. Because the nature of cancer as a stochastic 
process, each observed outcome represents a random draw from a 
Poisson distribution. Statistical dose-response modeling, such as 
the multistage model used by OSHA, is necessary to properly 
interpret the cancer dose-response. In the case of Glaser et al. 
(1986) study, such modeling would produce a maximum likelihood 
estimate of the risk at the middle dose that was greater than zero. 
In fact, the estimated risk at the middle dose would be on the order 
of several percent, not zero. Therefore, suggesting a lack of lung 
cancer risk at a similar human exposure would not be a health 
protective position (Ex. 44-5, p. 14).

    The U.S. Environmental Protection Agency applied a linearized (no 
threshold) multistage model to the Glaser data (Ex. 17-101). They 
reported a maximum likelihood estimate for lifetime lung cancer risk of 
6.3 per 1000 from continuous exposure to 1 [mu]g Cr(VI)/m\3\. This risk 
would be somewhat less for an occupational exposure (e.g. 8 hours/day, 
5 days/week) to the same air level and would be close to the excess 
lifetime risk predicted by OSHA (i.e. 2-9 per 1000).
    In summary, OSHA does not believe the animal evidence demonstrates 
that respiratory irritation is required for Cr(VI)-induced 
carcinogenesis. Significant elevation in lung tumor incidence was 
reported in rats that received Cr(VI) by instillation or inhalation at 
dose levels that caused minimal lung damage. Consequently, OSHA 
believes it inappropriate to consider a NOAEL (such as 25 [mu]g/m\3\) 
where lung tumors were not observed in a limited number of animals to 
be a threshold concentration below which there is no risk. Statistical 
analysis of the animal inhalation data using a standard dose-response 
model commonly employed for genotoxic carcinogens, such as Cr(VI), is 
reported to predict risks similar to those estimated by OSHA from the 
occupational cohorts of chromate production workers. While the rat 
intratracheal instillation study indicates that a dose rate effect may 
exist for Cr(VI)-induced carcinogenesis, it can not be reliably 
determined from the data whether the effect would occur at the 
occupational exposures of interest (e.g. working lifetime exposures at 
0.25 to 52 [mu]g Cr(VI)/m\3\) without a better quantitative 
understanding of Cr(VI) dosimetry within the lung. Therefore, OSHA does 
not believe that the animal data show that cumulative Cr(VI)
exposure is an inappropriate metric to estimate lung cancer risk.
    Exponent used the clinical findings from chromate production 
workers in the Gibb and Luippold cohorts to support their contention 
that 'respiratory irritation' was key to Cr(VI)-induced lung cancer 
(Ex. 28-233-4, p. 18-19). They noted that over 90 percent of chromate 
production workers employed at the Painesville plant during the 1930s 
and 1940s, including some Luippold cohort members, were reported to 
have damaged nasal septums. Based on this, Exponent concludes:

    Thus, it is possible that the increased incidence of lung cancer 
in these workers (i.e. SMR of 365 from Luippold et al. cohort 
exposed during the 1940s) is at least partially due to respiratory 
system tissue damage resulting from high Cr(VI) concentrations to 
which these workers were exposed. These exposures clearly exceed a 
threshold for both carcinogenic and non-carcinogenic (i.e. 
respiratory irritation) health effects (Ex. 38-233-4, p. 18).

Exponent noted that about 60 percent of the Gibb cohort also suffered 
ulcerated nasal septum tissue. The mean estimated annual Cr(VI) air 
level at time of diagnosis was about 25 [mu]g Cr(VI)/m\3\. Ulcerated 
nasal septum was found to be highly correlated with the average annual 
Cr(VI) exposure of the workers as determined by a proportional hazards 
model. These findings, again, led Exponent to suggest that:

    It may be reasonable to surmise that the high rates of lung 
cancer risk observed among the featured cohorts (i.e. Gibb and 
Luippold) was at least partially related to respiratory irritation 
(Ex. 38-233-4, p. 19).

    In its explanations, Exponent assumes that the irritation and 
damage to nasal septum tissue found in the exposed workers also occurs 
elsewhere in the respiratory tract. Exponent provided no evidence that 
Cr(VI) concentrations that damage tissue at the very front of the nose 
will also damage tissue in the bronchoalveolar regions where lung 
cancers are found. A national medical survey of U.S. chromate 
production workers conducted by the U.S. Public Health Service in the 
early 1950s found greater than half suffered nasal septum perforations 
(Ex. 7-3). However, there was little evidence of non-cancerous lung 
disease in the workers. The survey found only two percent of the 
chromate workers had chronic bronchitis which was only slightly higher 
than the prevalence in nonchromate workers at the same plants and less 
than had been reported for ferrous foundry workers. Just over one 
percent of the chromate production workers in the survey were found to 
have chest X-ray evidence consistent with pulmonary fibrosis. This led 
the U.S. Public Health Service to conclude "on the basis of X-ray data 
we cannot confirm the presence of pneumoconiosis from chromate 
exposure" (Ex. 7-3, p. 80). An earlier report noted fibrotic areas in 
the autopsied lungs of three Painesville chromate production workers 
employed during the 1940s who died of lung cancer (Ex. 7-12). The 
authors attributed the fibrotic lesions to the large amounts of 
chromite (a Cr(III) compound) ore found in the lungs.
    Exponent correctly noted that prevalence of nasal septum ulceration 
in the Gibb cohort was "significantly associated with [average annual] 
Cr(VI) exposure concentrations" using a proportional hazards model 
(Ex. 38-233-4, p. 19). However, other related symptomatology, such as 
nasal irritation and perforation, was not found to be correlated with 
annual average Cr(VI) air levels. This led the authors to suggest that 
nasal septum tissue damage was more likely related to short-term, 
rather than annual, Cr(VI) air levels. Nasal septum ulceration was also 
not a significant predictor of lung cancer when the confounding effects 
of smoking and cumulative Cr(VI) exposure were accounted for in the 
proportional hazards model (Ex. 31-22-11). The authors believed the 
lack of correlation probably reflected cumulative Cr(VI) as the 
dominant exposure metric related to the elevated lung cancer risk in 
the workers, rather than the high, short-term Cr(VI) air levels thought 
to be responsible for the high rate of nasal septum damage. The 
modeling results are not consistent with nasal septum damage as a 
predictor of Cr(VI)-induced lung cancer in chromate production workers. 
Dr. Herman Gibb confirmed this in oral testimony:

    * * * I was curious to see if [respiratory] irritation might be 
predictive of lung cancer. We did univariate analyses and found that 
a number of them were [predictive]. But whenever you looked at, when 
you put it into the regression model, none of them were. In other 
words, [respiratory] irritation was not predictive of the lung 
cancer response (Tr. 144).

    OSHA does not believe the evidence indicates that tissue damage in 
the nasal septum of chromate production workers exposed to Cr(VI) air 
levels around 20 [mu]g/m\3\ is responsible for the observed excess lung 
cancers. The lung cancers are found in the bronchioalveolar region, far 
removed from the nasal septum. Careful statistical analysis of the Gibb 
cohort did not find a significant relationship between clinical 
symptoms of nasal septum damage (e.g. ulceration, persistent bleeding, 
perforation) and lung cancer mortality. A 1951 U.S. Public Health 
Service medical survey found a high prevalence of nasal septum damage 
with few cases of chronic non-neoplastic lung disease (e.g. chronic 
bronchitis, pulmonary fibrosis). This suggests that the nasal septum 
damage caused by high Cr(VI) air concentrations was not mirrored by 
damage in lower regions of the respiratory tract where lung cancer 
takes place. Given these findings, it seems unlikely that the lower 
Cr(VI) air levels experienced by the Gibb cohort caused pervasive 
bronchioalveolar tissue damage that would be responsible for the 
clearly elevated lung cancer incidence in these workers. Therefore, the 
Agency does not concur with Exponent that there is credible evidence 
from occupational cohort studies that the high rates of lung cancer are 
related to tissue damage in the respiratory tract or that occupational 
exposure to 20 [mu]g Cr(VI)/m\3\ represents a 'no effect' level for 
lung cancer.
    Some commenters felt that certain physiological defense mechanisms 
that protect against the Cr(VI)-induced carcinogenic process introduce 
a threshold or sublinear dose-response (Exs. 38-233-4; 38-215-2; 38-
265). Some physiological defenses are thought to reduce the amount of 
biologically active chromium (e.g. intracellular Cr(V), Cr(III), and 
reactive oxygen species) able to interact with critical molecular 
targets within the lung cell. A prime example is the extracellular 
reduction of permeable Cr(VI) to the relatively impermeable Cr(III) 
which reduces Cr(VI) uptake into cells. Other defense mechanisms, such 
as DNA repair and apoptosis, can interfere with carcinogenic 
transformation and progression. These defense mechanisms are presented 
by commenters as highly effective at low levels of Cr(VI) but are 
overwhelmed at high dose exposures and, thus, could "provide a 
biological basis for a sublinear dose-response or a threshold below 
which there is expected to be no increased lung cancer risk (Ex. 38-
215-2, p. 29).
    One study, cited in support of an exposure-response threshold, 
determined the amount of highly soluble Cr(VI) reduced to Cr(III) in 
vitro by human bronchioalveolar fluid and pulmonary macrophage 
fractions over a short period (Ex. 31-18-7). These specific activities 
were used to estimate an "overall reducing capacity" of the lung. As 
previously discussed, cell membranes are permeable to Cr(VI) but not 
Cr(III), so only Cr(VI) enters cells to any appreciable extent. The 
authors interpreted these data to mean that high
levels of Cr(VI) would be required to "overwhelm" the reduction 
capacity before significant amounts of Cr(VI) could enter lung cells 
and damage DNA, thus creating a biological threshold to the exposure--
response (Ex. 31-18-8).
    There are several problems with this threshold interpretation. The 
in vitro reducing capacities were determined in the absence of cell 
uptake. Cr(VI) uptake into lung cells happens concurrently and in 
parallel with its extracellular reduction, so it cannot be concluded 
from the study data that a threshold reduction capacity must be 
exceeded before uptake occurs. The rate of Cr(VI) reduction to Cr(III) 
is critically dependant on the presence of adequate amounts of 
reductant, such as ascorbate or GSH (Ex. 35-65). It has not been 
established that sufficient amounts of these reductants are present 
throughout the thoracic and alveolar regions of the respiratory tract 
to create a biological threshold. Moreover, the in vitro activity of 
Cr(VI) reduction in epithelial lining fluid and alveolar macrophages 
was shown to be highly variable among individuals (Ex. 31-18-7, p. 
533). It is possible that Cr(VI) is not rapidly reduced to Cr(III) in 
some workers or some areas of the lung. Finally, even if there was an 
exposure threshold created by extracellular reduction, the study data 
do not establish the dose range in which the putative threshold would 
occur.
    Other commenters thought extracellular reduction and other 
physiological defenses were unlikely to produce a biological threshold 
(Exs. 44-5; 40-18-1). For example, Dr. Clewell remarked:

    Although studies attempted to estimate capacities of Cr(VI) (De 
Flora et al., 1997) the extracellular reduction and cellular uptake 
of Cr(VI) are parallel and competing kinetic processes. That is, 
even at low concentrations where reductive capacity is undiminished, 
a fraction of Cr(VI) will still be taken up into cells, as 
determined by the relative rates of reduction and transport. For 
this reason, reductive capacities should not be construed to imply 
"thresholds" below which Cr(VI) will be completely reduced prior 
to uptake. Rather, they indicate that there is possibly a "dose-
dependent transition", i.e. a nonlinearity in concentration 
dependence of the cellular exposure to Cr(VI). Evaluation of the 
concentration-dependence of the cellular uptake of Cr(VI) would 
require more data than is currently available on the relative 
kinetics of dissolution, extracellular reduction, and cellular 
uptake as well as on the homeostatic response to depletion of 
reductive resources (e.g. reduction of glutathione reductase) (Ex. 
44-5, p. 16)

    The same logic applies to other 'defense mechanisms' such as DNA 
repair and apoptosis. Despite the ability of cells to repair DNA damage 
or to undergo apoptosis (i.e. a form of programmed cell death) upon 
exposure to low levels of Cr(VI), these protections are not absolute. 
Since a single error in a critical gene may trigger neoplastic 
transformation and DNA damage increases with intracellular 
concentration of Cr(VI), it stands to reason that there may be some 
risk of cancer even at low Cr(VI) levels. If the protective pathways 
are saturable (e.g. protective capacity overwhelmed) then it might be 
manifested as a dose transition or nonlinearity. However, as explained 
above, an extensive amount of kinetic modeling data would be needed to 
credibly predict the dose level at which a potential dose transition 
occurs. OSHA agrees with Dr. Clewell that "in the absence of such a 
biologically based [kinetic] dose-response model it is impossible to 
determine either the air concentration of Cr(VI) at which the 
nonlinearity might occur or the extent of the departure from a linear 
dose-response that would result. Therefore, the assumption of a linear 
dose-response is justified" (Ex. 44-5, p.17-18).
    In conclusion, OSHA believes that examination of the Gibb and 
Luippold cohorts, the new U.S. cohorts analyzed in Luippold et al. 
(2005), and the best available animal and mechanistic evidence does not 
support a departure from the traditional linear, cumulative exposure-
based approach to cancer risk assessment for hexavalent chromium. 
OSHA's conclusion is supported by several commenters (see e.g. Tr. 121, 
186, Exs. 40-10-2, p. 6; 44-7). For example, NIOSH stated:

    It is not appropriate to employ a threshold dose-response 
approach to estimate cancer risk from a genotoxic carcinogen such as 
Cr(VI) [Park et al. 2004]. The scientific evidence for a 
carcinogenicity threshold for Cr(VI) described in the Preamble [to 
the proposed rule] consists of the absence of an observed effect in 
epidemiology studies and animal studies at low exposures, and in 
vitro evidence of intracellular reduction. The epidemiologic and 
animal studies lack the statistical power to detect a low-dose 
threshold. In both the NIOSH and OSHA risk assessments, linear no-
threshold risk models provided good fit to the observed cancer data. 
The in vitro extracellular reduction studies which suggested a 
theoretical basis for a non-linear reseponse to Cr(VI) exposure were 
conducted under non-physiologic conditions. These results do not 
demonstrate a threshold of response to Cr(VI) exposure (Ex. 40-10-2, 
p. 6).

OSHA's position is also supported by Dr. Herman Gibb's testimony at the 
hearing that a linear, no-threshold model best characterizes the 
relationship between Cr(VI) exposure and lung cancer risk in the Gibb 
cohort (Tr. 121). Statements from Ms. Deborah Proctor and Crump et al. 
(who conducted analyses utilizing the Luippold cohort) also indicated 
that these data are consistent with the traditional linear model (Tr. 
1845, Exs. 33-10, p. 456; 35-58, pp. 1159-1160). The significant excess 
risk observed in the Gibb cohort, which was best suited to address risk 
from low cumulative or average exposures, contradicts comments to the 
effect that "[i]ncreased lung cancers have been demonstrated only at 
workplace exposures significantly higher than the existing standard * * 
* " (Ex. 38-185, p. 4) or that characterized OSHA's risk assessment 
for the proposed PEL as "speculative" (Ex. 47-35-1, p. 4) or 
"seriously flawed" (Ex. 38-106, p. 23). OSHA believes that the clear 
excess risk among workers with cumulative exposures equivalent to those 
accrued over a 45-year working lifetime of low-level exposure to 
Cr(VI), combined with the good fit of linear exposure-response models 
to the Gibb and Luippold (2003) datasets and the lack of demonstrable 
nonlinearities or dose-rate effects, constitute strong evidence of risk 
at low exposures in the range of interest to OSHA.
3. Influence of Smoking, Race, and the Healthy Worker Survivor Effect
    A common confounder in estimating lung cancer risk to workers from 
exposure to a specific agent such as Cr(VI) is the impact of cigarette 
smoking. First, cigarette smoking is known to cause lung cancer. 
Ideally, lung cancer risk attributable to smoking among the Cr(VI)-
exposed cohorts should be controlled or adjusted for in characterizing 
exposure-response. Secondly, cigarette smoking may interact with the 
agent (i.e., Cr(VI)) or its biological target (i.e., susceptible lung 
cells) in a manner that enhances or even reduces the risk of developing 
Cr(VI)-induced lung cancer from occupational exposures, yet is not 
accounted for in the risk model. The Small Business Administration's 
Office of Advocacy commented that such an interactive effect may have 
improperly increased OSHA's risk estimates (Ex. 38-7, p. 4).
    OSHA believes its risk estimates have adequately accounted for the 
potential confounding effects of cigarette smoking in the underlying 
exposure-lung cancer response data, particularly for the Gibb cohort. 
One of the key issues in this regard is whether or not the reference 
population utilized to derive the expected number of lung cancers 
appropriately reflects the smoking behavior of the cohort members. The
risk analyses of the Gibb cohort by NIOSH and Environ indicate that 
cigarette smoking was properly controlled for in the exposure-response 
modeling. NIOSH applied a smoking-specific correction factor that 
included a cumulative smoking term for individual cohort members (Ex. 
33-13). Environ applied a generic correction factor and used lung 
cancer mortality rates from Baltimore City as a reference population 
that was most similar to the cohort members with respect to smoking 
behavior and other factors that might affect lung cancer rates (Ex. 33-
12). Environ also used internally standardized models that did not 
require use of a reference population and included a smoking-specific 
(yes/no) variable. All these models predicted very similar estimates of 
risk over a wide range of Cr(VI) exposures. There was less information 
about smoking status for the Luippold cohort. However, regression 
modeling that controlled for smoking indicated that it was not a 
significant confounding factor when relating Cr(VI) exposure to the 
lung cancer mortality (Ex. 35-58).
    Smoking has been shown to interact in a synergistic manner (i.e., 
combined effect of two agents are greater than the sum of either agent 
alone) with some lung carcinogens, most notably asbestos (Ex. 35-114). 
NIOSH reported a slightly negative but nonsignficant interaction 
between cumulative Cr(VI) exposure and smoking in a model that had 
separate linear terms for both variables (Ex. 33-13). This means that, 
at any age, the smoking and Cr(VI) contributions to the lung cancer 
risk appeared to be additive, rather than synergistic, given the 
smoking information in the Gibb cohort along with the cumulative 
smoking assumptions of the analysis. In their final linear relative 
risk model, NIOSH included smoking as a multiplicative term in the 
background rate in order to estimate lifetime lung cancer risks 
attributable to Cr(VI) independent of smoking. Although this linear 
relative risk model makes no explicit assumptions with regard to an 
interaction between smoking and Cr(VI) exposure, the model does assume 
a multiplicative relationship between the background rate of lung 
cancer in the reference population and Cr(VI) exposure. Therefore, to 
the extent that smoking is a predominant influence on the background 
lung cancer risk, the linear relative risk model implicitly assumes a 
multiplicative (e.g., greater than additive and synergistic, in most 
situations) relationship between cumulative Cr(VI) exposure and 
smoking. Since current lung cancer rates reflect a mixture of smokers 
and non-smokers, OSHA agrees with the Small Business Administration's 
Office of Advocacy that the excess lung cancer risks from Cr(VI) 
exposure predicted by the linear relative risk model may overestimate 
the risks to non-smokers to some unknown extent. By the same token, the 
model may underestimate the risk from Cr(VI) exposure to heavy smokers. 
Because there were so few non-smokers in the study cohorts 
(approximately 15 percent of the exposed workers and four lung cancer 
deaths in the Gibb cohort), it was not possible to reliably estimate 
risk for the nonsmoking subpopulation.
    Although OSHA is not aware of any convincing evidence of a specific 
interaction between cigarette smoking and Cr(VI) exposure, prolonged 
cigarette smoking does have profound effects on lung structure and 
function that may indirectly influence lung cancer risk from Cr(VI) 
exposure (Ex. 33-14). Cigarette smoke is known to cause chronic 
irritation and inflammation of the respiratory tract. This leads to 
decreases in airway diameter that could result in an increase in Cr(VI) 
particulate deposition. It also leads to increased mucous volume and 
decreased mucous flow, that could result in reduced Cr(VI) particulate 
clearance. Increased deposition and reduced clearance would mean 
greater residence time of Cr(VI) particulates in the respiratory tract 
and a potentially greater probability of developing bronchogenic 
cancer. Chronic cigarette smoking also leads to lung remodeling and 
changes in the proliferative state of lung cells that could influence 
susceptibility to neoplastic transformation. While the above effects 
are plausible consequences of cigarette smoking on Cr(VI)-induced 
carcinogenesis, the likelihood and magnitude of their occurrence have 
not been firmly established and, thus, the impact on risk of lung 
cancer in exposed workers is uncertain.
    Differences in lung cancer incidence with race may also introduce 
uncertainty in risk estimates. Gibb et al. reported differing patterns 
for the cumulative exposure-lung cancer mortality response between 
whites and non-whites in their cohort of chromate production workers 
(Ex. 31-22-11). In the assessment of risk from the Gibb cohort, NIOSH 
reported a strong interaction between cumulative Cr(VI) exposure and 
race, such that nonwhites had a higher cumulative exposure coefficient 
(i.e., higher lung cancer risk) than whites based on a linear relative 
risk model (Ex. 33-13). If valid, this might explain the slightly lower 
risk estimates in the predominantly white Luippold cohort. However, 
Environ found that including race as an explanatory variable in the Cox 
proportional hazards model C1 did not significantly improve model fit 
(p=0.15) once cumulative Cr(VI) exposure and smoking status had been 
considered (Ex. 33-12).
    NIOSH suggested that exposure or smoking misclassification might 
plausibly account for the Cr(VI) exposure-related differences in lung 
cancer by race seen in the Gibb cohort (Ex. 33-13, p. 15). It is 
possible that such misclassification might have occurred as a result of 
systematic differences between whites and non-whites with respect to 
job-specific Cr(VI) exposures at the Baltimore plant, unrecorded 
exposure to Cr(VI) or other lung carcinogens when not working at the 
plant, or in smoking behavior. Unknown differences in biological 
processes critical to Cr(VI)-induced carcinogenesis could also 
plausibly account for an exposure-race interaction. However, OSHA is 
not aware of evidence that convincingly supports any of these possible 
explanations.
    Another source of uncertainty that may impact the risk estimates is 
the healthy worker survivor effect. Studies have consistently shown 
that workers with long-term employment status have lower mortality 
rates than short-term employed workers. This is possibly due to a 
higher proportion of ill individuals and those with a less healthy 
lifestyle in the short term group (Ex. 35-60). Similarly, worker 
populations tend to be healthier than the general population, which 
includes both employed and unemployed individuals. As a result, 
exposure-response analyses based on mortality of long-term healthy 
workers will tend to underestimate the risk to short-term workers and 
vice versa, even when their cumulative exposure is similar. Also, an 
increase in disease from occupational exposures in a working population 
may not be detected when workers are compared to a reference population 
that includes a greater proportion less healthy individuals.
    The healthy worker survivor effect is generally thought to be less 
of a factor in diseases with a multifactorial causation and long onset, 
such as cancer, than in diseases with a single cause or short onset. 
However, there is evidence of a healthy worker effect in several 
studies of workers exposed to Cr(VI), as discussed further in the next 
section ("Suitability of Risk Estimates for Cr(VI) Exposures in Other 
Industries"). In these studies, the healthy worker survivor effect may 
mask increased lung cancer mortality due to occupational Cr(VI) exposure.
4. Suitability of Risk Estimates for Cr(VI) Exposures in Other 
Industries
    At issue is whether the excess lung cancer risks derived from 
cohort studies of chromate production workers are representative of the 
risks for other Cr(VI)-exposed workers (e.g., electroplaters, painters, 
welders). Typically, OSHA has used epidemiologic studies from one 
industry to estimate risk for other industries. For example, OSHA 
relied on a cohort of cadmium smelter workers to estimate the excess 
lung cancer risk in a wide range of affected industries for its cadmium 
standard (57 FR at 42102, 9/14/1992). This approach is usually 
acceptable because exposure to a common agent of concern is the primary 
determinant of risk and not some other factor unique to the workplace. 
However, in the case of Cr(VI), workers in different industries are 
exposed to various Cr(VI) compounds that may differ in carcinogenic 
potency depending to a large extent on water solubility. The chromate 
production workers in the Gibb and Luippold cohorts were primarily 
exposed to certain highly water-soluble chromates. As more fully 
described in section V.B. of the Cancer Effects section, the scientific 
evidence indicates that all Cr(VI) compounds are carcinogenic but that 
the slightly soluble chromates (e.g. calcium chromate, strontium 
chromate, and some zinc chromates) exhibit greater carcinogenicity than 
the highly water soluble chromates (e.g. sodium chromate, sodium 
dichromate, and chromic acid) or the water insoluble chromates (e.g. 
lead chromates) provided the same dose is delivered and deposited in 
the respiratory tract of the worker. It is not clear from the available 
scientific evidence whether the carcinogenic potency of water-insoluble 
Cr(VI) compounds would be expected to be more or less than highly 
water-soluble Cr(VI) compounds. Therefore, OSHA finds it prudent to 
regard both types of Cr(VI) compounds to be of similar carcinogenic 
potency.
    The primary operation at the chromate production plants in 
Painesville (Luippold cohort) and Baltimore (Gibb cohort) was the 
production of the highly water-soluble sodium dichromate. Sodium 
dichromate served as a starting material for the production of other 
highly water-soluble chromates such as sodium chromate, potassium 
dichromate, and chromic acid (Exs. 7-14; 35-61). As a result, the Gibb 
and Luippold cohorts were principally exposed to water-soluble Cr(VI). 
In the NPRM, OSHA requested comment on whether its risk estimates based 
on the exposure-response data from these two cohorts of chromate 
production workers were reasonably representative of the risks expected 
from equivalent exposures to different Cr(VI) compounds encountered in 
other industry sectors. Of particular interest was whether the 
preliminary risk estimates from worker cohorts primarily engaged in the 
production of the highly water soluble sodium chromate and sodium 
dichromate would substantially overpredict lung cancer risk for workers 
with the same level and duration of exposure to Cr(VI) but involving 
different Cr(VI) compounds or different operations. These operations 
include chromic acid aerosol in electroplating operations, the less 
water soluble Cr(VI) particulates encountered during pigment production 
and painting operations, and Cr(VI) released during welding, as well as 
exposure in other applications.
    OSHA received comments on this issue from representatives of a wide 
range of industries, including chromate producers, specialty steel 
manufacturers, construction and electric power companies that engage in 
stainless steel welding, the military and aerospace industry that use 
anti-corrosive primers containing Cr(VI), the surface finishing 
industry, color pigment manufacturers, and the Small Business 
Administration's Office of Advocacy (Exs. 38-231, 38-233; 38-8; 47-5; 
40-12-4; 38-215; 40-12-5; 38-106; 39-43; 38-7). Many industry 
commenters expressed concerns about the appropriateness of the 
underlying Gibb and Luippold data sets and the methodology (e.g. linear 
instead of threshold model) used to generate the lung cancer risk 
estimates. These issues have been addressed in other parts of section 
VI. The color pigment manufacturers asserted that lead chromate 
pigments, unlike other Cr(VI) compounds, lacked carcinogenic potential. 
This issue was addressed in section V.B.9 of the Health Effects 
section. In summary, OSHA finds lead chromate and other water-insoluble 
Cr(VI) compounds to be carcinogenic. The Agency further concludes that 
it is reasonable to regard water insoluble Cr(VI) compounds to be of 
similar carcinogenic potency to highly soluble Cr(VI) compounds. Based 
on this conclusion, OSHA no longer believes that its risk projections 
will underestimate the lung cancer risk for workers exposed to 
equivalent levels of water-insoluble Cr(VI), as suggested in the NPRM 
(69 FR at 59384).
    Several commenters encouraged OSHA to rely on cohort studies that 
examined the lung cancer mortality of workers in their particular 
industry in lieu of the chromate production cohorts. Members of the 
aircraft industry and their representatives commented that OSHA failed 
to consider the results from several large cohort studies that showed 
aerospace workers were not at increased risk of lung cancer (Exs. 38-
106; 38-215-2; 44-33; 47-29-2). In addition, Boeing Corporation and the 
Aeropspace Industries Association (AIA) provided data on the size 
distribution of Cr(VI) aerosols generated during primer spraying 
operations which showed most particles to be too large for deposition 
in the region of the respiratory tract where lung cancer typically 
occurs (Exs. 38-106-2; 38-215-2; 47-29-2). The Specialty Steel Industry 
maintained that epidemiological data specific to alloy manufacturing 
and experience within the their industry show that the lung cancer risk 
estimated by OSHA is unreasonably high for steel workers exposed to the 
proposed PEL of 1 [mu]g Cr(VI)/m\3\ (Ex. 38-233, p. 82). Several 
comments argued that there was a lack of scientific evidence for a 
quantifiable exposure-response relationship between Cr(VI) exposure 
from stainless steel welding (Exs. 38-8; 38-233-4). The commenters went 
on to suggest that the OSHA quantitative Cr(VI) exposure-lung cancer 
response model derived from the chromate production cohorts should not 
be used to characterize the risk to welders. The suitability of the 
OSHA risk estimates for these particular industries is further 
discussed below.
    a. Aerospace Manufacture and Maintenance. Most of the comments on 
suitability of OSHA risk estimates were provided by AIA (Exs. 38-215; 
47-29-2), Exponent on behalf of AIA (Exs. 38-215-2; 44-33), and the 
Boeing Corporation (Exs. 38-106; 38-106-1). Cr(VI) is used as an anti-
corrosive in primers and other coatings applied to the aluminum alloy 
structural surfaces of aircraft. The principal exposures to Cr(VI) 
occur during application of Cr(VI) primers and coatings and mechanical 
sanding of the painted surfaces during aircraft maintenance. Cr(VI) 
exposures are usually in the form of the slightly soluble strontium and 
zinc chromates used in primers and chromic acid found in other 
treatments and coatings designed to protect metal surfaces.
    Cohort Studies of Aerospace Workers. AIA commented that:

    OSHA has all but ignored a substantial body of evidence of 
studies showing no increased risk of lung cancer in aerospace 
workers * * *. While epidemiologic studies show a link between lung 
cancer and chromium VI exposure in other industries [e.g. chromate 
production], that relationship is not established in the aerospace 
industry (Ex.38-106, p. 16).

Aerospace commenters pointed to several cohort studies from aircraft 
manufacturing and maintenance sites that did not find significantly 
elevated lung cancer mortality in workers (Exs. 31-16-3; 31-16-4; 35-
213; 35-210). However, OSHA believes that the vast majority of workers 
in these cohorts were not routinely engaged in jobs involving potential 
Cr(VI) exposures.
    Only two of the above studies (i.e., the Alexander and Boice 
cohorts) specifically investigated the relationship between Cr(VI) 
exposures and lung cancer mortality (Exs. 31-16-3; 31-16-4). The 
Alexander cohort was evaluated as a supplemental data set for 
quantitative risk assessment in sections VI.B.6 and VI.E.4. Briefly, 
there were 15 observed lung cancer cases in the Alexander et al. study 
with 19.5 expected (Ex. 31-16-3). There was no evidence of a positive 
trend between cumulative Cr(VI) exposure and lung cancer incidence. The 
lack of excess lung cancers was probably, in large part, due to the 
short follow-up period (median nine years per member) and young age of 
the cohort (median 42 years at the end of follow-up). Lung cancer 
generally occurs 20 or more years after initial exposure to a 
carcinogenic agent and mostly in persons aged 55 years and older. There 
was no Cr(VI) air monitoring data for a significant portion of the 
study period and reconstruction of worker exposure was reduced to a 
limited number of 'summary time-weighted average exposure levels' based 
on job category (Ex. 31-16-3). These limitations may have caused 
inaccuracies in the worker exposure estimates that could lead to 
potential misclassification of exposure, and, thus may also have 
contributed to the lack of a positive Cr(VI) exposure--lung cancer 
response.
    In the their technical comments on behalf of the AIA, Exponent 
considered the Boice cohort to be "the largest, best defined, most 
completely ascertained, and followed for the longest duration" of the 
epidemiological studies examining lung cancer mortality and other 
health outcomes of aerospace workers (Ex. 38-215-2, p. 10). The Boice 
cohort (previously described in section V.B.6) consisted of 77,965 
aerospace workers employed over a thirty-year period at a large 
aircraft manufacturing plant in California (Ex. 31-16-4). The average 
duration of employment was over ten years and thirty percent of the 
cohort was deceased. Therefore, the Boice cohort was larger, older, and 
had greater follow-up than the Alexander cohort. Unfortunately, Cr(VI) 
air measurements were sparse in recent years and entirely absent during 
early years of plant operation so, unlike the Alexander cohort, 
quantitative Cr(VI) exposure reconstruction was not attempted. Instead, 
all jobs were qualitatively categorized by the chemicals involved 
(e.g., chromates, trichloroethylene, perchloroethylene, etc.) and their 
frequency of chemical usage (routine, intermittent, or no exposure). 
Duration of potential chemical exposure, including Cr(VI), was 
determined for the cohort members based on work history (Ex. 47-19-15). 
There were 3634 workers in the cohort believed to have routine 
exposures to Cr(VI), mostly in painting/primer operations or operating 
process equipment used for plating and corrosion protection. Another 
3809 workers were thought to have potential 'intermittent exposure' to 
chromates. Most workers with potential exposure to Cr(VI) also had 
potential exposures to the chlorinated solvents tricholoroethylene 
(TCE) and perchloroethylene (PCE). Because of an inadequate amount of 
Cr(VI) exposure data, OSHA was unable to use the Boice study for 
quantitative risk assessment.
    The Boice et al. study did not find excess lung cancer among the 
45,323 aircraft factory workers when compared against the race-, age-, 
calendar year-, and gender-adjusted rates for the general population of 
the State of California (SMR=97). This is not a surprising result 
considering more than 90 percent did not work in jobs that routinely 
involve Cr(VI) exposure. Factory workers potentially exposed to Cr(VI) 
also did not have significantly elevated lung cancer mortality 
(SMR=102; 95% CI: 82-126) relative to the California general population 
based on 87 observed lung cancer deaths. However, workers engaged in 
spray painting/priming operations that likely had the highest potential 
for Cr(VI) exposure did experience some excess lung cancer mortality 
(SMR=111; 95% CI: 80-151) based on 41 deaths, but the increase was not 
statistically significant.
    As commonly encountered in factory work, there was evidence of a 
'healthy worker effect' in this aerospace cohort that became 
increasingly pronounced in workers with long-term employment. The 
healthy worker effect (HWE) refers to the lower rate of disease 
relative to the general population sometimes observed in long-term 
occupational cohorts. For example, the Boice cohort factory workers 
employed for 20 years had statistically significant lower rates of 
death than a standardized California reference population for all 
causes (SMR=78; 95% CI: 75-81), lung cancer (SMR=70; 95% CI: 61-80), 
heart disease (SMR=79; 95% CI: 74-83), cerebrovascular disease (SMR=67; 
95% CI: 56-78), non-malignant respiratory disease (SMR=65; 95% CI: 57-
74), and cirrhosis of the liver (SMR=67; 95% CI: 51-88) among other 
specific causes (Ex. 31-16-4, Table 5). The study authors note that 
"these reductions [in disease mortality] seem in part due to the 
initial selection into the workforce and the continued employment of 
healthy people [i.e. healthy worker effect] that is often found in 
occupational studies" (Ex. 31-16-4, p. 592). If not properly accounted 
for in mortality analysis, HWE can mask evidence of disease risk. Mr. 
Robert Park, senior epidemiologist from NIOSH, confirmed this at the 
public hearing when addressing implications of HWE for Cr(VI) lung 
cancer risk in the Boice cohort.

    This [Boice cohort] is a population where you would expect to 
see a very dramatic healthy worker effect * * * so just off the top, 
I would say any [relative risk] estimates for lung cancer in the 
Boice population based on SMRs, I would want to adjust upwards by 
0.9, for example, if the real SMR ought to be around 0.9 due to the 
healthy worker effect. So if you do that in their population, they 
have classified some workers as [routinely] exposed to chromates, 
about 8 percent of the population. They observe a SMR of 1.02 in 
that group. If you look at some of the other groupings in that 
study, for example, assembly has an SMR of 0.92, fabrication, which 
is basically make all the parts, 0.92, maintenance, 0.79. So a lot 
of evidence for healthy worker effect in general in that population. 
So the chromate group actually is at least 10 or 12 percent higher 
in their lung cancer SMR. Now again, the numbers are small, you'd 
have to have a very huge study for an SMR of 1.1 or 1.15 to be 
statistically significant. So it is not. But it is a hint (Tr. 345-
347).

    OSHA agrees with Mr. Park that the relative risks for lung cancer 
in the Boice cohort are likely understated due to HWE. This is also 
illustrated in the study analysis of the lung cancer morality patterns 
by exposure duration to specific chemicals using internal cohort 
comparisons. The internal analysis presumably minimize any biases (e.g. 
smoking, HWE) that might exist from comparisons to the general 
population. The results for workers potentially exposed to Cr(VI), 
trichloroethylene (TCE), and perchloroethylene (PCE) are presented in 
Table VI-9.

Click here to view table VI-9

    As shown in the table, there was a statistically significant 
decline in relative risk of lung cancer among factory workers with 
duration of TCE exposure (p< 0.01) and PCE exposure (p=0.02). This 
mirrors the decline with increasing employment duration seen in 
comparison with the general California population and strongly suggests 
the internal cohort analysis failed to adequately adjust for HWE.
    The table shows that, despite the downward influence of HWE on lung 
cancer risk, there was a slight nonsignificant upward trend in excess 
lung cancer mortality with duration of exposure to Cr(VI). The result 
is that aircraft workers potentially exposed to chromate for five or 
more years had 50 to 70 percent greater lung cancer mortality than 
coworkers with a similar duration of potential exposure to the 
chlorinated solvents. The relative excess is even more noteworthy given 
that the subgroups had considerable overlap (e.g., many of the same 
workers in the PCE and TCE groups were also in the chromate group). 
This implies that a subset of Cr(VI) workers not exposed to chlorinated 
solvents, possibly spray painters routinely applying Cr(VI) primers 
over many years, may be at greater lung cancer risk than other Cr(VI)-
exposed members of the cohort.
    The AIA and its technical representative, Exponent, objected to 
OSHA reliance on the non-statistically significant upward trend in 
excess lung cancers with increasing Cr(VI) exposure duration described 
above (Exs. 38-215-2; 47-29-2). Exponent stated:

    Statistical tests for trend indicated there is no evidence for a 
trend of increasing risk of lung cancer with increasing years 
exposed to chromate (P< 0.20). OSHA seems to have 'eye-balled' the 
estimates and felt confident accepting the slight and non-
significant increases among risk estimates with overlapping 
confidence intervals as evidence of a "slightly positive" trend. 
However, OSHA's interpretation is an overstatement of the finding 
and should be corrected in the final rule (Ex. 38-215-2, p. 13).

    OSHA does not agree with these comments and believes it has 
objectively interpreted the trend data in a scientifically legitimate 
fashion. The fact that an upward trend in lung cancer risk with Cr(VI) 
exposure duration fails to meet a statistical confidence of 95 percent 
does not mean the relationship does not exist. For example, a trend 
with a p-value of 0.2 means random chance will not explain the 
relationship 80 percent of the time. The positive trend is all the more 
notable given that it occurs in spite of a significant downward trend 
in lung cancer mortality with years of employment. In other words, 
aerospace workers exposed to Cr(VI) experienced a slightly greater lung 
cancer mortality with increasing number of years exposed even while 
their co-workers exposed to other chemicals were experiencing a 
substantially lower lung cancer mortality with increasing years 
exposed.
    In its post-hearing comments, NIOSH calculated the observed excess 
lung cancer risk to the Boice spray painters expected to have the 
highest Cr(VI) exposures (SMR=1.11) to be 21 percent higher than the 
minimally Cr(VI)-exposed assembly workers (SMR=0.92). NIOSH assumed the 
painters were exposed to 15 [mu]g CrO3/m3 (i.e., 
the arithmetic mean of Cr(VI) air sampling data in the plant between 
1978 to 1991) for 10 years (i.e., the approximate average duration of 
employment) to derive an excess risk per mg CrO3/
m3 of 1.4 (Ex. 47-19-1). NIOSH noted that this was very 
close to the excess risk per mg CrO3/m3 of 1.44 
determined from their risk modeling of the Gibb cohort (Ex. 33-13). In 
a related calculation, OSHA derived the expected excess risk ratio from 
its linear relative risk model using a dose coefficient consistent with 
the Gibb and Luippold data sets. Assuming the Boice spray painters were 
exposed to 10 [mu]g Cr(VI)/m3 (90th percentile of plant air 
sampling data converted from [mu]g CrO3 to [mu]g Cr(VI)) for 
12 years (average employment duration of Boice factory workers), the 
model predicts a risk ratio 1.20 which is also very close to the 
observed excess risk ratio of 1.21 calculated from the observed SMR 
data for spray painters above. These calculations suggest that the 
excess lung cancer mortality observed in the Boice subcohort of Cr(VI)-
exposed aerospace workers is consistent with excess risks predicted 
from models based on the Gibb and Luippold cohort of chromate 
production workers.
    The other cohort studies of aerospace workers cited by AIA were not 
informative with regard to the association between Cr(VI) and lung 
cancer. A cohort study by Garabrandt et al. of 14,067 persons employed 
by an aircraft manufacturing company found significantly reduced excess 
lung cancer mortality (SMR=80; 95% CI: 68-95) compared to adjusted 
rates in the U.S. and San Diego County populations (Ex. 35-210). The 
mean duration of follow-up was only 16 years and the study authors are 
careful to state that the study can not rule out excess risk for 
diseases, such as lung cancer, that have long latencies of 20 years or 
more. The consistently low all-cause and cancer mortalities reported in 
the study strongly suggest the presence of a healthy worker effect. 
Another cohort study by Blair et al. of 14,457 aircraft maintenance 
workers at Hill Air Force base in Utah did not find elevated lung 
cancer mortality (SMR=90; 95% CI: 60-130) when compared to the general 
population of Utah (Ex. 35-213). However, the study was exclusively 
designed to investigate cancer incidence of chlorinated solvents (e.g. 
TCE, PCE, methylene chloride) and makes no mention of Cr(VI). This was 
also the case for a cohort study by Morgan et al. of 20,508 aerospace 
workers employed at a Hughes Aircraft manufacturing
plant, which found no excess lung cancer mortality (SMR=0.96; 95% CI: 
87-106) compared to the general U.S. population. However, a detailed 
investigation of jobs at a large aircraft manufacturing facility (i.e. 
facility studied by Boice et al.) found that only about 8 percent of 
employees had potential for routine Cr(VI) exposure (Ex. 47-19-15). If 
this is representative of the workforce in the other studies cited 
above, it is doubtful whether a Cr(VI)-related increase in lung cancer 
from a small proportion of workers would be reflected in the mortality 
experience of the entire cohort, most of whom would not have been 
exposed to Cr(VI).
    In summary, OSHA does not find convincing evidence from the 
aerospace cohort studies that the Agency's quantitative risk assessment 
overstates the lung cancer risk to Cr(VI)-exposed workers. An 
association between Cr(VI) exposure and lung cancer was never addressed 
in most cohorts relied upon by the aerospace industry. Job analysis 
shows that only a minor proportion of all aerospace workers are engaged 
in workplace activities that routinely lead to Cr(VI) exposure. This 
could explain the lack of excess lung cancer mortality found in studies 
characterizing the mortality experience of all aerospace workers. 
Alexander et al. identified a cohort of Cr(VI) exposed workers, made 
individual worker estimates of cumulative Cr(VI) exposures, and found 
no exposure-related trend with lung cancer incidence. However, the 
absence of exposure-response could be the result of a number of study 
limitations including the young age of the cohort (e.g. majority of 
workers were under 50 years of age, when lung cancer incidence is 
relatively uncommon), the inadequate follow-up period (e.g. majority of 
workers followed <  10 years), and the potential for exposure 
misclassification (e.g. Cr(VI) exposure levels prior to 1975 were not 
monitored). Boice et al. also identified a subcohort of aerospace 
workers with potential Cr(VI) exposure but lacked adequate air sampling 
to investigate a quantitative relationship between Cr(VI) exposure and 
lung cancer response. There was a significant decline in relative lung 
cancer risk with length of employment among factory workers as well as 
those exposed to chlorinated solvents, indicating a strong healthy 
worker survivor effect among this pool of workers. The healthy worker 
effect may have masked a significant trend in lung cancer with Cr(VI) 
exposure duration. Risk projections based on the OSHA linear model were 
found to be statistically consistent with the relative risk ratios 
observed in the Boice cohort.
    Cr(VI) Particle Size Distribution During Aerospace Operations. 
Differences in the size of Cr(VI) aerosols generated during chromate 
production and aerospace operations is another reason representatives 
of the aircraft industry believe the OSHA risk estimates overstate risk 
to aerospace workers (Exs. 38-106; 38-106-1; 38-215-2; 39-43; 44-33; 
47-29-2). The submitted particle size data indicated that spraying 
Cr(VI) primers mostly generates large aerosol droplets (e.g.
> 10 [mu]m) not expected to penetrate beyond the very upper portions of 
the respiratory tract (e.g. nasal passages, larynx). Some aerospace 
commenters also cited research showing that the few respirable primer 
particulates that reach the lower regions of the lung contain less 
Cr(VI) per particle mass than the larger non-respirable particles (Exs. 
44-33; 38-106; 39-43). As a result, aerospace commenters contend that a 
very small proportion of Cr(VI) aerosols generated by aircraft primer 
operations deposit in the bronchioalveolar regions of the lung where 
lung cancer occurs. OSHA agrees that the particle size studies 
submitted to the record sufficiently demonstrate that a relatively 
small proportion of Cr(VI) reaches the critical regions of the lung as 
a result of these aircraft spraying operations. However, the Agency 
believes the reduction in lung cancer risk from this lower Cr(VI) 
particle burden is likely offset by the greater carcinogenic activity 
of the slightly soluble strontium and zinc chromates inhaled during 
spray primer application. Evaluation of the study data provided to the 
record and the rationale behind the OSHA position are described below.
    The Agency reviewed the information provided by Boeing on the 
particle size of paint aerosols from typical spraying equipment used in 
aerospace applications. Boeing provided size characterization of paint 
aerosol from their in-house testing of spray paint equipment (Ex. 38-
106-1, p. 8-11). They measured droplet size distributions of non-
chromated polyurethane enamels generated by high volume low pressure 
(HVLP) and electrostatic air spray guns under typical settings. The 
particle size was measured 10 to 12 inches from the nozzle of the gun 
using laser diffraction techniques. Boeing found the median volumetric 
droplet diameter (Dv50) of the paint particles to be in the range of 17 
to 32 [mu]m under the test conditions. Less than 0.5 percent of 
droplets in the spray were 5 [mu]m and smaller (e.g. typical of 
particles that deposit in the bronchioalveolar region). Boeing 
concluded:

    In typical operations and products, the best aerosol size is a 
distribution with mass median diameter of about 30-40 microns, and a 
relatively monodisperse distribution. As a result, the fraction of 
the spray that is < 5 micron is about 1% or less; in overspray 
perhaps [ap]2%. Therefore the deposited dose would be far less than 
from exposure to an equal concentration of a smaller aerosol size, 
and estimates of risk based on studies of other industry sectors are 
not relevant to evaluation of risk in aerospace paint spraying (Ex. 
38-106-1, p. 16).

Although Boeing used a non-chromated enamel paint in their studies, 
they contend that the results would be representative of the particle 
size distribution for a Cr(VI) primer using the same equipment under 
similar conditions.
    Boeing also submitted recent publications by the UCLA Center for 
Occupational and Environmental Health measuring the Cr(VI) particle 
size distribution during spray painting operations at an aerospace 
manufacturing facility (Ex. 38-106-1). The UCLA group investigated 
particle size distributions of Cr(VI) primers sprayed from HVLP 
equipment in a lab bench-scale spray booth and in a field study of 
spray booths at an aerospace facility (Ex. 38-106-1, attachment 6). The 
tested primers contained the slightly soluble strontium chromate. The 
study data are presented in two papers by Sabty-Daily et al. The 
aerosol particles were collected at different locations several meters 
from the spray gun in the bench-scale paint booth using a cascade 
impactor. Full shift personal breathing zone samples from workers 
spraying primer were also collected with a cascade impactor in the 
field studies. The mass median aerodynamic diameter (MMAD) for Cr(VI) 
particles in the field study was reported to be 8.5 [mu]m with a 
geometric standard deviation of 2.2 [mu]m. On average, 62 percent of 
the Cr(VI) mass was associated with non-respirable particles >10 [mu]m. 
Taking into account deposition efficiency, it was estimated that less 
than five percent of the Cr(VI) would potentially deposit in the lower 
regions of the respiratory tract where lung cancer occurs. The bench 
scale study gave particle distributions similar to the field studies. 
It was shown that particle size decreases slightly as gun atomization 
pressure increases. Particles in the direct spray were generally larger 
than the overspray. Particle size was shown to decrease with distance 
to the target surface due to evaporation of solvent.
    Both Sabty-Daily articles and the Boeing submission made reference 
to another study that measured particle size distribution of a HVLP-
generated paint aerosol in the breathing zone of the worker (Ex. 48-3). 
Paint droplets were collected on polycarbonate filters with 0.2 [mu]m 
pore size. Aerosol size was measured using a microscopic method that 
minimizes bias from solvent evaporation. The breathing zone MMAD in the 
overspray was reported to be 15 to 19 [mu]m with a GSD of 1.7 [mu]m. In 
another study, LaPuma et al. investigated the Cr(VI) content of primer 
particles from an HVLP spray gun using a cascade impactor (Ex. 31-2-2). 
They reported that smaller particles (i.e. < 7 [mu]m) contained 
disproportionately less Cr(VI) per mass of dry paint than larger 
particles.
    Boeing concluded that "the particle size distribution reported by 
Sabty-Daily et al. (2004a) significantly underestimate the size 
distribution of paint aerosol" (Ex. 38-106-1, p. 14). They state that 
"in typical [spraying] operations and products the best aerosol size 
is a distribution with mass median diameter of about 30-45 microns" 
(Ex. 38-106-1, p. 16). This particle size is larger than 15 to 20 [mu]m 
reported in independent breathing zone measurements of spray paint 
aerosol collected on conventional sampling media (i.e. polycarbonate 
filters) (Carlton and Flynn, 1997).
    The Boeing rationale for dismissing the UCLA data was that the 
cascade impactor had low collection efficiency for larger particles 
relative to the Boeing laser diffraction method, which Boeing believes 
is more accurate over the entire size distribution. OSHA notes, 
however, that Boeing did not characterize aerosol particles in the 
breathing zone of workers spraying Cr(VI) primer. Their study 
characterized droplet size from an non-chromated enamel spray directly 
out of the spray gun prior to contact with the target surface. While 
collection efficiency accounts for some of the particle size 
difference, other factors may also have contributed. These factors 
include the composition of the spray paint, the sampling location, and 
the degree of solvent evaporation. OSHA considers Cr(VI) primer 
droplets with an average MMAD of 7 to 20 [mu]m, as measured in 
breathing zone studies, to best represent the particle size inhaled by 
a worker during spraying operations, since this range was measured in 
breathing zone studies. The majority of these droplet particles would 
not be expected to penetrate regions of the respiratory tract where 
lung cancers occur.
    While aerosol particle size during spray application of Cr(VI) 
primers has been measured, AIA acknowledged that the particle size 
distribution during sanding procedures has not been well studied (Exs. 
38-106; 47-29-2). However, they believe that most of the particles 
released as a result of sanding and grinding operations to remove old 
paint coatings from aircraft are non-respirable (e.g. >10 [mu]m). OSHA 
is not aware of reliable data in the record to support or refute this 
claim.
    The Cr(VI) particle size data from spray primer and sanding 
applications in aerospace need to be evaluated against Cr(VI) particle 
size during chromate production to determine its impact on OSHA risk 
estimates. Boeing observed that the high temperature calcination 
process that oxidizes chromite ore to sodium chromate would likely lead 
to a high proportion of respirable fume (Ex. 38-106). During post-
hearing comments, AIA provided a figure from the 1953 U.S. Public 
Health Service survey report that indicated the geometric mean airborne 
dust particle size in a chromate production plant was 0.3 to 0.4 m in 
size (Ex. 47-29-2, p. 3). The data came from a thermal precipitator 
analysis of one-hour dust samples collected from the roasting and 
leaching areas of the plant (Ex. 7-3). An independent 1950 industrial 
hygiene survey report of the Painesville plant from the Ohio Department 
of Health indicates the median size of the in-plant dust was 1.7 
microns and the median size of the mist generated during the leaching 
operations was 3.8 microns (Ex. 7-98). The measurement method used to 
determine this particle size was not clear from the survey report.
    The thermal precipitator used by the U.S. Public Health Service 
survey is an older sampling device specifically used to characterize 
particles smaller than 5 [mu]m. The thermal precipitator collection 
efficiency for particles >5 [mu]m was considered suspect due to 
gravitational and inertial effects caused by the very low air flow 
rates (e.g. 6 ml/min) necessary to operate the device. The survey 
figure shows that 95 percent of collected particles were smaller than 1 
[mu]m. However, this is probably an inflated percentage given that the 
thermal precipitator is unable to effectively collect particles outside 
the fine and ultrafine range (e.g. greater than about 5 [mu]m).
    In their post-hearing brief, AIA introduced an Exponent microscopic 
analysis of particles claimed to be landfilled 'roast residue' 
generated as airborne dust from the Painesville plant 'decades' earlier 
(Ex. 47-29-2). AIA stated that "the particle diameters ranged from 
0.11 to 9.64 [mu]m and that 82 percent of the particles were less than 
2.5 [mu]m (Ex. 47-29-2, p. 3). OSHA was unable to verify the nature of 
the landfill dust or determine its relevance from the information 
provided by AIA.
    In the same submission, AIA referenced several experimental and 
animal studies as evidence that small particles less than 2.5 [mu]m in 
diameter cause greater lung toxicity than larger particles (Ex. 47-29-
2). AIA concluded that:

    It is important for OSHA to recognize in the quantitative risk 
assessment that the particles to which the featured chromate 
production workers were exposed were fine [particle diameters 0.1-
2.5 [mu]m] and ultrafine particles [particle diameters < 0.1 [mu]m] 
and that particles of this size range are known to be associated 
with greater toxicity than larger particles. Thus, the quantitative 
cancer risk estimates based on these studies are very conservative 
and likely overestimate risks for Cr(VI) exposures in other 
industries, most notably aerospace (Ex. 47-29-2, p. 7).

    The above studies showed that fine/ultrafine particles penetrate 
into the alveolar region of the lung, are slowly cleared from 
respiratory tract, and can lead to pulmonary inflammation and non-
neoplastic respiratory disease. OSHA agrees that fine/ultrafine 
particles can disrupt pulmonary clearance and cause chronic 
inflammation if sufficient amounts are inhaled. However, AIA did not 
provide data that demonstrated the Gibb and Luippold workers were 
routinely exposed to levels of small particles that would trigger 
serious lung toxicity.
    AIA also referred to a human epidemiological study that reported 
the excess risk of lung cancer mortality from airborne fine/ultrafine 
particles (i.e. 8 percent increase per 10 [mu]g/m\3\ in particles) to 
be similar to the excess risk of cardiopulmonary disease (i.e. 6 
percent increase with each 10 [mu]g/m\3\ in particles). AIA suggested 
these results were evidence that the excess lung cancer mortality 
attributed to Cr(VI) in chromate production cohorts were, in large 
part, due to fine/ultrafine particles. However, the Luippold cohort had 
an excess mortality from lung cancer (SMR=239) that was 10.6-fold 
higher than the excess mortality of heart disease (SMR=113) (Ex. 33-
10). The Gibb cohort had an excess mortality from lung cancer that was 
5.7-fold higher than the excess mortality of arteriosclerotic heart 
disease (SMR=114) (Ex. 33-11). These mortality patterns are not 
consistent with the small particle study results above and strongly 
indicate fine/ultrafine particles are not the primary cause of excess 
lung cancer among the chromate production workers in the Luippold and 
Gibb cohorts. Given the information provided, OSHA does not have reason 
to expect that exposure to fine/ultrafine particles in the Luippold and 
Gibb cohorts had a substantial quantitative impact on its estimates of 
lung cancer risk from exposure to Cr(VI).
    Based on the evidence presented, OSHA believes the production of 
sodium chromate and dichromate likely generated a greater proportion of 
respirable Cr(VI) particles than the aerospace spray priming 
operations. The roasting operation that oxidizes trivalent chromite ore 
and soda ash to hexavalent sodium chromate salts would be expected to 
generate a small particle fume based on information from other high 
temperature calcination processes (e.g. beryllium oxide production). 
This is supported by a small amount of particle size information from 
the 1940s and 1950s (Ex. 7-98). However, there are insufficient data to 
reliably determine the median diameter of Cr(VI) particles or otherwise 
characterize the particle size distribution generated during sodium 
chromate production in the breathing zone of the worker. It should also 
be recognized that significant Cr(VI) exposures occurred during other 
chromate production operations, such as leaching sodium chromate from 
the roast, separating sodium dichromate crystals, and drying/bagging 
the final purified sodium dichromate product. There is no information 
on particle size for these operations, but it is reasonable to expect 
greater proportions of larger particles than generated during the 
roasting process. For these reasons, there is some degree of 
uncertainty with regard to size distribution of Cr(VI) aerosols inhaled 
by chromate production workers.
    OSHA agrees with the aerospace industry that the reduced proportion 
of respirable particles from spray primer operations relative to 
chromate production will tend to lower the lung cancer risk from 
equivalent Cr(VI) exposures. This is because less Cr(VI) will reach the 
bronchioalveolar regions of the respiratory tract where lung cancer 
occurs. However, the chemical form of Cr(VI) must also be considered. 
Spray primer and painting operations expose workers to the slightly 
soluble strontium and zinc chromates while chromate production workers 
are exposed primarily to highly soluble sodium chromate/dichromate.
    As explained earlier in section V.B.9 on carcinogenic effects, 
animal and mechanistic evidence suggest that the slightly soluble 
strontium and zinc chromates are more carcinogenic than the highly 
soluble Cr(VI) compounds when equivalent doses are delivered to 
critical regions of the respiratory tract. Slightly soluble Cr(VI) 
compounds produced a higher incidence of bronchogenic tumors than 
highly soluble Cr(VI) compounds (e.g. sodium dichromate, chromic acid) 
when instilled in the respiratory tract of rats at similar dosing and 
other experimental conditions (Ex. 11-2; 11-7). For example, 
intrabronchial instillation of strontium chromate produced a 40 to 60-
fold greater tumor incidence than instillation of sodium dichromate in 
one study (Ex. 11-2). Unlike the highly soluble Cr(VI) compounds, the 
less water soluble Cr(VI) compounds are better able to provide a 
persistent source of high Cr(VI) concentration within the immediate 
microenvironment of the lung epithelia facilitating cellular uptake of 
chromate ion into target cells. The greater carcinogenicity of the 
slightly soluble Cr(VI) compounds have led to ACGIH TLVs that are from 
5-fold (i.e. zinc chromates) to 100-fold (i.e. strontium chromates) 
lower than the TLV for highly water soluble Cr(VI) compounds.
    For these reasons, the risk reductions achieved from the lower 
Cr(VI) particle burden that reaches the bronchioalveolar region of the 
lung may, to a large extent, be offset by the greater carcinogenic 
activity of the Cr(VI) compounds that are inhaled during aircraft spray 
painting operations. Since significant lung cancer risk exists at 
Cr(VI) air levels well below the new PEL (e.g. 0.5-2.5 [mu]g/m\3\) 
based on chromate production cohorts, the risk would also likely be 
significant even if the lung cancer risk from similar Cr(VI) exposures 
in aerospace operations is slightly lower. Therefore, OSHA believes 
that the risk models based on the Gibb and Luippold data sets will 
provide reasonable estimates of lung cancer risk for aerospace workers 
exposed to equivalent levels of Cr(VI). However, based on the lower 
lung burden expected after considering the particle size distribution 
evidence submitted to the record, OSHA no longer believes that its risk 
projections will underestimate lung cancer risk for aerospace workers 
exposed to strontium or zinc chromates, as suggested in the NPRM (69 FR 
at 59384).
b. Specialty Steel Industry and Stainless Steel Welding.
    Collier Shannon Scott submitted comments to OSHA on behalf of a 
group of steel and superalloy industry trade associations and companies 
including the Specialty Steel Industry of North America (SSINA), the 
Steel Manufacturers Association (SMA), and the American Iron and Steel 
Institute (AISI) as well as various individual companies. They 
requested that OSHA "seriously consider" the results of the Arena et 
al. (1998) study of workers employed in the high nickel alloys industry 
(Tr. 661), as well as studies by Huvinen et al. (1996, 2002) and Moulin 
et al. (1990) on stainless steel production workers (Exs. 38-233, p. 
85; 47-5, p. 10) and by Danielsen et al. (1996) on Norweigen stainless 
steel welders (Ex. 47-5, p. 10). On behalf of the SSINA, Ms. Joan 
Fessler testified that the Arena et al. study (Ex. 38-233-2), also 
referred to as the "Redmond Study", found no relationship between 
Cr(VI) exposure and lung cancer, and in general " * * * no strong 
epidemiological evidence causally associating occupational exposures 
with excess risk" (Tr. 662). Ms. Fessler concluded that the study 
results " * * * stand in stark contrast to the extrapolated estimates 
of cancer risk OSHA has developed from the chromate worker cohorts to 
develop the proposed rule" (Tr. 662) and "[show] that there is no 
significant excess risk of lung cancer for workers in the steel 
industry" (Ex. 40-12-4, p. 2). She cited studies conducted by Huvinen 
et al. as additional evidence that workers in the stainless steel 
production industry do not have excess risk of lung cancer from Cr(VI) 
exposure (Tr. 663).
    OSHA reviewed the Arena et al. (1998) study, which examined 
mortality in a cohort of 31,165 workers employed at 13 U.S. high nickel 
alloy plants for at least one year between 1956 and 1967 (Ex. 38-233-2, 
p. 908). The focus of the study is nickel exposure; it does not report 
how many of the cohort members were exposed to Cr(VI) or the levels of 
Cr(VI) exposure to which they may have been exposed. Therefore there 
does not appear to be any basis for SSINA's conclusion that "[t]here 
was no strong epidemiological evidence causally associating 
occupational exposures with excess risk" in the study and that "[n]o 
dose response relationship was demonstrated * * * " (Tr. 662). Ms. 
Fessler stated, in response to a question by Dr. Lurie of Public 
Citizen, that there is no information in the study on Cr(VI) exposures 
with which to assess a dose-response relationship between occupational 
exposure to Cr(VI) and excess lung cancer risk in the cohort (Tr. 685). 
Without any information on the proportion of workers that were exposed 
to Cr(VI) or the levels to which they were exposed, one cannot 
determine that there is no carcinogenic effect of Cr(VI) exposure, or 
that the results of the Arena study contradict OSHA's risk estimates.
    To more meaningfully compare the lung cancer risk predicted by 
OSHA's risk model and that observed in the Arena et al. study, OSHA 
estimated Cr(VI) exposures for the cohort members based in part on 
exposures in the stainless steel industry. High-nickel alloys that 
contain chromium are roughly comparable to stainless steel in terms of 
chromium content and the temperatures at which they are melted. This 
in turn determines the amount of trivalent chromium that converts to h
exavalent chromium in the heating process. For example, cast stainless steels 
with high nickel composition (e.g. Cast 18-38, Cast 12-60, Cast 15-65, 
and Cast 15-35) have chromium content ranging from 10-21% and have 
melting points between 2350 and 2450 degrees Fahrenheit. Other high-nickel 
alloys with chromium content, such as Hastelloy alloys C and G, Incoloy, 
Nimonic, and Inconel, range from 13 to 22% chromium (except Incoloy 804=29.7% Cr) 
with melting points of 2300-2600 degrees Fahrenheit. Stainless steels, 
in general, have 12-30% chromium content and melting points between 
2350 and 2725 degrees Fahrenheit.
    For this analysis OSHA projected that the proportion of workers in 
each production job category is approximately similar in stainless 
steel and high-nickel alloy production. For example, OSHA assumed that 
the percent of alloy production workers who are furnace operators is, 
as in steel production, about 5%. Assuming that both the Cr(VI) 
exposures typical of various production jobs and the proportion of 
workers employed in each job are roughly similar, workers in the Arena 
cohort producing high-nickel stainless steels and alloys containing 
chromium are likely to have Cr(VI) exposures comparable to those 
generally found in stainless steel production. Workers' exposures were 
estimated using the exposure profile shown in Table III-62 of the Final 
Economic Analysis section on steel mills (Ex. 49-1).
    Not all workers in the Arena et al. cohort had Cr(VI) exposures 
comparable to those in stainless steel facilities. As discussed by Ms. 
Fessler at the hearing, exposure to " * * * [c]hrome was not uniform 
in all [industries included in the study] because some of those 
industries * * * did only high nickel work or nickel mining or whatever 
specific nickel work there was" (Tr. 683). OSHA assumed that Cr(VI) 
exposures of workers producing high-nickel alloys without chromium 
content, such as Duranickel, Permanickel, Hastelloy alloys B, D, and G, 
and Monel alloys, are similar to those found in carbon steel mills and 
other non-stainless facilities, which according to comments submitted 
by Collier Shannon Scott:

    * * * may generate Cr(VI) due to trace levels of chromium in 
feedstock materials or the inadvertent melting of stainless steel 
scrap, as well as during various maintenance and welding operations 
(Ex. 38-233, p. 10).

Exposure levels for Arena cohort workers producing these alloys were 
estimated using the carbon steel exposure profile shown in Table III-64 
of the Final Economic Analysis section on steel mills (Ex. 49-1).
    Table VI-10 below shows the risk ratios (ratio of excess plus 
background cancers to background only cancers) predicted by OSHA's 
model for workers producing high-nickel alloys with and without 
chromium content. The percentage of workers with 8-hour TWA exposures 
in each range shown below are calculated for Ni-Cr alloys and non-Cr 
alloys using profiles developed for the Final Economic Analysis 
sections on stainless steel and carbon steel industries, respectively 
(Ex. 49-1). An average exposure duration of 20 years was assumed. While 
it was not clear how long workers were exposed on average, the reported 
length of follow-up in the study indicates that the duration of 
exposure was probably less than 20 years for most workers. Risk ratios 
were calculated assuming that workers were followed through age 70. The 
average age at end of follow-up was not clear from the Arena et al. 
publication. Over half of the original cohort was under 30 as of 1978, 
and follow-up ended in 1988 (Ex. 38-233-2, p. 908). Follow-up through 
age 70 may therefore lead OSHA's model to overestimate risk in this 
population, but would probably not lead to underestimation of risk.

Click here to view table VI-10

    The Arena et al. study reported lung cancer rates among white males 
(who comprised the majority of the cohort) about 2%-13% higher than 
background depending on the reference population used. The table above 
illustrates that with reasonable assumptions about exposures in the 
Arena cohort, OSHA's risk model predicts excess risks as low as those 
reported by Arena et al. OSHA's model predicts the highest risks (1-6% 
higher than background) among workers producing alloy mixtures similar 
to stainless steel in chromium content. Unfortunately, it is not clear 
from the Arena et al. publication how many of the workers were involved 
in production of chromium-containing alloys. If an even split is 
assumed between workers producing alloys with and without chromium 
content in the Arena et al. cohort, OSHA's model predicts a lung cancer 
rate between 0.8% and 3.8% higher than background.
    More precise information about the level or duration of cohort 
members' exposures might increase or decrease OSHA's model predictions 
somewhat. For example, some workers in the historical alloy industry 
would have had higher exposures than their modern-day counterparts, so 
that better exposure information may lead to somewhat higher model 
predictions. On the other hand, better information on the duration of 
exposure and workers' age at the end of follow-up would lower the model 
predictions, because this analysis made assumptions likely to 
overestimate both. The analysis presented here should be interpreted 
cautiously in light of the considerable uncertainty about the actual 
exposures to the Arena cohort members, and the fact that OSHA's model 
predictions are based on a lifetable using year 2000 U.S. all-cause 
mortality data (rather than data from the time period during which the 
cohort was followed). This analysis is not intended to provide a 
precise estimate of risk from exposure to Cr(VI) in the Arena cohort, 
but rather to demonstrate that the relatively low excess risk seen in 
the cohort is reasonably consistent with the excess risk that OSHA's 
model would predict at low exposures. It illustrates that OSHA's risk 
model does not predict far higher risk than was observed in this 
cohort. Rather, the majority of workers in alloy production would be 
predicted to have relatively low risk of occupational lung cancer based 
on their relatively low exposure to Cr(VI).
    Regarding the Huvinen et al. (1996, 2002) studies, the comments 
submitted by Collier Shannon Scott state that "there was not a 
significant increase in the incidence of any disease, including lung 
cancer, as compared to the control population" (Ex. 38-233, p. 85). 
However, the authors also noted that risk of cancer could not be 
excluded because the follow-up time was short and the exposed group was 
young and small (Ex. 38-233-3, p. 747).
    In addition to the small size (109 workers) and young age (mean 
43.3 years) of the Cr(VI)-exposed group in the Huvinen et al. study 
population, the design of this study limits its relevance to the issue 
of lung cancer risk among stainless steel workers. The subjects were 
all employed by the company at the time of the study. Individuals with 
lung cancer would be expected to leave active employment, and would not 
have been surveyed in the study. The authors made only a limited 
attempt to track former workers: Those who met the study criteria of 8 
years' employment in a single production department were surveyed by 
mailed questionnaire (Ex. 38-233-3, p. 743), and no follow-up on 
nonrespondents was reported. A second study conducted on the original 
study group five years later was again limited to employed workers, as 
those who had left the company " * * * could not be contacted" (Ex. 
38-233-3, p. 204). Due to the short follow-up period and the 
restriction to living workers (still employed or survey respondents), 
these studies are not well suited to identify lung cancer cases.
    Post-hearing comments stated that " * * * OSHA has failed to even 
consider specific epidemiological studies performed on stainless steel 
production workers and welders that would be far more relevant than the 
chromate production studies OSHA relied upon for its analysis" (Ex. 
47-5, p. 10). In particular, they suggest that OSHA should consider a 
study by Danielsen et al. (1996) on Norweigian boiler welders and a 
study by Moulin et al. (1990) on French stainless steel production 
workers (Ex. 47-5, p. 10). However, the Moulin et al. study (Ex. 35-
282), was discussed in the Preamble to the Proposed Rule (69 FR at 
59339). OSHA concluded that the association between Cr(VI) and 
respiratory tract cancer in this and similar studies is difficult to 
assess because of co-exposures to other potential carcinogens such as 
asbestos, polycyclic aromatic hydrocarbons, nickel, and the lack of 
information on smoking (69 FR at 59339).
    The Danielsen et al. study was not evaluated in the NPRM, but is 
similar to other studies of welders evaluated by OSHA in which excess 
risk of lung cancer did not appear to be associated with stainless 
steel welding. In Danielsen et al., as in most other welding studies, 
no quantitative information on Cr(VI) exposure was available, there was 
potential confounding by smoking and asbestos exposure, and there 
appeared to be an overall healthy worker effect in the study (625 
deaths vs. 659 expected). Therefore, OSHA does not believe that 
Danielsen et al. contributes significant information beyond that in the 
studies that are reviewed in Section V.B.4 of this preamble. OSHA's 
interpretation and conclusions regarding the general findings of 
welding cohort studies, discussed below in the context of comments 
submitted by the Electric Power Research Institute, apply to the 
results of Danielsen et al. as well.
    The Electric Power Research Institute (EPRI), Exponent, and others 
submitted comments to OSHA that questioned whether the Agency's 
exposure-response model, based on the Gibb and Luippold chromate 
production industry cohorts, should be used to estimate lung cancer 
risks to welders exposed to Cr(VI) (Exs. 38-8; 38-233-4; 39-25, pp. 2-
3). EPRI stated that:

    OSHA's review of the toxicology, epidemiology, and mechanistic 
data associated with health effects among welders was thorough and 
accurate. We concur with the selection of the two focus cohorts 
(Luippold et al. 2003 and Gibb et al. 2000) as the best data 
available upon which to base an estimate of the exposure-response 
relationship between occupational exposure to Cr(VI) and an 
increased lung cancer risk"; however * * * it may be questionable 
whether that relationship should be used for stainless steel welders 
given that a positive relationship between exposure to Cr(VI) and 
lung cancer risk was not observed in most studies of welder cohorts 
(Ex. 38-8, pp. 6-7).

EPRI's concerns, like other comments submitted to OSHA on risk to 
welders, are based primarily on the results of the Gerin et al. (1993) 
study and on several studies comparing stainless steel and mild steel 
welders.
    As discussed above in Section V., Gerin et al. (1993) is the only 
available study that attempts to relate estimated cumulative Cr(VI) 
exposure and lung cancer risk among welders. While excess lung cancer 
risks were found among stainless steel welders, there was no clear 
relationship observed between the estimated amount of Cr(VI) exposure 
and lung cancer (Ex. 38-8, p. 8). This led the authors to suggest that 
the elevated risks might be " * * * related to other exposures such as 
cigarette smoking, background asbestos exposure at work or other 
occupational or environmental risks * * * " rather than to Cr(VI) 
exposure. On the other hand, Gerin et al. stated that " * * * the 
welding fume exposures in these populations may be too low to demonstrate 
a gradient of risk", or misclassification of exposure might obscure the 
dose-response relationship (Ex. 7-120, pp. S25-S26), a point with which EPRI 
expressed agreement (Ex. 38-8, p. 8).
    OSHA agrees with Gerin et al. that co-exposures to carcinogens such 
as nickel, asbestos, and cigarette smoke may have contributed to the 
elevated lung cancer risks among welders. OSHA also agrees with the 
authors that exposure misclassification may explain the absence of a 
clear relationship between Cr(VI) and lung cancer in this study. Gerin 
et al. derived their exposure data primarily from literature on welding 
fume, as well as from a limited number of industrial hygiene 
measurements taken in the mid 1970s in eight of the 135 companies 
participating in the study (Ex. 7-120, p. S24, p. S27). Their exposure 
estimates took account of the welding process used and the base metal 
welded by individuals in the cohort, but they apparently had no 
information on other important items, such as the size of the work 
piece and weld time, which were identified by EPRI as factors affecting 
the level of Cr(VI) exposure from welding (Ex. 38-8, p. 5).
    EPRI also identified ventilation as a particularly important 
determinant of exposure (Ex. 38-8, p. 5). Gerin et al. did not appear 
to have individual information on ventilation use for their exposure 
estimates, relying instead on "information on the history of welding 
practice * * * obtained from each company on the basis of an ad hoc 
questionnaire" that described for each company the average percent of 
time that welders used local ventilation, operated in confined or open 
areas, and worked indoors or outdoors (Ex. 7-120, p. S23). The use of 
local ventilation, time spent welding in confined areas, and time spent 
welding outdoors may have varied considerably from worker to worker 
within any single company. In this case exposure estimates based on 
company average information would tend to overestimate exposure for 
some workers and underestimate it for others, thus weakening the 
appearance of an exposure-response relationship in the cohort.
    Gerin et al. also stated that the average exposure values they 
estimated do not account for a number of factors which affect welders' 
exposure levels, including " * * * type of activity (e.g. maintenance, 
various types of production), special processes, arcing time, voltage 
and current characteristics, welder position, use of special electrodes 
or rods, presence of primer paints and background fumes coming from 
other activities" (Ex. 7-120, p. S25). They noted that the resulting 
difficulty in the construction of individual exposure estimates is 
exacerbated by aggregation of data across small cohorts from many 
different companies that may have different exposure conditions (Ex. 7-
120, p. S25). According to Gerin et al., exposure misclassification of 
this sort may have obscured a dose-response relationship in this cohort 
(Ex. 7-120, p. S25). The authors suggest that their estimates should be 
checked or corrected " * * * with data coming from well-documented 
industrial hygiene studies or industrial hygiene data banks including 
information on the major relevant factors" (Ex. 7-120, p. S26). OSHA 
believes that there is insufficient information to determine why a 
clear relationship between Cr(VI) exposure and lung cancer is not 
observed in the Gerin et al. study, but agrees with the authors that 
exposure misclassification and the influence of background exposures 
may explain this result.
    EPRI noted the apparent lack of a relationship between exposure 
duration and lung cancer risk in the Gerin et al. cohort (Ex. 38-8, p. 
10). Duration of exposure is expected to show a relationship with 
cancer risk if duration serves as a reasonable proxy for a measure of 
exposure (e.g. cumulative exposure) that is related to risk. Since 
cumulative exposure is equal to exposure duration multiplied by average 
exposure level, duration of exposure may correlate reasonably well with 
cumulative exposure if average exposure levels are similar across 
workers, or if workers with longer employment tend to have higher 
average exposure levels. In a cohort where exposure duration is 
believed to correlate well with cumulative exposure, the absence of a 
relationship between exposure duration and disease risk could be 
interpreted as evidence against a relationship between cumulative 
exposure and risk.
    High variation in average exposures among workers, unrelated to the 
duration of their employment, would tend to reduce the correlation 
between exposure duration and cumulative exposure. If, as EPRI states, 
Cr(VI) exposure depends strongly on process, base metal, and other work 
conditions that vary from workplace to workplace, then duration of 
exposure may not correlate well with cumulative exposure across the 135 
companies included in the Gerin et al. study. The lack of a positive 
relationship between exposure duration and lung cancer in the Gerin et 
al. cohort may therefore signify that duration of exposure is not a 
good proxy for the amount of exposure accumulated by workers, and 
should not be interpreted as evidence against an exposure-response 
relationship.
    In post-hearing comments Mr. Robert Park of NIOSH discussed other 
issues related to exposure duration in the Gerin et al. and other 
welding cohorts:

    Several factors may impact the interpretation of [the Gerin et 
al. (1993) and Simonato et al. (1991) welder cohort studies] and are 
consistent with an underlying risk associated with duration * * *. 
The healthy worker survivor effect is a form of confounding in which 
workers with long employment durations systematically diverge from 
the overall worker population on risk factors for mortality. For 
example, because smoking is a risk factor for disease, disability 
and death, long duration workers would tend to have a lower smoking 
prevalence, and hence lower expected rates of diseases that are 
smoking related, like lung cancer. Not taking this into account 
among welders might result in long duration welders appearing to 
have diminished excess risk when, in fact, excess risk continues to 
increase with time (Ex. 47-19-1, p. 6).

Mr. Park also emphasized the special importance of detailed information 
for individual workers in multi-employer studies with exposure 
conditions that vary widely across employers. He notes that high worker 
turnover in highly exposed jobs " * * * could result in long duration 
welding employment appearing to have lower risk than some shorter 
duration [welding] employment when it does not" (Ex. 47-19-1, p. 6).
    EPRI compared the risk of lung cancer among a subset of workers in 
the Gerin cohort exposed to high cumulative levels of Cr(VI) to the 
risk found among chromate production workers in the Gibb et al. and 
Luippold et al. studies. "Focusing on the highest exposure group, SMRs 
for the cohorts of stainless steel workers studied by Gerin et al 
(1993) * * * range from 133 to 148 for exposures >1.5 mg-yrs/m\3\ * * 
*. By comparison, the SMR from the Luippold et al. (2003) cohort is 365 
for cumulative exposures of 1.0 to 2.69 mg-yrs/m\3\", a difference 
that EPRI argues " * * * draws into question whether the exposure-
specific risk estimates from the chromate production industry can be 
extrapolated to welders" (Ex. 38-8, p. 25). It is not clear why EPRI 
chose to focus on the high exposure group, which had a minimum of 1.5 
mg/m\3\-years cumulative Cr(VI) exposure, a mean of 2.5 mg/m\3\-years, 
and no defined upper limit. Compared to the other exposure groups 
described by Gerin et al., this group is likely to have had more 
heterogenous exposure levels; may be expected to have a stronger
healthy worker effect due to the association between high cumulative 
exposure and long employment history; and is the least comparable to 
either workers exposed for a working lifetime at the proposed PEL (1 
[mu]g/m\3\ * 45 years = 0.045 mg/m\3\-years cumulative exposure) or 
welders in modern-day working conditions, who according to an IARC 
review cited in EPRI's comments typically have exposure levels less 
than 10 [mu]g/m\3\ (<  0.45 mg/m\3\-years cumulative exposure over 45 
years) (Ex. 38-8, p. 4). In addition, the majority of the observation 
time in the Luippold et al. cohort and the vast majority in the Gibb et 
al. cohort is associated with exposure estimates lower than 1.5 mg/
m\3\-years Cr(VI) (Ex. 33-10, p. 455, Table 3; 25, p. 122, Table VI).
    It should be noted that the levels of excess lung cancer risk 
observed among welders in the Gerin et al. cohort and chromate 
production workers in the Gibb and Luippold cohorts are quite similar 
at lower cumulative exposure ranges that are more typical of Cr(VI) 
exposures experienced in the cohorts. For example, the group of welders 
with estimated cumulative exposures ranging from 50 to 500 [mu]g-yrs/
m\3\ has an SMR of 230. Chromate production workers from the Gibb and 
Luippold cohorts with cumulative exposures within this range have 
comparable SMRs, ranging from 184 to 234, as shown in Table VI-11 
below. For reference, 45 years of occupational exposure at 
approximately 1.1 [mu]g/m\3\ Cr(VI) would result in a cumulative 
exposure of 50 [mu]g-yrs/m\3\; 45 years of occupational exposure at 
approximately 11.1 [mu]g/m\3\ Cr(VI) would result in a cumulative 
exposure of 500 [mu]g-yrs/m\3\.

Click here to view table VI-11

    OSHA performed an analysis comparing the risks predicted by OSHA's 
models, based on the Gibb and Luippold data collected on chromate 
production workers, with the lung cancer deaths reported for the 
welders in the Gerin et al. study. Gerin et al. presented observed and 
expected lung cancer deaths for four categories of cumulative exposure: 
< 50 [mu]g-yrs/m\3\, 50-500 [mu]g-yrs/m\3\, 500-1500 [mu]g-yrs/m\3\, and 
1500+ [mu]g-yrs/m\3\. The great majority of the Gerin et al. data on 
stainless steel welders (98% of person-years) are in the highest three 
categories, while the lowest category is extremely small (< 300 person-
years of observation). OSHA's preferred risk models (based on the Gibb 
and Luippold cohorts) were used to predict lung cancer risk for each of 
the three larger exposure categories. The OSHA predictions were derived 
using the mean values from each exposure range, except for the open-
ended highest category, for which Gerin et al. reported a mean exposure 
level of 2500 [mu]g-yrs/m\3\ (Ex. 7-120, p. S26). The ratio of 
predicted to background lung cancer deaths, which approximately 
characterizes the expected SMRs for these exposure groups, was 
calculated for each group.
    The OSHA model predictions were calculated assuming that workers 
were first exposed to Cr(VI) at age 29, the average age at the start of 
employment reported by Gerin et al. (Ex. 7-120, p. S26). The SMRs 
reported by Gerin et al. were calculated for welders with at least five 
years of employment and at least 20 years of follow-up. However, the 
average duration of employment and follow-up was not evident from the 
publication. The OSHA model predictions were therefore calculated using 
a range of reasonable assumptions about the duration of employment over 
which workers were exposed (5, 10, 15, and 20 years) and the length of 
follow-up (30, 40, and 50 years).
    Table VI-12 below presents the SMRs reported by Gerin et al. for 
stainless steel welders in the three highest exposure categories, 
together with the ratio of predicted to background lung cancer deaths 
from OSHA's risk models. It should be noted that the ratio was 
calculated using year 2000 U.S. lung cancer mortality rates, while the 
SMRs reported by Gerin et al. were calculated using national lung 
cancer mortality rates for the nine European countries represented in 
the study (Ex. 7-114).

Click here to view table VI-12

    Table VI-12 shows that the range of risk ratios predicted by OSHA's 
model is higher than the ratios reported for the highest exposure group 
in the Gerin et al. cohort, consistent with EPRI's observations (Ex. 
38-8, p. 25). However, the risk ratios predicted by OSHA's model are 
consistent with the Gerin SMRs for the 500-1500 [mu]g-yrs/m\3\ 
cumulative exposure range. For the 50-500 [mu]g-yrs/m\3\ cumulative 
exposure range, the OSHA prediction falls slightly below the lung 
cancer mortality ratio observed for the Gerin et al. cohort. The OSHA 
predictions for each group overlap with the 95% confidence intervals of 
the Gerin et al. SMRs, suggesting that sampling error may partly 
account for the discrepancies between the observed and predicted risk 
ratios in the lowest and highest exposure groups.
    As previously discussed, OSHA believes that the lack of a clear 
exposure-response trend in the Gerin et al. study may be partly 
explained by exposure misclassification. As shown in Table VI-12, the 
highest exposure group has lower risk than might be expected based on 
OSHA's preferred risk models, while the lowest exposure group appears 
to have higher risk than OSHA's models would predict. This overall 
pattern of generally elevated but non-increasing SMRs across the three 
larger exposure groups in the Gerin study is consistent with 
potentially severe exposure misclassification. The higher-than-
predicted risks among welders in the lowest exposure group could 
similarly reflect misclassification. However, it is not possible to 
determine with certainty that exposure misclassification is the cause 
of the differences between the risk predicted by OSHA's model and that 
observed in the Gerin cohort.
    Finally, EPRI cites the generally similar relative risks found 
among stainless steel and mild steel welders as further evidence that 
exposure to Cr(VI) may not carry the same risk of lung cancer in 
welding operations as it does in the chromate production industry. EPRI 
states:

    [I]t is reasonable to expect that if Cr(VI) were a relevant risk 
factor for welders in the development of lung cancer, and certain 
types of welding involve Cr(VI) more than other types, then 
subgroups of welders who are more exposed to Cr(VI) by virtue of the 
type of welding they do should have higher rates of lung cancer than 
welders not exposed to Cr(VI) in their welding occupation;

in particular, " * * *stainless steel welders should have a higher 
risk of lung cancer than welders of mild steel" (Ex. 38-8, p. 13). 
OSHA believes that EPRI's point would be correct if the subgroups in 
question are similar in terms of other important risk factors for lung 
cancer, such as smoking, co-exposures, and overall population health. 
However, no analysis comparing stainless steel welders with mild steel 
welders has properly controlled for these factors, and in fact there 
have been indications that mild steel welders may be at greater risk of 
lung cancer than stainless steel welders from non-occupational causes. 
As discussed by EPRI, "[r]esults from cohort studies of stainless 
steel welders with SMRs much less than 100 support an argument that the 
healthy worker effect might be more marked among stainless steel 
workers compared to mild steel welders'; also " * * *stainless steel 
welders are generally more qualified and paid more than other welders" 
(Ex. 38-8, p. 16), a socioeconomic factor that suggests possible 
differences in lung cancer risk due to smoking, community exposures, or 
occupational exposures from employment other than welding.
    Comments submitted by Exponent (Ex. 38-233-4) and EPRI (Ex. 38-8) 
compare the Cr(VI) compounds found in welding fumes and those found in 
the chromate production environments of the Gibb and Luippold cohorts. 
Exponent stated that "[t]he forms of Cr(VI) to which chromate 
production workers were historically exposed are primarily the soluble 
potassium and sodium chromates" found in stainless steel welding 
fumes. Less soluble forms of Cr(VI) are also found in stainless steel 
welding fumes in limited amounts, as discussed in the 1990 IARC 
monograph on welding (Ex. 35-242, p. 460), and are believed to have 
been present in limited amounts at the plants where the Gibb and 
Luippold workers were employed (Ex. 38-233-4, p. 4). Exponent concludes 
that, while it is difficult to compare the exposures of welders to 
chromate production workers, " * * *there is no obvious difference * * 
* in solubility * * * " that would lead to a significantly lesser risk 
from Cr(VI) exposure in welding as compared to the Gibb and Luippold 
cohort exposures (Ex. 38-233-4, p. 3, p. 11). OSHA believes that the 
similarity in the solubility of Cr(VI) exposures to welders and 
chromate production workers supports the Agency's use of its risk model 
to describe Cr(VI)-related risks to welders.
    Exponent and others (Exs. 38-8; 39-25) commented on the possibility 
that the bioavailability of Cr(VI) may nevertheless differ between 
welders and chromate production workers, stating that " * * * 
bioavailability of Cr(VI)-containing particles from welding fumes may 
not be specifically related to solubility of the Cr(VI) chemical 
species in the fume" (Ex. 38-233-4, p. 11). In this case, Exponent 
argues,

delivered doses of Cr(VI) to the lung could be quite dissimilar 
among welders as compared to chromate production industry workers 
exposed to the same Cr(VI) chemical species at the same Cr(VI) 
airborne concentrations (Ex. 38-233-4, p. 11).

However, Exponent provided no data or plausible rationale that would 
support a Cr(VI) bioavailability difference between chromate production 
and welding. The low proportion of respirable Cr(VI) particles that 
apparently limits bioavailability of inhaled Cr(VI) during aircraft 
spray priming operations described previously is not an issue with 
welding. High temperature welding generates fumes of small
respirable-size Cr(VI) particles able to penetrate the bronchoalveolar 
region of the lung. OSHA finds no evidence indicating that Cr(VI) from 
welding is less bioavailable than Cr(VI) from soluble chromate 
production.
    In summary, OSHA agrees with EPRI and other commenters that 
evidence of an exposure-response relationship is not as strong in 
studies of Cr(VI)-exposed welders compared to studies of chromate 
production workers. OSHA believes that the available welding studies 
are less able to detect an exposure-response relationship, due to the 
potentially severe exposure misclassification, occupational exposure to 
other cancer causing agents, and the general lack of information with 
which to control for any differences in background lung cancer risk 
between Cr(VI)-exposed and unexposed welders. In contrast, the two 
featured cohorts had sufficient information on workers' Cr(VI) 
exposures and potential confounding exposures to support a reliable 
exposure-response assessment. These are the primary factors that led 
OSHA to determine (like EPRI and Exponent) that the Luippold and Gibb 
cohorts are the best data available on which to base a model of 
exposure-response between Cr(VI) and lung cancer (Exs. 38-8, p. 6; 38-
233-4, p. 1). Moreover, EPRI admitted that examination of " * * * the 
forms of Cr(VI) to which welders are exposed, exposure concentrations, 
and other considerations such as particle size * * * " identified " * 
* * no specific basis * * * " for a difference in Cr(VI)-related lung 
cancer risk among welders and the Gibb and Luippold chromate production 
cohorts (Ex. 38-8, p. 7). OSHA concludes that it is reasonable and 
prudent to estimate welders' risk using the exposure-response model 
developed on the basis of the Gibb et al. and Luippold et al. datasets.

H. Conclusions

    OSHA believes that the best quantitative estimates of excess 
lifetime lung cancer risks are those derived from the data sets 
described by Gibb et al. and Luippold et al. Both data sets show a 
significant positive trend in lung cancer mortality with increasing 
cumulative Cr(VI) exposure. The exposure assessments for these two 
cohorts were reconstructed from air measurements and job histories over 
three or four decades and were superior to those of other worker 
cohorts. The linear relative risk model generally provided the best fit 
among a variety of different models applied to the Gibb et al. and 
Luippold et al. data sets. It also provided an adequate fit to three 
additional data sets (Mancuso, Hayes et al., and Gerin et al.). Thus, 
OSHA believes the linear relative risk model is the most appropriate 
model to estimate excess lifetime risk from occupational exposure to 
Cr(VI). Using the Gibb et al. and Luippold et al. datasets and a linear 
relative risk model, OSHA concludes that the lifetime lung cancer risk 
is best expressed by the three-to five-fold range of risk projections 
bounded by the maximum likelihood estimates from the two featured data 
sets. This range of projected risks is within the 95 percent confidence 
intervals from all five data sets.
    OSHA does not believe that it is appropriate to employ a threshold 
dose-response approach to estimate cancer risk from a genotoxic 
carcinogen, such as Cr(VI). Federal agencies, including OSHA, assume an 
exposure threshold for cancer risk assessments to genotoxic agents only 
when there is convincing evidence that such a threshold exists (see 
e.g. EPA, Guidelines for Carcinogen Risk Assessment, March 2005, pp. 3-
21). In addition, OSHA does not consider absence of a statistically 
significant effect in an epidemiologic or animal study that lacks power 
to detect such effects to be convincing evidence of a threshold or 
other non-linearity. OSHA also does not consider theoretical reduction 
capacities determined in vitro with preparations that do not fully 
represent physiological conditions within the respiratory tract to be 
convincing evidence of a threshold. While physiological defense 
mechanisms (e.g. extracellular reduction, DNA repair, apoptosis) can 
potentially introduce dose transitions, there is no evidence of a 
significantly non-linear Cr(VI) dose-lung cancer response in the 
exposures of interest to OSHA. Finally, as previously discussed, linear 
no-threshold risk models adequately fit the existing exposure-response 
data.
    The slightly soluble Cr(VI) compounds produced a higher incidence 
of respiratory tract tumors than highly water soluble or highly water 
insoluble Cr(VI) compounds in animal studies that tested Cr(VI) 
compounds under similar experimental conditions. This likely reflects 
the greater tendency for chromates of intermediate water solubility to 
provide a persistent high local concentration of solubilized Cr(VI) in 
close proximity to the target cell. Highly soluble chromates rapidly 
dissolve and diffuse in the aqueous fluid lining the epithelia of the 
lung and are more quickly cleared from the respiratory tract. Thus, 
these chromates are less able to achieve the higher and more persistent 
local concentrations within close proximity of the lung cell surface 
than the slightly water soluble chromates. Water insoluble Cr(VI) 
particulates are also able to come in close contact with the lung cell 
surface but do not release readily absorbed chromate ions into the 
biological environment as rapidly. OSHA concludes that slightly soluble 
Cr(VI) compounds are likely to exhibit a greater degree of 
carcinogenicity than highly water soluble or water insoluble Cr(VI) 
when the same dose is delivered to critical target cells in the 
respiratory tract of the exposed worker. OSHA also believes it 
reasonable to regard water insoluble Cr(VI) to be of similar 
carcinogenic potency to highly water soluble Cr(VI) compounds in the 
absence of convincing scientific evidence to indicate otherwise.
    The Gibb and Luippold cohorts were predominantly exposed to highly 
water-soluble chromates, particularly sodium chromate and dichromate. 
After evaluating lung cancer rates in other occupational cohort studies 
with respect to the forms of Cr(VI) in the workplace, reliability in 
the Cr(VI) exposure data, and the presence of potentially confounding 
influences (e.g. smoking) and bias (e.g. healthy worker survivor bias) 
as well as information on solubility, particle size, cell uptake, and 
other factors influencing delivery of Cr(VI) to lung cells, OSHA finds 
the risks estimated from the Gibb and Luippold cohorts adequately 
represent risks to workers exposed to equivalent levels of Cr(VI) 
compounds in other industries.
    As with any risk assessment, there is some degree of uncertainty in 
the projection of risks that results from the data, assumptions, and 
methodology used in the analysis. The exposure estimates in the Gibb et 
al. and Luippold et al. data sets relied, to some extent, on a paucity 
of air measurements using less desirable sampling techniques to 
reconstruct Cr(VI) exposures, particularly in the 1940s and 1950s. 
Additional uncertainty is introduced when extrapolating from the cohort 
exposures, which usually involved exposures to higher Cr(VI) levels for 
shorter periods of time to an equivalent cumulative exposure involving 
a lower level of exposure for a working lifetime. The study cohorts 
consisted mostly of smokers, but detailed information on their smoking 
behavior was unavailable. While the risk assessments make some 
adjustments for the confounding effects of smoking, it is unknown 
whether the assessments fully account for any interactive effects that 
smoking and Cr(VI) exposure may have on
carcinogenic action. In any case, OSHA does not have reason to believe 
the above uncertainties would introduce errors that would result in 
serious overprediction or underprediction of risk.
    OSHA's estimate of lung cancer risk from a 45 year occupational 
exposure to Cr(VI) at the previous PEL of 52 [mu]g/m\3\ is 101 to 351 
excess deaths per 1000 workers. This range, which is defined by maximum 
likelihood estimates based on the Gibb and Luippold epidemiological 
cohorts, is OSHA's best estimate of excess risk. It does not account 
for statistical uncertainty, or for other potential sources of 
uncertainty or bias. The wider range of 62 to 493 excess deaths per 
1000 represents the statistical uncertainty associated with OSHA's 
excess risk estimate at the previous PEL, based on lowest and highest 
95% confidence bounds on the maximum likelihood estimates for the two 
featured data sets. The excess lung cancer risks at alternative 8 hour 
TWA PELs that were under consideration by the Agency were previously 
shown in Table VI-7, together with the uncertainty bounds for the 
primary and supplemental studies at these exposure concentrations. The 
45-year exposure estimates satisfy the Agency's statutory obligation to 
consider the risk of material impairment for an employee with regular 
exposure to the hazardous agent for the period of his working life (29 
U.S.C. 651 et seq.). Occupational risks from Cr(VI) exposure to less 
than a full working lifetime are considered in Section VII on the 
Significance of Risk and in Section VIII on the Benefits Analysis.

VII. Significance of Risk

    In promulgating health standards, OSHA uses the best available 
information to evaluate the risk associated with occupational 
exposures, to determine whether this risk is severe enough to warrant 
regulatory action, and to determine whether a new or revised rule will 
substantially reduce this risk. OSHA makes these findings, referred to 
as the "significant risk determination", based on the requirements of 
the OSH Act and the Supreme Court's interpretation of the Act in the 
"benzene" decision of 1980 (Industrial Union Department, AFL-CIO v. 
American Petroleum Institute, 448 U.S. 607). The OSH Act directs the 
Secretary of Labor to:

    set the standard which most adequately assures, to the extent 
feasible, on the basis of the best available evidence, that no 
employee will suffer material impairment of health or functional 
capacity even if such employee has regular exposure to the hazard * 
* * for the period of his working life [6(b)(5)].

OSHA's authority to promulgate regulations to protect workers is 
limited by the requirement that standards be "reasonably necessary and 
appropriate to provide safe or healthful employment" [3(8)].
    In the benzene decision, the Supreme Court's interpretation of 
Section 3(8) further defined OSHA's regulatory authority. The Court 
stated:

    By empowering the Secretary to promulgate standards that are 
"reasonably necessary or appropriate to provide safe or healthful 
employment and places of employment," the Act implies that, before 
promulgating any standard, the Secretary must make a finding that 
the workplaces in question are not safe (IUD v. API 448 U.S. at 
642).

    "But 'safe' is not the equivalent of 'risk-free' ", the Court 
maintained. "[T]he Secretary is required to make a threshold finding 
that a place of employment is unsafe-in the sense that significant 
risks are present and can be eliminated or lessened by a change in 
practices" (IUD v. API, 448 U.S. at 642). It has been Agency practice 
in regulating health hazards to establish this finding by estimating 
risk to workers using quantitative risk assessment, and determining the 
significance of this risk based on judicial guidance, the language of 
the OSH Act, and Agency policy considerations.
    The Agency has considerable latitude in defining significant risk 
and in determining the significance of any particular risk. The Court 
did not stipulate a means to distinguish significant from insignificant 
risks, but rather instructed OSHA to develop a reasonable approach to 
the significant risk determination. The Court stated that "it is the 
Agency's responsibility to determine in the first instance what it 
considers to be a 'significant' risk", and it did not express "any 
opinion on the* * *difficult question of what factual determinations 
would warrant a conclusion that significant risks are present which 
make promulgation of a new standard reasonably necessary or 
appropriate" (448 U.S. at 659). The Court also stated that, while 
OSHA's significant risk determination must be supported by substantial 
evidence, the Agency "is not required to support the finding that a 
significant risk exists with anything approaching scientific 
certainty" (448 U.S. at 656). Furthermore,

    A reviewing court [is] to give OSHA some leeway where its 
findings must be made on the frontiers of scientific knowledge [and] 
* * * the Agency is free to use conservative assumptions in 
interpreting the data with respect to carcinogens, risking error on 
the side of overprotection rather than underprotection [so long as 
such assumptions are based on] a body of reputable scientific 
thought (448 U.S. at 655, 656).

    To make the significance of risk determination for a new or 
proposed standard, OSHA uses the best available scientific evidence to 
identify material health impairments associated with potentially 
hazardous occupational exposures, and, when possible, to provide a 
quantitative assessment of exposed workers' risk of these impairments. 
OSHA has reviewed extensive epidemiological and experimental research 
pertaining to adverse health effects of occupational Cr(VI) exposure, 
including lung cancer, and has established quantitative estimates of 
the excess lung cancer risk associated with previously allowable Cr(VI) 
exposure concentrations and the expected impact of the new PEL. OSHA 
has determined that long-term exposure at the previous PEL would pose a 
significant risk to workers' health, and that adoption of the new PEL 
and other provisions of the final rule will substantially reduce this 
risk.

A. Material Impairment of Health

    As discussed in Section V of this preamble, there is convincing 
evidence that exposure to Cr(VI) may cause a variety of adverse health 
effects, including lung cancer, nasal tissue damage, asthma, and 
dermatitis. OSHA considers these conditions to be material impairments 
of health, as they are marked by significant discomfort and long-
lasting adverse effects, can have adverse occupational and social 
consequences, and may in some cases have permanent or potentially life-
threatening consequences. Based on this finding and on the scientific 
evidence linking occupational Cr(VI) to each of these effects, OSHA 
concludes that exposure to Cr(VI) causes "material impairment of 
health or functional capacity" within the meaning of the OSH Act.
1. Lung Cancer
    OSHA considers lung cancer, an irreversible and frequently fatal 
disease, to be a clear material impairment of health. OSHA's finding 
that inhaled Cr(VI) causes lung cancer is based on the best available 
epidemiological data, reflects substantial evidence from animal and 
mechanistic research, and is consistent with the conclusions of other 
government and public health organizations, including NIOSH, EPA,
ACGIH, NTP, and IARC (Exs. 35-117; 35-52; 35-158; 17-9-D; 18-3, p. 
213). The Agency's primary evidence comes from two epidemiological 
studies that show significantly increased incidence of lung cancer 
among workers in the chromate production industry (Exs. 25; 33-10). The 
high quality of the data collected in these studies and the analyses 
performed on them has been confirmed by OSHA and by independent peer 
review. Supporting evidence of Cr(VI) carcinogenicity comes from 
occupational cohort studies in chromate production, chromate pigment 
production, and chromium plating, and by cell culture research into the 
processes by which Cr(VI) disrupts normal gene expression and 
replication. Studies demonstrating uptake, metabolism, and genotoxicity 
of a variety of soluble and insoluble Cr(VI) compounds support the 
Agency's position that all Cr(VI) compounds should be regulated as 
occupational carcinogens (Exs. 35-148; 35-68; 35-67; 35-66; 12-5; 35-
149; 35-134).
2. Non-Cancer Impairments
    While OSHA has relied primarily on the association between Cr(VI) 
inhalation and lung cancer to demonstrate the necessity of the 
standard, the Agency has also determined that several other material 
health impairments can result from exposure to airborne Cr(VI). As 
shown in several cross-sectional and cohort studies, inhalation of 
Cr(VI) can cause ulceration of the nasal passages and perforation of 
the nasal septum (Exs. 35-1; 7-3; 9-126; 35-10; 9-18; 3-84; 7-50; 31-
22-12). Nasal tissue ulcerations are often accompanied by swelling and 
bleeding, heal slowly, and in some cases may progress to a permanent 
perforation of the nasal septum that can only be repaired surgically. 
Inhalation of Cr(VI) may also lead to asthma, a potentially life-
threatening condition in which workers become allergic to Cr(VI) 
compounds and experience symptoms such as coughing, wheezing, and 
difficulty in breathing upon exposure to small amounts of airborne 
Cr(VI). Several case reports have documented asthma from Cr(VI) 
exposure in the workplace, supporting Cr(VI) as the sensitizing agent 
by bronchial challenge (Exs. 35-7; 35-12; 35-16; 35-21).
    During the comment period, NIOSH requested that OSHA consider 
allergic contact dermatitis (ACD) as a material impairment of health 
due to occupational exposure to Cr(VI). NIOSH reasoned:

    Dermal exposure to Cr(VI) through skin contact * * * may lead to 
sensitization or allergic contact dermatitis. This condition, while 
not life-threatening, is debilitating and marked by significant 
discomfort and long-lasting adverse effects; it can have adverse 
occupational and social consequences and should be a material 
impairment to the health of affected workers * * * Including 
allergic contact dermatitis in OSHA's determination of material 
impairment of health draws attention to the fact that Cr(VI) is both 
a dermal exposure hazard and an inhalation hazard, and alerts 
employers that they should seek to minimize exposure to both routes 
(Ex. 40-10-2, p. 3)

    OSHA fully agrees with the NIOSH comment. There is strong evidence 
that unprotected skin contact with Cr(VI)-containing materials and 
solutions can cause ACD as well as irritant dermatitis and skin 
ulceration (see section V.D). ACD is a delayed hypersensitivity 
response. The worker initially becomes sensitized to Cr(VI) following 
dermal exposure. Once a worker becomes sensitized, brief exposures to 
small amounts of Cr(VI) can trigger symptoms such as redness, swelling, 
itching, and scaling. ACD is characterized by the initial appearance of 
small raised papules that can later develop into blisters and dry 
thickened, cracked skin. The allergic condition is persistent, causing 
some workers to leave their jobs (Ex. 35-320). Symptoms of ACD 
frequently continue long after occupational exposure to Cr(VI) ends, 
since sensitized individuals can react to contact with Cr(VI) in 
consumer products and other non-occupational sources.
    Skin exposure to Cr(VI) compounds can also cause a non-allergic 
form of dermatitis. This skin impairment results from direct contact 
with Cr(VI) doses that damage or irritate the skin, but do not involve 
immune sensitization. This form of dermatitis can range from mild 
redness to severe burns and ulcers, known as "chrome holes", that 
penetrate deep into tissues. Once the worker is removed from exposure, 
the skin ulcers heal slowly, often with scarring.

B. Risk Assessment

    When possible, epidemiological or experimental data and statistical 
methods are used to characterize the risk of disease that workers may 
experience under the currently allowable exposure conditions, as well 
as the expected reduction in risk that would occur with implementation 
of the new PEL. The Agency finds that the available epidemiological 
data are sufficient to support quantitative risk assessment for lung 
cancer among Cr(VI)-exposed workers. Using the best available studies, 
OSHA has identified a range of expected risk from regular occupational 
exposure at the previous PEL (101-351 excess lung cancer deaths per 
1000 workers) and at the new PEL of 5 [mu]g/m\3\ (10-45 per 1000 
workers), assuming a working lifetime of 45 years' exposure in each 
case. These values represent the best estimates of multiple analysts 
working with data from two extensively studied worker populations, and 
are highly consistent across analyses using a variety of modeling 
techniques and assumptions. While some attempts have been made to 
assess the relationship between Cr(VI) exposure level and noncancer 
adverse health effects, the Agency does not believe that a reliable 
quantitative risk assessment can be performed for noncancer effects at 
this time, and has therefore characterized noncancer risk 
qualitatively.
    For estimates of lung cancer risk from Cr(VI) exposure, OSHA has 
relied upon data from two cohorts of chromate production workers. The 
Gibb cohort, which originates from a chromate production facility in 
Baltimore, Maryland, includes 2357 workers who began work between 1950 
and 1974 and were followed up through 1992 (Ex. 33-11). The extensive 
exposure documentation available for this cohort, the high statistical 
power afforded by the large cohort size, and the availability of 
information on individual workers' race and smoking status provide a 
strong basis for risk analysis. The Luippold cohort, from a facility in 
Painesville, Ohio, includes 482 workers who began work between 1940 and 
1972, worked for at least one year at the plant, and were followed up 
through 1997 (Ex. 33-10). This cohort also provides a strong basis for 
risk analysis, in that it has high-quality documentation of worker 
Cr(VI) exposure and mortality, a long period of follow-up, and a large 
proportion of relatively long-term employees (55% were employed for 
longer than 5 years).
1. Lung Cancer Risk Based on the Gibb Cohort
    Risk assessments were performed on the Gibb cohort data by Environ 
International Corporation (Ex. 33-12), under contract with OSHA; Park 
et al., as part of an ongoing effort by NIOSH (Ex. 33-13); and Exponent 
on behalf of the Chrome Coalition (Ex. 31-18-15-1). A variety of 
statistical models were considered, allowing OSHA to identify the most 
appropriate models and assess the resulting risk estimates' sensitivity 
to alternate modeling approaches. Models were tried with additive and 
relative risk assumptions; various exposure groupings and lag times; 
linear and nonlinear exposure-response functions; external and internal
standardization; reference lung cancer rates from city-, state-, and 
national-level data; inclusion and exclusion of short-term workers; and 
a variety of ways to control for the effects of smoking. OSHA's 
preferred approach, a relative risk model using Baltimore lung cancer 
reference rates, and NIOSH's preferred approach, a relative risk model 
using detailed smoking information and U.S. lung cancer reference 
rates, are among several models that use reasonable assumptions and 
provide good fits to the data. As discussed in section VI, the Environ, 
Park et al., and linear Exponent models yield similar predictions of 
excess risk from exposure at the previous PEL and the new PEL (see 
Tables VI-2 and VI-3). OSHA's preferred models (from the Gibb data set) 
predict about 300-350 excess lung cancers per 1000 workers exposed for 
a working lifetime of 45 years at the previous PEL and about 35-45 
excess lung cancers per 1000 workers at the new PEL of 5 [mu]g/m\3\.
    Environ and Crump et al. performed risk assessments on the Luippold 
cohort, exploring additive and relative risk models, linear and 
quadratic exposure-response functions, and several exposure groupings 
(Exs. 35-59; 35-58). Additive and relative risk models by both analyst 
groups fit the data adequately with linear exposure-response. All 
linear models predicted similar excess risks, from which OSHA has 
selected preferred estimates based on the Crump et al. analysis of 
about 100 excess lung cancer deaths per 1000 workers exposed for 45 
years at the previous PEL, and ten excess lung cancer deaths per 1000 
workers at the new PEL.
2. Lung Cancer Risk Based on the Luippold Cohort
    The risk assessments performed on the Luippold cohort yield 
somewhat lower estimates of lung cancer risk than those performed on 
the Gibb cohort. This discrepancy is probably not due to statistical 
error in the risk estimates, as the confidence intervals for the 
estimates do not overlap. The risk estimates based on the Gibb and 
Luippold cohorts are nonetheless reasonably close. OSHA believes that 
both cohorts support reasonable estimates of lung cancer risk, and 
based on their results has selected a representative range of 101-351 
per 1000 for 45 years' occupational exposure at the previous PEL and 
10-45 per 1000 for 45 years' occupational exposure at the new PEL for 
the significant risk determination. OSHA's confidence in these risk 
estimates is further strengthened by the results of the independent 
peer review to which the risk assessment was submitted, which supported 
the Agency's approach and results. OSHA also received several comments 
in support of its risk estimates (Exs. 44-7, 38-222; 39-73-1). A full 
analysis of major comments on the results of OSHA's quantitative risk 
assessment can be found in section VI.F.
3. Risk of Non-Cancer Impairments
    Although nasal damage and asthma may be associated with 
occupational exposure to airborne Cr(VI), OSHA has determined that 
there are insufficient data to support a formal quantitative risk 
assessment for these effects. Available occupational studies of Cr(VI)-
induced nasal damage are either of cross-sectional study design, do not 
provide adequate data on short-term airborne Cr(VI) exposure over an 
entire employment period, or do not account for possible contribution 
from hand-to-nose transfer of Cr(VI) (Exs. 31-22-12; 9-126; 35-10; 9-
18). Occupational asthma caused by Cr(VI) has been documented in 
clinical case reports but asthma occurrence has not been linked to 
specific Cr(VI) exposures in a well-conducted epidemiological 
investigation. The Agency has nonetheless made careful use of the best 
available scientific information in its evaluation of noncancer health 
risks from occupational Cr(VI) exposure. In lieu of a quantitative 
analysis linking the risk of noncancer health effects, such as damage 
to nasal tissue, with specific occupational exposure conditions, the 
Agency has qualitatively considered information on the extent of these 
effects and occupational factors affecting risk, as discussed below.
    Damage to the nasal mucosa and septum can occur from inhalation of 
airborne Cr(VI) or transfer of Cr(VI) on workers' hands to the interior 
of the nose. Epidemiological studies have found varying, but 
substantial, prevalence of nasal damage among workers exposed to high 
concentrations of airborne Cr(VI). In the cohort of 2357 chromate 
production workers studied by Gibb et al., over 60% experienced nasal 
tissue ulceration at some point during their employment, with half of 
these workers' first ulcerations occurring within 22 days from the date 
they were hired (Ex. 31-22-12). The authors found a statistically 
significant relationship between nasal ulceration and workers' 
contemporaneous exposures, with about half of the workers who developed 
ulcerations first diagnosed while employed in a job with average 
exposure concentrations greater than 20 [mu]g/m3. Nasal 
septum perforations were reported among 17% of the Gibb cohort workers, 
and developed over relatively long periods of exposure (median time 172 
days from hire date to diagnosis).
    A high prevalence of nasal damage was also found in a study of 
Swedish chrome platers (Ex. 9-126). Platers exposed to average 8-hour 
Cr(VI) concentrations above 2 [mu]g/m3 with short-term 
excursions above 20 [mu]g/m3 from work near the chrome bath 
had a nearly 50 percent prevalence (i.e. 11 out of 24 workers) of nasal 
ulcerations and septum perforations. These data, along with that from 
the Gibb cohort, suggest a substantial and clearly significant risk of 
nasal tissue damage from regular short-term exposures above 20 [mu]g/
m3. More than half of the platers (i.e. 8 of 12 subjects) 
with short-term excursions to somewhat lower Cr(VI) concentrations 
between 2.5 and 11 [mu]g/m3 had atrophied nasal mucosa (i.e. 
cellular deterioration of the nasal passages) but not ulcerations or 
perforations. This high occurrence of nasal atrophy was substantially 
greater than found among the workers with mean Cr(VI) levels less than 
2 [mu]g/m3 (4 out of 19 subjects) and short-term Cr(VI) 
exposures less than 1 [mu]g/m3 (1 of 10 subjects) or among 
the office workers not exposed to Cr(VI) (0 of 19 subjects). This 
result is consistent with a concentration-dependant gradation in 
response from relatively mild nasal tissue atrophy to the more serious 
nasal tissue ulceration with short-term exposures to Cr(VI) levels 
above about 10 [mu]g/m3. For this reason, OSHA believes 
short-term Cr(VI) exposures regularly exceeding about 10 [mu]g/
m3 may still result in a considerable risk of nasal 
impairment. However, the available data do not allow a precise 
quantitative estimation of this risk.
    While dermal exposure to Cr(VI) can cause material impairment to 
the skin, a credible quantitative assessment of the risk is not 
possible because few occupational studies have measured the amounts of 
Cr(VI) that contact the skin during job activities; studies rarely 
distinguish dermatitis due to Cr(VI) from other occupational and non-
occupational sources of dermatitis; and immune hypersensitivity 
responses, such as ACD, have an exceedingly complex dose-response.

C. Significance of Risk and Risk Reduction

    The Supreme Court's benzene decision of 1980 states that "before 
he can promulgate any permanent health or safety standard, the 
Secretary [of Labor] is required to make a threshold finding that a 
place of employment is unsafe--in the sense that significant risks are
present and can be eliminated or lessened by a change in practices" 
(IUD v. API, 448 U.S. at 642). The Court broadly describes the range of 
risks OSHA might determine to be significant:

    It is the Agency's responsibility to determine in the first 
instance what it considers to be a "significant" risk. Some risks 
are plainly acceptable and others are plainly unacceptable. If, for 
example, the odds are one in a billion that a person will die from 
cancer by taking a drink of chlorinated water, the risk clearly 
could not be considered significant. On the other hand, if the odds 
are one in a thousand that regular inhalation of gasoline vapors 
that are 2 percent benzene will be fatal, a reasonable person might 
well consider the risk significant and take the appropriate steps to 
decrease or eliminate it. (IUD v. API, 448 U.S. at 655).

The Court further stated, "The requirement that a "significant" risk 
be identified is not a mathematical straitjacket * * *. Although the 
Agency has no duty to calculate the exact probability of harm, it does 
have an obligation to find that a significant risk is present before it 
can characterize a place of employment as "unsafe"' and proceed to 
promulgate a regulation (IUD v. API, 448 U.S. at 655).
    Table VII-1 presents the estimated excess risk of lung cancer 
associated with various levels of Cr(VI) exposure allowed under the 
current rule, based on OSHA's risk assessment and assuming either 20 
years' or 45 years' occupational exposure to Cr(VI) as indicated. The 
purpose of the OSH Act, as stated in Section 6(b), is to ensure "that 
no employee will suffer material impairment of health or functional 
capacity even if such employee has regular exposure to the hazard * * * 
for the period of his working life." 29 U.S.C. 655(b)(5). Taking a 45-
year working life from age 20 to age 65, as OSHA has always done in 
significant risk determinations for previous standards, the Agency 
finds an excess lung cancer risk of approximately 100 to 350 per 1000 
workers exposed at the previous PEL of 52 [mu]g/m3 Cr(VI). 
This risk is clearly significant, falling well above the level of risk 
the Supreme Court indicated a reasonable person might consider 
acceptable. Even assuming only a 20-year working life, the excess risk 
of about 50 to 200 per 1000 workers is still clearly significant. The 
new PEL of 5 [mu]g/m3 Cr(VI) is expected to reduce these 
risks substantially, to below 50 excess lung cancers per 1000 workers. 
However, even at the new PEL, the risk posed to workers with a lifetime 
of regular exposure is still clearly significant.

Click here to view table VII-1

    Workers exposed to concentrations of Cr(VI) lower than the new PEL 
and for shorter periods of time may also have significant excess cancer 
risk. The Agency's risk estimates are roughly proportional to duration 
for any given exposure concentration. The estimated risk to workers 
exposed at any fixed concentration for 10 years is about one-half the 
risk to workers exposed for 20 years; the risk for five years' exposure 
is about one-fourth the risk for 20 years. For example, about 11 to 55 
out of 1000 workers exposed at the previous PEL for five years are 
expected to develop lung cancer as a result of their exposure. Those 
exposed to 10 [mu]g/m3 Cr(VI) for 5 years have an estimated 
excess risk of about 2-12 lung cancer deaths per 1000 workers. It is 
thus not only workers exposed for many years at high levels who have 
significant cancer risk under the old standard; even workers exposed 
for shorter periods at levels below the previous PEL are at substantial 
risk, and will benefit from implementation of the new PEL.
    To further demonstrate significant risk, OSHA compares the risk 
from currently permissible Cr(VI) exposures to risks found across a 
broad variety of occupations. The Agency has used similar occupational 
risk comparisons in the significant risk determination for substance-
specific standards promulgated since the benzene decision. This 
approach is supported by evidence in the legislative record that 
Congress intended the Agency to regulate unacceptably severe 
occupational hazards, and not "to establish a utopia free from any 
hazards"(116 Cong. Rec. 37614 (1970), Leg. Hist 480), or to address 
risks comparable to those that exist in virtually any occupation or 
workplace. It is also consistent with Section 6(g) of the OSH Act, 
which states:

    In determining the priority for establishing standards under 
this section, the Secretary shall give due regard to the urgency of 
the need for mandatory safety and health standards for particular 
industries, trades, crafts, occupations, businesses, workplaces or 
work environments.

    Fatal injury rates for most U.S. industries and occupations may be 
obtained from data collected by the Bureau of Labor Statistics. Table 
VII-2 shows average annual fatality rates per 1000 employees for 
several industries between 1992 and 2001, as well as projected 
fatalities per 1000 employees for periods of 20 and 45 years based on 
these annual rates (Ex. 35-305). While it is difficult to compare 
aggregate fatality rates meaningfully to the risks estimated in the 
quantitative risk assessment for Cr(VI), which target one specific 
hazard (inhalation exposure to Cr(VI)) and health outcome (lung 
cancer), these rates provide a useful frame of reference for 
considering risk from Cr(VI) inhalation. Regular exposures at high 
levels, including the previous PEL of 52 [mu]g/m3 Cr(VI), 
are expected to cause substantially more deaths per 1000 workers from 
lung cancer than result from occupational injuries in most private 
industry. At the new PEL of 5 [mu]g/m3 Cr(VI) the Agency's 
estimated range of excess lung cancer mortality overlaps the fatality 
risk for mining and approaches that for construction, but still clearly exceeds 
the risk in lower-risk industries such as manufacturing.

Click here to view table VII-2

    Because there is little available information on the incidence of 
occupational cancer, risk from Cr(VI) exposure cannot be compared with 
overall risk from other workplace carcinogens. However, OSHA's previous 
risk assessments provide estimates of risk from exposure to certain 
carcinogens. These risk assessments, like the current assessment for 
Cr(VI), were based on animal or human data of reasonable or high 
quality and used the best information then available. Table VII-3 shows 
the Agency's best estimates of cancer risk from 45 years' occupational 
exposure to several carcinogens, as published in the preambles to final 
rules promulgated since the benzene decision in 1980.

Click here to view table VII-3

    The Cr(VI) risk estimate at the previous PEL is higher than many 
risks the Agency has found to be significant in previous rules (Table 
VII-3, "Risk at Previous PEL"). The estimated risk from lifetime 
occupational exposure to Cr(VI) at the new PEL is 10-45 excess lung 
cancer deaths per 1000 workers, a range which overlaps the estimated 
risks from exposure at the current PELs for benzene and cadmium (Table 
VII-3, "Risk at new PEL").
    Based on the results of the quantitative risk assessment, the 
Supreme Court's guidance on acceptable risk, comparison with rates of 
occupational fatality in various industries, and comparison with cancer 
risk estimates developed in previous rules, OSHA finds that the risk of 
lung cancer posed to workers under the previous permissible level of 
occupational Cr(VI) exposure is significant. The new PEL of 5 is 
expected to reduce risks to workers in Cr(VI)-exposed occupations 
substantially (by about 8- to 10-fold). OSHA additionally finds that 
nasal tissue ulceration and septum perforation can occur under exposure 
conditions allowed by the previous PEL leading to an additional health 
risk beyond the significant lung cancer risk present. The reduction of 
the Cr(VI) PEL from 52 [mu]g/m3 to 5 [mu]g/m3 is 
expected to substantially reduce workers' risk of nasal tissue damage. 
With regard to dermal effects from Cr(VI) exposure, OSHA believes that 
provision of appropriate protective clothing and adherence to 
prescribed hygiene practices will serve to protect workers from the 
risk of Cr(VI)-induced skin impairment.

VIII. Summary of the Final Economic and Regulatory Flexibility Analysis

A. Introduction

    OSHA's Final Economic and Regulatory Flexibility Analysis (FEA) 
addresses issues related to the costs, benefits, technological and 
economic feasibility, and economic impacts (including small business 
impacts) of the Agency's Occupational Exposure to Hexavalent Chromium 
rule. The full Final Economic and Regulatory Flexibility Analysis has 
been placed in the docket as Ex. 49. The analysis also evaluates 
alternatives that were considered by the agency before adopting the final 
rule. This rule is an economically significant rule under Section 3(f)(1) 
of Executive Order 12866 and has been reviewed by the Office of Information and 
Regulatory Affairs in the Office of Management and Budget, as required 
by executive order. The purpose of this Final Economic and Regulatory 
Flexibility Analysis is to:
     Identify the establishments and industries potentially 
affected by the final rule;
     Estimate current exposures and the technologically 
feasible methods of controlling these exposures;
     Estimate the benefits of the rule in terms of the 
reduction in lung cancer and dermatoses employers will achieve by 
coming into compliance with the standard;
     Evaluate the costs and economic impacts that 
establishments in the regulated community will incur to achieve 
compliance with the final standard;
     Assess the economic feasibility of the rule for affected 
industries; and
     Evaluate the principal regulatory alternatives to the 
final rule that OSHA has considered.
    The full Final Economic Analysis contains the following chapters:

Chapter I. Introduction
Chapter II. Industrial Profile
Chapter III. Technological Feasibility
Chapter IV. Costs of Compliance
Chapter V. Economic Impacts
Chapter VI. Benefits and Net Benefits
Chapter VII. Final Regulatory Flexibility Analysis
Chapter VIII. Environmental Impacts
Chapter IX. Assessing the Need for Regulation.

    These chapters are summarized in sections B to H of this Preamble 
summary.

B. Introduction and Industrial Profile (Chapters I and II)

    The final standard for occupational exposure to hexavalent chromium 
was developed by OSHA in response to evidence that occupational 
exposure to Cr(VI) poses a significant risk of lung cancer, nasal 
septum ulcerations and perforations, and dermatoses. Exposure to Cr(VI) 
may also lead to asthma. To protect exposed workers from these effects, 
OSHA has set a Permissible Exposure Limit (PEL) of 5 [mu]g/m\3\ 
measured as an 8-hour time weighted average. OSHA also examined 
alternative PELs ranging from 20 [mu]g/m\3\ to 0.25 [mu]g/m\3\ measured 
as 8-hour time weighted averages.
    OSHA's final standards for occupational exposure to Cr(VI) are 
similar in format and content to other OSHA health standards 
promulgated under Section 6(b)(5) of the Act. In addition to setting 
PELs, the final rule requires employers to:
     Monitor the exposure of employees (though allowing a 
performance-oriented approach to monitoring);
     Establish regulated areas when exposures may reasonably be 
expected to exceed the PEL (except in shipyards and construction);
     Implement engineering and work practice controls to reduce 
employee exposures to Cr(VI);
     Provide respiratory protection to supplement engineering 
and work practice controls where those controls are not feasible, where 
such controls are insufficient to meet the PEL, or in emergencies;
     Provide other protective clothing and equipment as 
necessary for dermal protection;
     Make industrial hygiene facilities (hand washing stations) 
available in some situations;
     Provide medical surveillance when employees are exposed 
above the action level for 30 days or more;
     Train workers about the hazards of Cr(VI) (including 
elements already required by OSHA's Hazard Communication Standard); and
     Keep records related to the standard.
    The contents of the standards, and the reasons for issuing separate 
standards for general industry, construction and shipyard employment, 
are more fully discussed in the Summary and Explanation section of this 
Preamble.
    Chapter II of the full FEA describes the uses of Cr(VI) and the 
industries in which such uses occur. Employee exposures are defined in 
terms of "application groups," i.e., groups of firms where employees 
are exposed to Cr(VI) when performing a particular function. This 
methodology is appropriate to exposure to Cr(VI) where a widely used 
chemical like chromium may lead to exposures in many kinds of firms in 
many industries but the processes used, exposures generated, and 
controls needed to achieve compliance may be the same. For example, 
because a given type of welding produces Cr(VI) exposures that are 
essentially the same regardless of whether the welding occurs in a 
ship, on a construction site, as part of a manufacturing process, or as 
part of a repair process, it is appropriate to analyze such processes 
as a group. However, OSHA's analyses of costs and economic feasibility 
reflect the fact that baseline controls, ease of implementing ancillary 
provisions, and the economic situation of the employer may differ 
within different industries in an application group.
    The most common sources of occupational exposure to Cr(VI), in 
addition to the production and use of chromium metal and chromium metal 
alloys, are chromium electroplating; welding of metals containing 
chromium, particularly stainless steel or other high-chromium steels, 
or with chromium coatings; and the production and use of Cr(VI)-
containing compounds, particularly Cr(VI) pigments, but also Cr(VI) 
catalysts, chromic acid, and the production of chromium-containing 
pesticides.
    Some industries are seeing a sharp decline in chromium use. 
However, many of the industries that are seeing a sharp decline have 
either a small number of employees or have low exposure levels (e.g., 
wood working, printing ink manufacturers, and printing). In the case of 
lead chromate in pigment production, OSHA's sources indicate that there 
is no longer domestic output containing lead chromates. Therefore, this 
trend has been recognized in the FEA. Painting activities in general 
industry primarily involve the application of strontium chromate 
coatings to aerospace parts; these exposures are likely to continue 
into the foreseeable future. Similarly, removal of lead chromate paints 
in construction and maritime is likely to present occupational risks 
for many years.
    In application groups where exposures are particularly significant, 
both in terms of workforce size and exposure levels--notably in 
electroplating and welding--OSHA anticipates very little decline in 
exposures to hexavalent chromium due to the low potential for 
substitution in the foreseeable future.
    OSHA has made a number of changes to the industrial profile of the 
application groups as a result of comments on the proposed rule. Among 
the most important are:
     Additions to the electroplating application group to 
include such processes as chrome conversion, which were not considered 
at the time of the proposal;
     Additions to the painting application group to cover 
downstream users, particularly automobile repair shops and construction 
traffic painting;
     Additions to glass manufacturing to cover fiberglass, flat 
glass, and container glass industries;
     Addition of the forging industry;
     Addition of the ready mixed concrete industry;
     Additions to the welding application group to include 
welding on low-chromium steel and increase the estimated number of 
exposed workers in the maritime sector; and
     More careful division of the many different industries in 
which electroplating, welding and painting may appear as applications.
    Table VIII-1 shows the application groups analyzed in OSHA's FEA, 
as well as the industries in each application group, and for each 
provides the number of establishments affected, the number of employees 
working in those establishments, the number of entities (firms or 
governments) fitting SBA's small business criteria for the industry, 
and the number of employees in those firms. (The table shows data for 
both establishments and entities--defined as firms or governments. An 
entity may own more than one establishment.) The table also shows the 
revenues of affected establishment and entities, updated to reflect 
2002 data. (This table provides the latest available data at the time 
this analysis was produced.) As shown in the table, there are a total 
of 52,000 establishments affected by the final standard.
    Various types of welding applications account for the greatest 
number of establishments and number of employees affected by the final 
standard.
BILLING CODE 4510-26-P

Click here to view table VIII-1

BILLING CODE 4510-26-C
    Table VIII-2 shows the current exposures to Cr(VI) by application 
group. The exposure data relied on by OSHA in developing the exposure 
profile and evaluating technological feasibility were compiled in a 
database of exposures taken from OSHA compliance officers, site visits 
by OSHA contractors and the National Institute for Occupational Safety 
and Health (NIOSH), the U.S. Navy, published literature, commenters on 
the proposed rule and other interested parties.
    It is also important to note that Table VIII-2 and OSHA's cost and 
feasibility analyses reflect the full range of exposures occurring in 
each application group, not the median exposures. Some commenters 
(e.g., Ex. 47-27-1) misunderstood this and believed OSHA determined 
that only employers with median exposures above the PEL would incur 
costs for engineering and work practice controls. OSHA did not use 
exposure medians to assign compliance costs in this rulemaking. OSHA 
made limited use of exposure medians for only a few purposes. The first 
was in the analysis of baseline controls, described in the 
technological feasibility discussion below. Where both exposure data 
and information on the controls in place were available, OSHA used the 
median exposure level experienced in the presence of a specific type of 
control to assign an effectiveness level to the control. Second, to 
determine whether to assume baseline controls were already in place in 
cases where OSHA only had exposure data available, it compared median 
exposure levels to the median exposure levels previously assigned to 
baseline controls.
BILLING CODE 4510-26-P

Click here to view table VIII-2

BILLING CODE 4510-26-C

    In all sectors OSHA has used the best available information to 
determine baseline exposures and technological feasibility. Throughout 
the rulemaking process OSHA requested industry-specific information. 
These requests included site visits, discussions with industry experts 
and trade associations, the 2002 Request for Information (RFI), and the 
SBREFA process. These requests continued through the proposal and the 
public hearing process where OSHA continued to request information. 
OSHA reviewed all the data submitted to the record and where 
appropriate updated the exposure profile. For exposure information to 
be useful in the profile, only individual personal exposures 
representing a full shift were used.
    As noted earlier, OSHA used a variety of sources to obtain 
information about exposures in each application group. These sources 
include: NIOSH Health Hazard Evaluations (HHEs), OSHA's Integrated 
Management Information System (IMIS) exposure data, data from other 
government agencies, published literature, OSHA/NIOSH site visits, 
discussions with industry experts and trade associations, and data 
submitted to the OSHA record. In some instances OSHA's contractor had 
difficulty obtaining permission to perform site visits in a specific 
application group. For instance, OSHA's contractor could obtain 
permission to conduct a site visit only at a steel mill that used the 
teeming and primary rolling method--in contrast to continuous casting, 
now used in approximately 95 percent of steel mills. In these few 
cases, OSHA acknowledged these potential problems and OSHA (or its 
contractor) discussed its concerns with industry experts and used their 
professional judgment to determine technological feasibility.
    In response to the exposure data submitted to the record OSHA has 
made the following major changes to the exposure profile:
     Electroplating--Revised the exposure distribution for hard 
chrome electroplating to use only the more-detailed exposure data from 
site visits and other NIOSH reports.
     Welding--In construction, OSHA used exposure data from the 
maritime sector for analogous operations to supplement the exposure 
profile. Added additional exposure data to the profile as provided to 
the record.
     Painting--Revised the exposure profile to reflect the 
additional aerospace exposure data submitted to the record.
     Steel Mills--Revised the exposure profile to reflect 
additional exposure data supplied to the record; welders were added 
directly to this application group.
     Chromium Catalyst Users--Revised the exposure profile 
based on additional exposure data from a NIOSH HHE.
     Wood working--Added information from the record.
     Construction--Revised the exposure profile to reflect the 
additional exposure information submitted to the record.
    Detailed information on the changes made in the exposure profile 
for each application group can be found in Chapter III of the Final 
Economic Analysis.
    OSHA's analysis of technological feasibility examined employee 
exposures at the operation or task level to the extent that such data 
were available. There are approximately 558,000 workers exposed to 
Cr(VI), of which 352,000 are exposed above 0.25 micrograms per cubic 
meter and 68,000 above the PEL of 5 micrograms per cubic meter.

C. Technological Feasibility

    In Chapter III of OSHA's FEA, OSHA assesses the current exposures 
and the technological feasibility of the final standard in all affected 
industry sectors. The analysis presented in this chapter is organized 
by application group and analyzes employee exposures at the operation 
or task level to the extent that such data are available. Accordingly, 
OSHA collected exposure data at the operation or task level to identify 
the Cr(VI)-exposed workers or job operations that need to improve their 
process controls to achieve exposures at or below the PEL. In the few 
instances where there were insufficient exposure data, OSHA used 
analogous operations to characterize these operations.
    In general, OSHA considered the following kinds of controls that 
could reduce employee exposures to Cr(VI): local exhaust ventilation 
(LEV), which could include maintenance or upgrade of the current local 
exhaust ventilation or installation of additional LEV; process 
enclosures that would isolate the worker from the exposure; process 
modifications that would reduce the generation of Cr(VI) dust or fume 
in the work place; improved general dilution ventilation including 
assuring that adequate make-up air is supplied to the work place; 
improved housekeeping; improved work practices; and the supplemental 
use of respiratory protection if engineering and work practice controls 
were not sufficient to meet the PEL.
    The technologies used in this analysis are commonly known, readily 
available and are currently used to some extent in the affected 
industries and processes. OSHA's assessment of feasible controls and 
the exposure levels they can achieve is based on information collected 
by Shaw Environmental, Inc. (Ex. 50), a consultant to OSHA, on the 
current exposure levels associated with existing controls, on the 
availability of additional controls needed to reduce employee 
exposures, and on other evidence presented in the docket.
    Through the above analysis, OSHA finds that a PEL of 5 [mu]g/m\3\ 
is technologically feasible for most operations in all affected 
industries through the use of engineering and work practice controls. 
As discussed further below, the final rule requires that when painting 
of aircraft or large aircraft parts is performed in the aerospace 
industry, the employer is only required to use engineering and work 
practice controls to reduce employee exposures to Cr(VI) to or below 25 
[mu]g/m\3\. The employer must then use respiratory protection to 
achieve the PEL. Apart from this limited exception, all other 
industries can achieve the PEL with only minimal reliance on 
respiratory protection. Table VIII-3 shows OSHA's estimate of 
respirator use by industry for each of the PELs that OSHA considered. 
At the final PEL of 5 [mu]g/m\3\, only 3.5 percent of exposed employees 
will be required to use respirators.
    In only three sectors will respirator use be required for more than 
5 percent of exposed employees. In two of these sectors, chromate 
pigment producers and chromium dye producers, use of respirators will 
be intermittent. The third sector, stainless steel welding, presents 
technological challenges in certain environments such as confined 
spaces. OSHA has concluded that, with a few limited exceptions which 
are discussed below, employers will be able to reduce exposures to the 
PEL through the use of engineering and work practice controls.
BILLING CODE 4510-26-P

Click here to view table VIII-3

BILLING CODE 4510-26-C

    In determining technological feasibility OSHA has used the median 
to describe the exposure data. Since the median is a statistical term 
indicating the central point of a sequence of numbers (50 percent below 
and 50 percent above) it best describes exposures for most people. The 
median is also a good substitute for the geometric mean for a log 
normal distribution which often describes exposure data. As described 
by the Color Pigments Manufacturers Association, Inc. (CPMA) in an 
economic impact study by IES Engineers:

    The exposure distribution (assuming it is log normal) can be 
characterized by the geometric mean and standard deviation. The 
median (not the average) is a reasonable estimate of the geometric 
mean (Ex. 47-3, p. 54).

    In contrast, the use of an arithmetic mean (or average) may tend to 
misrepresent the exposure of most people. For example, if there are a 
few workers with very high exposures due to poor engineering or work 
practice controls, the arithmetic mean will be artificially high, not 
representing realistic exposures for the workers.
    The technological feasibility chapter of the FEA is broken down 
into five main parts: Introduction, Exposure Profile, Baseline 
Controls, Additional Controls and Substitution. The first part is an 
introduction to the application group, which outlines the major changes 
in the analysis between the Preliminary Economic Analysis and the Final 
Economic Analysis and addresses comments specific to the application 
group.
    The next part of the technological feasibility analysis is the 
exposure profile. The exposure profile describes the prevailing 
exposures in each application group on a job-by-job basis. The exposure 
profile represents exposure situations that may be well controlled or 
poorly controlled. The data used to determine the current exposures 
were obtained from any of the following sources: OSHA site visits; the 
OSHA compliance database, Integrated Management Information System 
(IMIS); NIOSH site visits; NIOSH control technology or health hazard 
evaluation reports (HHE); information from the U.S. Navy; published 
literature; submissions by individual companies or associations; or, in 
a few cases, by consideration of analogous operations. While the 
exposure profile was developed from current exposures and is not 
intended to demonstrate feasibility, there were a few instances where 
the exposure profile was used as ancillary support for technological 
feasibility if there were a significant number of facilities already 
meeting the PEL. An example of this case can be seen in the production 
of colored glass, where over 90 percent of the exposure data were below 
0.25 [mu]g/m3.
    In the cases where analogous operations were used to determine 
exposures, OSHA used data from industries or operations where materials 
and exposure routes are similar. OSHA also tended to be conservative 
(over-estimating exposures). For example, exposure data for the bagging 
of pigments were used to estimate exposures for the bagging of plastic 
colorants. In both cases the operation consists of bagging a pigmented 
powder. However, exposures would tend to be higher for bagging pigments 
due to the fact that in pigments there is a higher percentage of Cr(VI) 
and the pigments tend to consist of finer particles than those in 
plastic colorants where the Cr(VI) particles are diluted with other 
ingredients. As Mr. Jeff Cox from Dominion Colour Corporation stated:

    Exposure of packers in the pigment industry, who are making a 
fine powder, is very much higher than packers in the plastics 
colorants industry, who are basically packing pellets of 
encapsulated product which are a few millimeters in diameter (Tr. 
1710).

    The use of operations that are more difficult to control to 
estimate analogous operations would result in an overestimate of 
exposures, subsequently resulting in an overestimate of the controls 
needed to reduce the exposures to Cr(VI) in those analogous operations.
    The next section of OSHA's analysis of technological feasibility in 
the FEA describes the baseline controls. OSHA determined controls to be 
"baseline" if OSHA believed that such controls are commonly used in 
the application group. This should not be interpreted to mean that OSHA 
believes that all firms use these controls, but rather that the 
controls are common and widely available in the industry. Information on 
the controls used in each specific application group was obtained from 
several different sources such as: site visits, NIOSH HHEs, industry 
experts, industry associations, published literature, submissions to the 
docket, and published reports from other federal agencies. OSHA used the 
median to estimate the exposure level associated with the baseline controls. 
For the majority of the operations, the median was calculated using the 
exposures directly associated with the baseline controls. However, 
there were a few cases where the median was calculated from the 
exposure profile and OSHA determined these exposures reflected the 
baseline controls (e.g., fiberglass production).
    The fourth section of the technological feasibility analysis 
determined the need for additional controls. If the median exposure was 
above the PEL with the use of baseline controls, OSHA would recommend 
additional engineering or work practice controls that would reduce 
exposures to or below the PEL. The final rule does not require an 
employer to use these specific controls. The engineering controls or 
work practices are, however, OSHA's suggestions for possible ways to 
achieve the PEL. Through this process a few situations could arise when 
the exposures with baseline exposures are above the PEL:
     Engineering and work practice controls alone: OSHA 
determined that additional controls would reduce worker's exposure 
below the PEL if: 1) the proposed additional controls were already in 
use at other facilities in the same application group and exposures 
there were below the PEL, or 2) the additional controls were used in 
analogous industries or operations and they were effective.
     Respiratory protection required to meet the PEL: There 
were a few instances where workers' exposures would remain above the 
PEL even with the installation of additional controls. In these cases 
OSHA indicated that the supplemental use of respirators may be needed 
(e.g. enclosed spray-painting operations in aerospace).
     Intermittent respiratory protection: There were instances 
where a worker performs specific job-related activities that could 
result in higher exposures above the PEL for limited periods of time. 
In these cases OSHA noted that the supplemental use of respirators 
during these activities may be necessary. For example, an employee who 
works in pigment production generally, may need to use a respirator 
only when entering the enclosure where the bagging operations take 
place because the enclosure is the engineering control in this 
operation.
    The final component of the technological feasibility section in the 
FEA is a discussion of substitution. Here, OSHA describes the options 
available for eliminating or reducing the use of ingredients that 
either contain or can produce Cr(VI) during processing. This is 
primarily a discussion of the possibility of substitution. In some 
cases there is no readily available substitute for either chromium 
metal or Cr(VI) ingredients such as a non-Cr(VI) coating for corrosion 
control in the aerospace industry. In other cases an application group 
has been steadily reducing their use of Cr(VI), such as in the printing 
industry. In some industries there are substitutes available for at 
least some operations, such as the use of trivalent chromium in some 
decorative electroplating operations. Finally, through hearing 
testimony and docket submissions, OSHA received information regarding 
new technologies that can be used to reduce some of the sources of 
exposure to the workers.
    In most cases OSHA does not rely on material substitution for 
reducing exposures to Cr(VI) to determine technological feasibility. 
For example, in the case of some welding operations, OSHA has 
determined that the use of an alternate welding process that reduces 
fume generation, such as the switching from shielded metal arc welding 
(SMAW) to gas metal arc welding (GMAW), could be effective in reducing 
a worker's exposure to hexavalent chromium to a level at or below the 
PEL. Alternatively, experiments have also shown that elimination or 
reduction of sodium and potassium in the flux reduces the production of 
Cr(VI) in the welding fume (Ex. 50). However, this technology has yet 
to be commercialized due to potential weld quality problems. Thus, OSHA 
ultimately determined that material substitution was currently not 
feasible for SMAW welding operations.
    There were comments submitted to the record that did not agree with 
certain aspects of OSHA's feasibility analysis. These comments 
addressed:
     OSHA's use of median values to describe exposure data and 
failure to address costs for exposures above the PEL where the median 
was below the PEL;
     OSHA's use of the number of workers to determine the 
number of facilities needing additional controls;
     The use/validity of OSHA's analytical method; and
     The lack of data/site visits to properly characterize an 
application group.
    Several commenters objected to OSHA's use of the median in the 
technological feasibility analysis. The National Coil Coating 
association stated:

    It is inappropriate to use median exposure values to reach a 
conclusion that no coil coating facility will be subject to 
regulatory requirements associated with exceedances of the proposed 
PEL. Of the 15 samples supplied, one sample exceeded the proposed 
PEL and another one was equal to the proposed PEL (Ex. 39-72-1).

Collier Shannon Scott, representing the Specialty Steel Industry of 
North America, stated:

    OSHA conducted a technological feasibility analysis to determine 
what engineering or administrative controls would be necessary to 
achieve the proposed PEL only where the median exposure value for 
any particular job category exceeded the proposed PEL. If correct, 
this means that where the median exposure value fell below 1 ug/m3, 
even though numerous of the exposure values for that job category 
were above 1 ug/m3, OSHA's analysis does not recognize that controls 
would have to be implemented for that job category at any facilities 
where that job is conducted (Ex. 47-27-1).

    OSHA believes that these commenters misunderstood OSHA's use of the 
median value and the term "additional controls." As stated earlier, 
OSHA used the median value to describe either the overall exposures or 
the effectiveness of various controls. However, to estimate the cost of 
controls, OSHA used the entire exposure profile. Thus, if any exposures 
were over the PEL, then costs for engineering controls would be 
assigned. If for a job category the "baseline controls" have been 
determined to reduce employee exposures to below the PEL, then OSHA 
would include costs for "baseline controls" for the percentage of the 
facilities that had exposures over the PEL. However, if the 
"baseline" controls would not be sufficient to reduce worker 
exposures to below the PEL then OSHA would cost the "additional 
controls."
    Collier Shannon Scott, representing the Specialty Steel Industry of 
North America also stated:

    OSHA wrongly uses percentage distribution by job category to 
estimate the number of facilities that would be required to install 
engineering controls. This is a logical error. There is no 
connection between the number of facilities that must install 
controls and the percentage of employees above a given exposure 
level (Ex. 47-27-1).

    OSHA was also concerned about accurately using individual exposures 
to represent the number of facilities that would need to implement either 
baseline controls or additional controls. Thus, whenever exposure data 
were associated with individual facilities, OSHA normalized the 
exposure data by job category to the facility, with each facility 
having a weighting factor of 1. However, if exposure data varied 
significantly, OSHA accounted for this. For example, if fifty percent 
of the exposure data for a job class in a facility was above the PEL 
and fifty percent below the PEL, then OSHA counted this as representing 
0.5 facilities above the PEL and 0.5 facilities below the PEL.
    The use of this weighting system ensured that each facility 
received the same weight so that one facility that supplied a large 
amount of data would not overwhelm the exposure profile and skew the 
distribution in an application group. This is particularly important 
when there is a wide range of sizes of facilities and a large facility 
could outweigh a smaller facility. OSHA then used this weighting system 
to determine the percentage of facilities affected, so that the costs 
were based on a per-facility versus a per-employee basis. However, in a 
few instances OSHA could not use the weighting factor system because 
certain exposure data were presented to OSHA as representing the 
industry. For examples, in maritime welding and aerospace painting the 
exposure data could not be attributed to individual facilities but were 
presented to OSHA as representing a group of facilities.
    There were comments about several different aspects of OSHA's 
analytical method. The Policy Group, representing the Surface Finishing 
Industry Council, was concerned about how OSHA interpreted the term 
non-detect (ND):

    Appropriate assessment of ND qualitative value would require 
that the sample specific quantitation limit be lower than any 
targeted analytical value, such as the new proposed AL and PEL. 
According to a leading OSHA/NIOSH contract laboratory (DataChem 
Laboratories) in the field of IH analyses, laboratories only report 
to the lowest calibration standard. Thus, the lowest standard value 
in the curve is the quantitation limit or reporting limit. This 
limit is the minimum value the labs generally report, regardless of 
any theoretical LOD value (Ex. 47-17-8).

    OSHA agrees with The Policy Group's assessment and has updated the 
exposure profiles to reflect non-detect samples as the Limit of 
Quantification (LOQ) where the source of the data did not indicate the 
limit of detection. This is discussed in more detail in the 
electroplating section of the technological feasibility chapter in the 
FEA.
    Several comments questioned whether OSHA's analytical method truly 
represents a worker's exposure (Ex. 38-216-1). Several other sources 
indicate that OSHA's analytical method ID 215 is appropriate and it 
accurately represents a worker's exposure. In a Journal of 
Environmental Monitoring article the authors conclude:

    * * * a field comparison of three recently developed or modified 
CrVI sampling and analytical methods showed no statistically 
significant differences among the means of the three methods based 
on statistical analysis of variance. The overall performances of the 
three CrVI methods were comparable in electroplating and spray 
painting operations where soluble CrVI was present. Although the 
findings reported herein are representative of workplace operations 
utilizing soluble forms of CrVI, these analytical methods (using 
identical sample preparation procedures) also have been shown to 
quantitatively measure insoluble forms of CrVI in other occupational 
settings. There were no significant differences observed among CrVI 
concentrations measured by NIOSH 7605 and OSHA ID 215 (Ex. 40-10-5).

In addition URS Corporation stated:

    The new OSHA method 215 was used to analyze samples collected 
during the Site Visits for Company 1 and Company 18. This method is 
far superior to the old OSHA method ID 103 and to other relative 
older methods. The new method utilizes separations of the hexavalent 
chromium from potential interferences prior to the analysis. It is 
also designed to detect much lower CrVI concentrations levels and to 
remove both positive and negative interferences at these lower 
concentrations. Furthermore, this method has been fully validated in 
the presence of interferences over a CrVI concentration range that 
includes the proposed new AL and PEL values (Ex. 47-17-8).

OSHA's analytical method ID 215 is a fully validated analytical method 
that can analyze Cr(VI) well below the PEL within the accuracy of 
measurement as specified in the final standard.
    Dr. Joel Barnhart, on behalf of the Chrome Coalition, questioned 
how the samples were taken during the OSHA-sponsored site visits (Ex. 
40-12-1). At all site visits conducted by OSHA's contractors, certified 
industrial hygienists (CIHs) were responsible for either taking samples 
or reviewing sampling data provided by the facility visited. All 
samples were taken following procedures from either NIOSH or OSHA which 
detail the type of sampler, filter and flow rates appropriate for the 
analytical methods used. Full details about the samples, operations 
they represent and engineering controls can be found in each site visit 
report.
    Several commenters mentioned that OSHA relied solely on one site 
visit for an entire application group (Exs. 38-218; 38-205). While the 
OSHA/NIOSH site visits were important to OSHA's understanding of the 
processes used in the different application groups, the site visits 
were not the sole source of information. OSHA, as stated earlier, used 
many different sources to properly characterize an application group. 
These sources included: OSHA site visits, OSHA's compliance data base 
(IMIS), NIOSH site visits, NIOSH engineering control technology reports 
or health hazard evaluation reports, published literature, submissions 
by individual companies, as well as detailed discussions with industry 
experts. In addition, throughout the rulemaking process OSHA has 
requested information regarding processes, exposures, engineering 
controls, substitutes and other information pertinent to Cr(VI) 
application groups. These requests came in many forms such as 
stakeholder meetings, site visits, OSHA's 2002 Request for Information, 
and the SBREFA review. OSHA continued to update the technological 
feasibility analysis based on information submitted to the docket 
during the hearings and during the pre- and post-hearing comment 
periods.
    OSHA also received comments specific to application groups 
regarding issues such as the number of employees potentially exposed, 
additional exposure data, and the effectiveness of controls. Comments 
that were application group-specific are addressed in the FEA in the 
individual sections on those application groups.
    The major changes made to the technological feasibility analysis 
for the Final Economic Analysis are listed below:
     Electroplating--The number of affected workers and 
establishments was revised, the exposure distribution was revised for 
hard chrome electroplating, and chromate conversion workers and 
establishments were added.
     Welding--The number of maritime welders was increased, 
mild steel welding was added, and control technology for reducing 
worker exposure was revised.
     Painting--Auto body repair workers were added to general 
industry and traffic painting was added to construction. Control 
technology for reducing worker exposure was revised for aerospace spray 
painting.
     Chromium Catalyst Production--Control technology for 
reducing worker exposure was revised.
     Steel Mills--OSHA revised the distribution of steel 
workers, carbon steel workers were added, and downstream users (e.g. 
rolling mills and forging operations) were added to this application 
group.
     Glass Production--Fiber, flat, and container glass 
production were added.
     Producers of Pre-Cast Concrete Products--Ready mixed 
concrete workers were added.
     Throughout the analysis the exposure profiles were updated 
to reflect additional exposure data submitted to the docket.
    Technological Feasibility of the New PEL: There are over 558,000 
workers exposed to Cr(VI). Table VIII-2 shows the current exposures to 
Cr(VI) by application group. There are employers and some entire 
application groups that already have nearly all exposures below the 
PEL. However, many others will need to install or improve engineering 
and work practice controls to achieve the PEL.
    OSHA has determined that the primary controls most likely to be 
effective in reducing employee exposure to Cr(VI) are local exhaust 
ventilation (LEV), process enclosure, process modification, and 
improving general dilution ventilation. In some cases, a firm may not 
need to upgrade its local exhaust system, but instead must ensure that 
the exhaust system is working to design specification throughout the 
process. In other cases, employers will need to upgrade or install new 
LEV. This includes installing duct work, a type of hood and/or a 
collection system. OSHA estimates that process enclosures may be 
necessary for difficult-to-control operations such as dusty operations. 
These enclosures would isolate the employees from high exposure 
processes and reduce the need for respirators. Process modifications 
can also be effective in reducing exposures in some industries to a 
level at or below the PEL.
    Below are discussions of the types of engineering and work practice 
controls that may be needed for the application groups where exposures 
are more difficult to control.
    Electroplating: OSHA has determined that the PEL of 5 [mu]g/m\3\ is 
technologically feasible for all job categories through the use of a 
combination of engineering controls. For decorative plating and 
anodizing the vast majority (over 80 percent) of workers are already 
below 5 [mu]g/m\3\. For the workers above the PEL, there are several 
control options to reduce exposures, such as properly maintained 
ventilation and the use of fume suppressants. Some firms may not need 
to upgrade their local exhaust systems, but must ensure that their 
current exhaust systems are working according to design specification. 
For example, in hard chrome electroplating (where Cr(VI) exposures are 
highest) nearly 100 percent of hard chrome electroplating baths have 
LEV at the tank; however, none of the systems inspected during site 
visits and for NIOSH reports were operating at the designed 
capabilities. Many had disconnected supply lines or holes in the hoods 
and were working at 40 percent of their design capabilities. In such 
cases, OSHA recommends that these facilities perform the proper 
maintenance necessary to bring the system back to its initial 
parameters. Even with these deficiencies in engineering controls, over 
75 percent of workers are below 5 [mu]g/m\3\.
    In addition to improving LEV, the use of fume suppressants can 
further reduce the volume of Cr(VI) fumes released from the plating 
bath. However, OSHA was unable to conclude, based on the evidence in 
the record, that the proposed PEL of 1 [mu]g/m\3\ would have been 
technologically feasible for all hard chrome electroplating operations. 
In particular, OSHA has significant concerns about the technological 
feasibility of the proposed PEL for hard chrome electroplating 
operations in which fume suppressants cannot be used to control 
exposures to Cr(VI) because they would interfere with product 
specifications and render the resulting product unusable.
    Welding: The welding operations OSHA expects to trigger 
requirements under the new Cr(VI) rule are those performed on stainless 
steel, as well as those performed on high-chrome-content carbon steel 
and those performed on carbon steel in confined and enclosed spaces. At 
the time of the proposal, OSHA believed that carbon steel contained 
only trace amounts of chromium and therefore that welding on carbon 
steel would not be affected by the standard. Comments and evidence 
received during the rulemaking, however, led OSHA to conclude that 10 
percent of carbon steel contains chromium in more than trace amounts; 
OSHA adjusted its analysis accordingly. See Tr. 581-82.
    OSHA has determined that the PEL of 5 [mu]g/m\3\ is technologically 
feasible for all affected welding job categories on carbon steel. OSHA 
has concluded that no carbon steel welders are exposed to Cr(VI) above 
5 [mu]g/m\3\, with the exception of a small portion of workers welding 
on carbon steel in enclosed and confined spaces. Furthermore, OSHA has 
determined that engineering and work practice controls are available to 
permit the vast majority (over 95 percent) of welding operations on 
carbon steel in enclosed and confined spaces to comply with a PEL of 5 
[mu]g/m\3\.
    Although stainless steel welding generally results in higher 
exposures than carbon steel welding, OSHA has determined that the PEL 
of 5 [mu]g/m\3\ is also technologically feasible for all affected 
welding job categories on stainless steel. Many welding processes, such 
as tungsten-arc welding (TIG) and submerged arc welding (SAW), already 
achieve Cr(VI) exposures below the PEL because they inherently generate 
lower fume volumes. However, the two most common welding processes, 
shielded metal arc welding (SMAW) and gas metal arc welding (GMAW), 
generate greater exposures and may require the installation or 
improvement of LEV (defined to include portable LEV systems such as 
fume extraction guns (FEG)).
    OSHA has found process substitution to be the most effective method 
of reducing Cr(VI) exposures. For example, the generation of Cr(VI) in 
GMAW welding fume is approximately 4 percent of the total Cr content, 
compared to upwards of 50 percent for SMAW. In the proposal, OSHA 
estimated that all SMAW workers outside of confined spaces (over 90 
percent of the welders) could switch welding processes. However, 
hearing testimony and comments indicated that switching to GMAW is not 
feasible to the extent that OSHA had originally estimated.
    Some comments indicated that this conversion has already taken 
place where possible. For example, Atlantic Marine stated they have 
already "greatly reduced the use of SMAW and replaced it with GMAW 
over the last several years' (Ex. 39-60). Other comments indicated it 
is still an ongoing process. For instance, General Dynamics stated, 
"There are ongoing efforts to reduce the use of SMAW and replace it 
with GMAW for both efficiency and health reasons" (Ex. 38-214). In 
addition, some comments expressed concerns about the quality of the 
weld if GMAW is used instead of SMAW. (Ex. 39-70).
    In view of these concerns OSHA has revised its estimate of the 
percentage of SMAW welders that can switch to GMAW from 90 percent to 
60 percent. This estimate is consistent with the estimate made by 
Edison Welding Institute in a report for the Department of Defense on 
Cr(VI) exposures which "identifies engineering controls that can be 
effective in reducing worker exposure for many applications in the 
shipbuilding and repair industry" (Ex. 35-410).
    For those stainless steel SMAW operations that cannot switch to 
GMAW, and even for some GMAW operations, the installation or 
improvement of LEV may be needed and can be used to reduce exposures. 
OSHA has found that LEV would permit most SMAW and GMAW operations to 
comply with a PEL of 5 [mu]g/m\3\. OSHA recognizes that the 
supplemental use of respirators may still be necessary in some 
situations. A significant portion of the welders who may need 
supplemental respiratory protection are working in confined spaces or 
other enclosed areas, where the use of engineering controls may be 
limited due to space constraints. However, respirator use in those 
circumstances will not be extensive and does not undermine OSHA's 
finding that the PEL of 5 [mu]g/m\3\ is technologically feasible.
    For a more detailed explanation of OSHA's technological feasibility 
analysis for all welding operations, see Chapter III of the FEA.
    Aerospace: OSHA has determined that most operations in the 
aerospace industry can achieve a PEL of 5 [mu]g/m\3\. These operations 
include sanding Cr(VI) coated parts, assembly, and two-thirds of the 
spray painting operations. Field studies have shown that use of LEV at 
the sanding source can reduce exposures by close to 90 percent, with 
workers exposures well below the final PEL of 5 [mu]g/m\3\. Exposure 
data provided to the docket show that the spray painting operations in 
paint booths or paint rooms using optimum engineering controls can 
achieve worker exposures below the final PEL of 5 [mu]g/m\3\ (excluding 
large parts, whole planes, or the interior of the fuselage)
    OSHA recognizes that there are certain instances where the 
supplemental use of respirators may be necessary because engineering 
and work practice controls are not sufficient to reduce exposures below 
the PEL. For example, when spray painting large parts or entire planes 
in hangars, engineering controls become less effective because of the 
large area needing ventilation and the constantly changing position of 
workers in relationship to these controls. As a result, OSHA estimates 
that engineering and work practice controls can limit exposures to 
approximately 25 [mu]g/m\3\ under the conditions described above and 
supplemental use of respirators will be needed to achieve the PEL of 5 
[mu]g/m\3\. Accordingly, OSHA has adopted a provision for the painting 
of whole aircrafts (interior or exterior) and large aircraft parts that 
requires employers to reduce exposures to 25 [mu]g/m\3\ with 
engineering and work practice controls and supplement these controls 
with the use of respiratory protection to achieve the PEL. For a more 
detailed explanation of OSHA's technological feasibility analysis for 
aerospace painting, see Chapter III of the FEA.
    Other Industries: Other application groups that generate fine dusts 
such as chromate pigment production, chromium catalyst production, and 
chromium dye production may require new or improved ventilation to 
achieve the PEL of 5 [mu]g/m\3\. Housekeeping measures are also 
important for controlling Cr(VI) exposures in these industries. General 
housekeeping and the use of HEPA vacuums instead of dry sweeping will 
minimize background exposures for most job categories. For a more 
detailed explanation of OSHA's technological feasibility analysis for 
chromate pigment producers, chromium catalyst producers, and chromium 
dye producers, see Chapter III of the FEA.
    Apart from the aerospace painting operations discussed above, OSHA 
recognizes that there are a few limited operations where the 
supplemental use of respirators may be necessary to achieve the PEL of 
5 [mu]g/m\3\. However, OSHA believes that the final PEL can be achieved 
in most operations most of the time with engineering and work practice 
controls. As noted previously, Table VIII-3 shows OSHA's estimate of 
respirator use by industry for each of the PELs that OSHA considered.
    Technological Feasibility of the Proposed PEL: As discussed more 
thoroughly in paragraph (c) of the Summary and Explanation of the 
Standard and in Chapter III of the FEA, OSHA has determined that the 
proposed PEL of 1 [mu]g/m\3\ is not feasible across all industries 
because it cannot be achieved using engineering and work practice 
controls in a substantial number of industries and operations employing 
a large number of workers covered by the standard (in particular, see 
"Technological Feasibility of the Proposed 1 [mu]g/m\3\ 8-Hour TWA 
PEL" in Chapter III of the FEA). Specifically, OSHA has determined 
that a PEL of 1 [mu]g/m\3\ is not feasible for welding, which affects 
the largest number of establishments and employees.
    A PEL of 1 [mu]g/m\3\ is also technologically infeasible for 
aerospace painting, where two-thirds of all spray painting operations 
cannot reduce exposures to at or below 1 [mu]g/m\3\ using engineering 
and work practice controls. Finally, OSHA was unable to conclude that 
the proposed PEL was technologically feasible for existing facilities 
in several other industries or operations, such as pigment production, 
catalyst production, and some hard chrome electroplating operations, 
where a PEL of 1 [mu]g/m\3\ would significantly increase the number of 
workers requiring respiratory protection.

D. Costs

    The costs employers are expected to incur to comply with the final 
standard are $282 million per year. In addition, OSHA estimates that 
employers will incur $110 million per year to comply with the personal 
protective equipment and hygiene requirements already present in 
existing generic standards. The final requirements to provide 
protective clothing and equipment and hygiene areas are closely aligned 
with the requirements of OSHA's current generic PPE and sanitation 
standards (e.g., 1910.132 and 1926.95 for PPE and 1910.142 and 1926.51 
for the hygiene requirements). Therefore, OSHA estimates that the 
marginal cost of complying with the new PPE and sanitation requirements 
of the Cr(VI) standard was lower for firms currently subject to and in 
compliance with existing generic standards. OSHA's research on these 
current standards, however, uncovered some noncompliance. The baseline 
chosen for the Cr(VI) regulatory impact analysis reflects this non-
compliance with current requirements. Although OSHA estimates that 
employers would need to spend an additional $110 million per year to 
bring themselves into compliance with the personal protective equipment 
and hygiene requirements already prescribed in existing generic 
standards, this additional expenditure is not attributable to the 
Cr(VI) rulemaking. However, the rule does require employers to pay for 
PPE. In some cases where employers do not now pay for PPE, employers 
will incur costs they did not previously have. However, because these 
costs were previously borne by employees, this change does not 
represent a net cost to the country. OSHA estimates that employers 
would be essentially transferring a benefit to employees of $6 million 
per year, the value of the portion of the total expense now paid by 
employees.
    All costs are measured in 2003 dollars. Any one-time costs are 
annualized over a ten-year period, and all costs are annualized at a 
discount rate of 7 percent. (A sensitivity analysis using a discount 
rate of 3 percent is presented in the discussion of net benefits.) The 
derivation of these costs is presented in Chapter IV of the full FEA. 
Table VIII-4 provides the annualized costs by provision and by 
industry. Engineering control costs represent 41 percent of the costs 
of the new provisions of the final standard, and respiratory protection costs 
represent 25 percent of the costs of the new provisions of the final 
standard. Costs for the new provisions for general industry are $192 
million per year, costs for constructions are $67 million per year, and 
costs for the shipyard sector are $23 million per year. In developing 
the costs for construction, OSHA assumed that all work by construction 
firms would be covered by the construction standard. However, in 
practice some work by construction firms takes the form of maintenance 
operations that would be covered by the general industry standard. 
(OSHA sought comment on this issue but received none.)
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    Table VIII-4 also shows the costs by application group. The various 
types of welding represent the most expensive application group, 
accounting for 51 percent of the total costs.
    Table VIII-5 presents OSHA's final total annualized costs by cost 
category for each of the alternative PELs considered by OSHA in the 
proposed rule. At a discount rate of 7 percent, total costs range from 
$112 million for a PEL of 20 [mu]g/m\3\ to $1.8 billion for a PEL of 
0.25 [mu]g/m\3\.
    OSHA also presents, in Table VIII-6, the distribution of compliance 
costs at the time they are imposed. Because firms will have the choice 
of whether to finance expenditures in a single year, or spread them out 
over four years, OSHA considers it unlikely that a firm would be 
impacted in an amount equal to the entire startup cost in the year that 
the initial requirements are imposed. On the other hand, capital 
markets are not perfectly liquid and particular firms may face 
additional lending constraints, therefore OSHA believes that 
identifying startup costs, in addition to the annualized costs, is 
relevant when exploring the question of economic feasibility and the 
overall impact of this rulemaking.
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E. Economic Impacts

    To determine whether the final rule's projected costs of compliance 
would raise issues of economic feasibility for employers in affected 
industries, i.e., would adversely alter the competitive structure of 
the industry, OSHA first compared compliance costs to industry revenues 
and profits. OSHA then examined specific factors affecting individual 
industries where compliance costs represent a significant share of 
revenue, or where the record contains other evidence that the standard 
could have significant impact on the competitive structure of the 
industry.
    OSHA compared the baseline financial data with total annualized 
incremental costs of compliance by computing compliance costs as a 
percentage of revenues and profits. This impact assessment for all 
firms is presented in Table VIII-7. This table is considered a 
screening analysis and is the first step in OSHA's analysis of whether 
the compliance costs potentially associated with the standard would 
lead to significant impacts on establishments in the affected 
industries. The actual impact of the standard on the viability of 
establishments in a given industry, in a static world, depends, to a 
significant degree, on the price elasticity of demand for the services 
sold by establishments in that industry.
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    Price elasticity refers to the relationship between the price 
charged for a service and the demand for that service; that is, the 
more elastic the relationship, the less able is an establishment to 
pass the costs of compliance through to its customers in the form of a 
price increase and the more it will have to absorb the costs of 
compliance from its profits. When demand is inelastic, establishments 
can recover most of the costs of compliance by raising the prices they 
charge for that service; under this scenario, profit rates are largely 
unchanged and the industry remains largely unaffected. Any impacts are 
primarily on those using the relevant services. On the other hand, when 
demand is elastic, establishments cannot recover all the costs simply 
by passing the cost increase through in the form of a price increase; 
instead, they must absorb some of the increase from their profits. 
Commonly, this will mean both reductions in the quantity of goods and 
services produced and in total profits, though the profit rate may 
remain unchanged. In general, "when an industry is subject to a higher 
cost, it does not simply swallow it, it raises its price and reduces 
its output, and in this way shifts a part of the cost to its consumers 
and a part to its suppliers," in the words of the court in American 
Dental Association v. Secretary of Labor (984 F.2d 823, 829 (7th Cir. 
1993)).
    The Court's summary is in accordance with micro-economic theory. In 
the long run, firms can only remain in business if their profits are 
adequate to provide a return on investment that assures that investment 
in the industry will continue. Over time, because of rising real 
incomes and productivity, firms in most industries are able to assure 
an adequate profit. As technology and costs change, however, the long 
run demand for some products naturally increases and the long run 
demand for other products naturally decreases. In the face of rising 
external costs, firms that otherwise have a profitable line of business 
may have to increase prices to stay viable. Commonly, increases in 
prices result in reduced demand, but rarely eliminate all demand for 
the product. Whether this decrease in the total production of the 
product results in smaller production for each establishment within the 
industry, or the closure of some plants within the industry, or a 
combination of the two, is dependent on the cost and profit structure 
of individual firms within the industry.
    If demand is completely inelastic (i.e., price elasticity is 0), 
then the impact of compliance costs that are 1 percent of revenues for 
each firm in the industry would result in a 1 percent increase in the 
price of the product or service, with no decline in quantity demanded. 
Such a situation represents an extreme case, but might be correct in 
situations in which there are few if any substitutes for the product or 
service in question, or if the products or services of the affected 
sector account for only a very small portion of the income of its 
consumers.
    If the demand is perfectly elastic (i.e., the price elasticity is 
infinitely large), then no increase in price is possible and before-tax 
profits would be reduced by an amount equal to the costs of compliance 
(minus any savings resulting from improved employee health and/or 
reduced insurance costs) if the industry attempted to keep producing 
the same amount of goods and services as previously. Under this 
scenario, if the costs of compliance are such a large percentage of 
profits that some or all plants in the industry can no longer invest in 
the industry with hope of an adequate return on investment, then some 
or all of the firms in the industry will close. This scenario is highly 
unlikely to occur, however, because it can only arise when there are 
other goods and services that are, in the eyes of the consumer, perfect 
substitutes for the goods and services the affected establishments 
produce.
    A common intermediate case would be a price elasticity of one. In 
this situation, if the costs of compliance amount to 1 percent of 
revenues, then production would decline by 1 percent and prices would 
rise by 1 percent. In this case, the industry revenues would stay the 
same, with somewhat lower production, but similar profit rates (in most 
situations where the marginal costs of production net of regulatory 
costs would fall as well). Consumers would, however, get less of the 
product or the service for their expenditures, and producers would 
collect lower total profits; this, as the court described in ADA v. 
Secretary of Labor, is the more typical case.
    If there is a price elasticity of one, the question of economic 
feasibility is complicated. On the one hand, the industry will 
certainly not be "eliminated" with the level of costs found in this 
rulemaking, since under these assumptions the change in total profits 
is somewhat less than the costs imposed by the regulation. But there is 
still the question of whether the industry's competitive structure will 
be significantly altered. For example, given a 20 percent increase in 
costs, and an elasticity of one, the industry will not be eliminated. 
However, if the increase in costs is such that all small firms in an 
industry will have to close, this could reasonably be concluded to have 
altered its competitive structure. For this reason, when costs are a 
significant percentage of revenues, OSHA examines the differential 
costs by size of firm, and other classifications that may be important.
    Some commenters (Ex. 38-265; Ex. 38-202; Ex. 40-12) questioned the 
screening analysis approach for several reasons: (1) It fails to 
provide for a facility-by-facility analysis; (2) it fails to consider 
that, in some plants, there may be product lines that do not involve 
hexavalent chromium; and (3) the concept of cost pass-through is 
largely negated by foreign competition. It should be noted that almost 
all commenters arguing for the inadequacy of screening analysis also 
argued for much higher costs than those estimated by OSHA (criticisms 
of costs were examined in Chapter 4). No one in the record presented an 
argument as to why costs representing less than one percent of revenues 
would be economically infeasible.
    First, some commenters (Ex. 38-265; Ex. 40-12; Ex. 47-5) argued 
that industry ratios of costs to profits or costs to revenues cannot 
adequately determine economic feasibility--instead the analysis must be 
conducted on a facility-by-facility basis. OSHA rejects this argument 
for two reasons. First, the judicial definition of economic feasibility 
notes that a regulation may be economically feasible and yet cause some 
marginal facilities to close. (American Textile Mfrs. Institute, Inc. 
v. Donovan 452 U.S. 490, 530-532 (1981))
    OSHA's obligation is not to determine whether any plants will 
close, or whether some marginal plants may close earlier than they 
otherwise might have, but whether the regulation will eliminate or 
alter the competitive structure of an industry. OSHA has an obligation 
to examine industries, and to consider its industry definitions 
carefully, so that they compare like with like. However, OSHA does not 
have an obligation to conduct facility-by-facility analysis of the 
thousands of facilities in the dozens of industries covered by a major 
standard. OSHA criteria can be examined through examination of industry 
ratios, particularly when the costs represent a very small percentage 
of revenues. Again, it must be noted that almost all commenters arguing 
for the inadequacy of screening analysis also argued for much higher 
costs than those estimated by OSHA, and while not agreeing with the 
need for facility-by-facility analysis, OSHA agrees that as costs 
become high as a percentage of revenues, something more than industry 
ratio analysis may be needed.
    Second, some commenters argued that some facilities and industries 
have some lines of production involving hexavalent chromium, and some 
that do not, and, in such cases, OSHA should analyze only the revenues 
and profits associated with the lines using hexavalent chromium. Even 
if this were desirable, the data for such an analysis is simply not 
publicly available. No
government data source collects data in a way that could be used for 
this purpose, and there is little privately collected data that could 
be used for this purpose. Even if such data were available, there are 
reasons to produce a product line even if it has profits lower than 
other product lines, and the data to examine this issue is even more 
unavailable. Further, OSHA's mandates, as interpreted by the courts, 
focus on the effect of a standard on industries, not on product lines 
within those industries. (American Iron & Steel Institute v. OSHA, 939 
F.2d 975, 986 (D.C. Cir, 1991))
    Finally, some commenters (SFIC, Ex. 38-265; SSINA, Ex. 40-12, Ex. 
47-5; Engelhard, Ex. 38-202) questioned the above analysis by bringing 
up the issue of foreign competition, and some presented the argument 
that foreign competition made price increases impossible.
    While foreign competition is an important issue to consider in 
analyzing economic feasibility, the presence of foreign competition 
does not mean that price increases are impossible. In economic terms, 
the case that foreign competition makes price increases impossible 
would be an argument that foreign competition puts all firms into the 
situation of having infinite elasticity of domestic demand, because 
foreign firms are not subject to the regulation, and, as a result can 
underprice American firms and drive them out of business.
    Is this the case? Both theory and history suggest that it is not. 
From a theoretical viewpoint, the ability to sell to a consumer is 
determined by the price at the site, plus the cost of transportation, 
plus or minus intangible factors (such as quality or timeliness). Under 
these circumstances, a specific establishment can be competitive even 
if its cost of production is greater than that of foreign competitors--
if the U.S. producer has other advantages.
    From a practical viewpoint, econometric studies typically talk 
about the elasticity of domestic production with respect to foreign 
prices. No one assumes that a lower foreign price simply and totally 
assures that the domestic industry will be eliminated. Foreign 
competition has been a fact for decades--this does not mean that any 
domestic regulation assures that the domestic industry will be 
eliminated.
    However, foreign competition does mean the elasticity of demand for 
domestic production will be greater than the total elasticity of demand 
for the product in question. Thus foreign competition is a factor that 
can result in greater elasticity of demand for domestic firms, and that 
needs to be considered in the context of the overall feasibility 
analysis, just as other factors such as the presence or absence of good 
substitutes need to be considered in the analysis.
    A different problem with the formulation in terms of demand 
elasticity given above is that it ignores other things besides the 
regulatory costs that may act to shift either the costs of the 
production or demand for a product or service. In the normal course of 
events, neither demand nor supply is static. Costs of inputs needed 
commonly increase (at least in nominal terms). Productivity may 
increase or decrease as technology changes. Increases in income or GDP 
normally serve to increase demand for a good or service from year to 
year (for the majority of goods with positive income elasticity). In a 
typical year for most manufacturing industries, some costs will rise, 
productivity will also improve, and increases in GDP will increase 
demand. Adjusting to cost increases is thus a part of the normal 
economic scene. Even a real cost increase brought about by a regulation 
may be partially offset by productivity improvement. Finally, even real 
price increases may not decrease the quantities sold (and thus force 
employers to close) if the price increases are offset by income-driven 
increased demand for the good or service. A real price increase caused 
by the costs of a regulation will mean that the quantity sold will be 
lower than it otherwise would have been, but does not imply that actual 
quantity sold for the product will decline as compared to past years.
    Table VIII-7 provides costs as percentage of revenues and profits 
for all affected establishments. OSHA believes that this is the best 
starting point for fulfilling its statutory responsibility to determine 
whether the standard affects the viability of an industry as a whole.
    Table VIII-8 shows costs as a percentage of profits and revenues 
for firms classified as small by the Small Business Administration and 
Table VIII-9 shows costs as a percentage of revenues and profits for 
establishments with fewer than 20 employees. (These tables use costs 
with a discount rate of 7 percent.) These small-business tables show 
greater potential impacts, especially for small electroplating 
establishments. Based on these results, OSHA has prepared a Final 
Regulatory Flexibility Analysis (see Chapter VII of the FEA) to examine 
the impacts on small businesses and how they can be alleviated. (Tables 
V-5, V-6, and V-7 in the FEA show the same information using a discount 
rate of 3 percent.)
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Economic Feasibility for Many Industries With Low Potential Impacts

    To determine whether a rule is economically feasible, OSHA 
evaluates evidence from a number of sources. And while there is no hard 
and fast rule, in the absence of evidence to the contrary OSHA 
generally considers a standard economically feasible when the costs of 
compliance are less than one percent of revenues. Common-sense considerations 
indicate that potential impacts of such a small magnitude are unlikely to 
eliminate an industry or significantly alter its competitive structure 
particularly since most industries have at least some ability to raise 
prices to reflect increased costs. Of course, OSHA recognizes that even 
when costs are within this range, there could be unusual circumstances 
requiring further analysis. In addition, as a second check, OSHA also 
looks to see whether even such low costs may represent more than ten 
percent of the profit in a particular industry. If either of these 
factors is present, or if there is other evidence of industry demise or 
potential disruption in an industry's competitive structure because of 
the standard, OSHA examines the effect of the rule on that industry 
more closely. Finally, OSHA reviews the record for any other unusual 
circumstances, such as excellent substitutes of equal cost that might 
make an industry particularly sensitive to price change. In this case, 
the only argument of this kind that OSHA noted was an argument by one 
commenter that trivalent chromium plating might be substituted in some 
applications for hexavalent chromium. However, even if this is the case 
(some in the record did not agree), a plating operation could switch to 
trivalent plating with minimal capital investment and thus remain in 
business.
    OSHA believes that a potential one percent revenue effect is an 
appropriate way to begin the analysis in light of the fact that the 
United States has a dynamic and constantly changing economy. There is 
an enormous variety of year-to-year events that could cause a one 
percent increase in a business's costs, e.g., increasing fuel costs, an 
unusual one-time expense, changes in costs of materials, increased 
rents, increased taxes, etc. Table V-8, which shows year to year 
changes in prices for a number of industries affected by the standard, 
reflects this phenomenon.
    Changes in profits are also subject to the dynamics of the economy. 
A recession, or a downturn in a particular industry, will typically 
cause profit declines in excess of ten percent for several years in 
succession. Table V-9, which shows annual profits for several years in 
succession, illustrates this phenomenon. While a permanent loss of 
profits presents a greater problem than a temporary loss, these year-
to-year variations do serve to show that small changes in profits are 
quite normal without affecting the viability of industries.
    The potential impacts of this regulation on the affected employers, 
for the most part, are within the range of normal year-to-year 
variation that firms and industries expect and survive. Table V-8 in 
the FEA shows year-to-year price variations for selected industries 
with hexavalent chromium exposure, and Table V-9 (in the FEA) shows 
year-to-year profit variations for selected industries with hexavalent 
chromium exposures. Table V-8 serves the purpose of showing that, for 
many industries, annual price changes of one percent or more are 
commonplace without affecting the viability of the industry. Table V-9 
serves to show that temporary profit swings of significantly more than 
ten percent are also well within the boundaries of normal year-to-year 
change.
    Because a permanent decrease in profits is much more significant 
than a temporary swing of the same magnitude, OSHA has also used the 
fact that a very large short term decline can be compared in effect to 
a smaller long-term decrease in profits to calculate the extent to 
which the temporary changes shown in Table V-9 may demonstrate an 
industry's ability to withstand a long-term change. For example, using 
a 7 percent discount rate, and the assumption that profits return to 
the long term average following a temporary decline, the following 
short term declines are approximately equivalent to a 10 percent long-
term decline:

50 percent decline for one year;
30 percent decline for two years;
20 percent decline for three years.

    Looking at profits of the average corporation for the period of 
1990 to 2002, events of one of the above magnitudes have occurred twice 
in that 12-year period without threatening industrial viability. (Based 
on corporate profit rate data from IRS, Statistics of Income: Corporate 
Income Tax Returns, as Reported in U.S. Department of Commerce, U.S. 
Statistical Abstract 2006). And since, as discussed below, demand is 
not perfectly elastic in any of the affected industries, it is unlikely 
that the actual effect on profits will be as high as indicated in Table 
VIII-7.
    The record does not contain evidence that any of the affected 
industries for which OSHA found that the costs of complying with the 
standard will be less than both one percent of prior revenue and ten 
percent of prior profits will in fact be threatened by the standard. 
Although some industry representatives asserted that compliance would 
threaten their existence, these assertions (with one exception, 
discussed below) were not supported by empirical evidence that even the 
proposed PEL of 1 would be economically infeasible. As noted above, 
cost changes of less than one percent are routinely passed on and 
impacts that are less than 10 percent of profits have not been shown to 
be likely to affect the viability or competitive structure of any of 
the industries affected by this standard.

Economic Feasibility for Industries With Higher Potential Impacts

    In Table VIII-7, OSHA found that there were 9 industries in three 
application groups in which costs were greater than 1 percent of 
revenues, and an additional 22 industries in six application groups in 
which costs were greater than 10 percent of profits.
    However, this number of industries is somewhat misleading. Seven of 
the industries in which costs exceed one percent of revenues, and an 
additional twelve of those in which costs exceeded 10 percent of 
profits (without exceeding 1 percent of revenues) are industries in the 
plating and welding application groups in which plating or welding are 
exceedingly rare, such as electroplating in the performing arts, 
spectator sports and related industries (NAICS 711) and welding in 
religious, governmental, civil, and professional organizations (NAICS 
813). In both cases, only one establishment in the entire industry 
reported engaging in either welding or plating. It is difficult to 
determine whether reports of welding or plating in such industries 
represent an extremely unusual situation or, perhaps, simply someone 
inadvertently checking the wrong box on a survey. In either case, OSHA 
concludes that if such establishments do indeed engage in welding or 
plating, they could maintain their primary line of business, as almost 
everyone else in their industries does, by dropping welding or plating 
operations if such operations represented any threat whatsoever to the 
viability of their businesses.
    The same is true of the other industries that are in the general 
category of extremely rare and unusual users of plating operations: 
Specialty trade contractors (NAICS 238); wholesale trade and durable 
goods (NAICS 423); motor vehicle and parts dealers (NAICS 441); 
furniture and home furnishing stores (NAICS 442); electronics and 
appliance stores (NAICS 443); building materials and garden equipment 
dealers (NAICS 444); health and personal care stores (NAICS 446); 
miscellaneous store retailers (NAICS 453); nonstore retailers (NAICS 
454); information services and data processing service (NAICS 519); 
rental and leasing services (NAICS 532); professional, scientific and 
technical services (NAICS 541); performing arts, spectator sports and 
related industries (NAICS 711); and personal and laundry services 
(NAICS 812). In the welding application groups, the industries in this 
category are: gasoline stations (NAICS 447); nursing and residential 
care (NAICS 623); social assistance (NAICS 624); food services and 
drinking places (NAICS 722); and religious, governmental, civil, and 
professional organizations (NAICS 813).
    The remainder of this section examines those industries with higher 
potential impacts where their businesses may be dependent on Cr (VI) 
applications.
    Electroplating Job Shops: Electroplating job shops (NAICS 332813: 
electroplating, plating, polishing anodizing and coloring services) are 
a service industry for the manufacturing sector, and, to a lesser 
extent, to those maintaining, restoring, or customizing objects with 
metal parts. At a PEL of 5, job shops have costs as a percentage of 
profits of 30 percent and costs as a percentage of revenues of 1.24 
percent. These firms sell a service rather than a product. (Firms that 
directly sell the products they plate end up in other NAICS codes.) As 
a result, plating firms are primarily affected by foreign competition 
through the loss of other manufacturing in the United States, rather 
than through their customers sending products or their component parts 
abroad for electroplating. However, some commenters noted that there 
may be cases of sending products abroad for the sole purpose of 
electroplating. This seems unlikely to be commonplace however, because 
of the shipping times and costs for a process that normally represents 
a very small part of the value added for the ultimate product. In 
addition, because electroplating is essential to the manufacture of 
most plated products, the ultimate demand for plating services is 
unlikely to decrease significantly.
    Finally, independent electroplating shops have been subject to 
annual profit changes larger in magnitude than those associated with 
this standard. Table V-9 in the FEA shows that, over the past ten 
years, profits in this industry have risen and fallen as much as 49 
percent in one year without affecting the viability of the industry. 
Although these kinds of temporary changes would not have the effect of 
permanent decline of profits by 30 percent, OSHA believes that all of 
the factors discussed above indicate that there is sufficient price 
elasticity and other flexibility in this industry to absorb these 
costs.
    The price increase of 1.24 percent required to fully restore 
profits at a PEL of five is significantly less than the average annual 
increase in price of electroplating services, as shown by Table V-8 in 
the FEA. Further, during the period shown in Table V-8, the industry 
successfully survived, without any real price increase, the regulatory 
costs imposed by EPA's Chrome MACT standard. The costs of that standard 
are somewhat uncertain. Some commenters argued that that standard could 
be quite expensive. One commenter suggested that one facility had 
incurred costs of $80,000 per year to meet that standard, and that such 
high costs were not atypical. (Tr. 2003) Another commenter noted, 
however, that "the effect of the MACT Standard was minimized when 
people realized that the combination of a mist suppressant and the 
development of a mist suppressant that would work in a hard chrome 
installation along with the use of mesh pads puts you below the MACT 
standard." (Tr. 2203) The commenter apparently felt that, in the 
latter case, the costs would not have been significant. Nevertheless, 
in either event, probably due to productivity improvement in other 
aspects of the industry, there was no real price increase or massive 
dislocation in the industry.
    SFIC (Ex. 38-265) also argued that it was difficult to pass on 
costs in electroplating based on an EPA study that estimated a cost 
pass through elasticity of 0.58. This study was based on pre-1996 data, 
and found a statistical relationship between nominal price increases 
and increases in a nominal cost index. Whatever the difficulties in 
passing increased costs to its customers the industry might have had 
before 1996, since that time nominal prices have increased in ways that 
did not have the effects on profit predicted by the EPA study.
    Even in the event of a real price increase, we believe that demand 
for electroplating services is relatively inelastic. For most products 
that are plated, plating is basically essential to the function of the 
product. The EPA study for the MACT standard found that products 
incorporating electroplating had relatively inelastic demand, on the 
order of less than 0.5, and the cost of plating represented a very 
small percentage of the total costs of the products in question. In 
this situation, the chief danger associated with a real cost increase 
of less than 1 percent is that there would be some increased foreign 
penetration of U.S. markets. However, the small size of the change, and 
the difficulty of sending products abroad solely for plating services, 
assures that the price change in question would not eliminate the 
industry, and is unlikely to alter the competitive structure of the 
industry.
    However, OSHA is concerned about the economic feasibility of the 
standard for electroplating at a PEL of 1. At this lower PEL, costs of 
the standard represent 2.7 percent of revenues and 65 percent of 
profits. In almost all OSHA health standards in which this figure was 
developed, the costs for the most affected industry have been less than 
2 percent of revenues. (The major exception was brass and bronze 
foundries, where the lead standard PEL was found economically 
infeasible with the use of engineering controls.) Further, in standards 
where the costs might have been in excess of 2 percent of revenues, 
OSHA has sought ways to lower the cost through long term phase-ins of 
engineering controls. OSHA examined this possibility for job-shop 
electroplaters, and found that even allowing the use of respirators 
rather than engineering controls would not significantly lower the 
costs as percentage of revenues. OSHA also examined the issue of 
whether there were particular types of platers that might have 
unusually high or low costs, and found that even quite different 
plating shop configurations with respect to the type of plating done 
would have approximately equal average costs.
    Given the high level of costs as a percentage of revenues and 
profits, and the inability to alleviate those impacts without a higher 
PEL, OSHA further examined the economic feasibility of the standard at 
a PEL of 1. It seems unlikely that a price increase of 2.7 percent, 
although significantly larger than the average nominal price increases 
in recent years, would eliminate the industry entirely. OSHA has 
concluded, however, that the costs associated with such a PEL could 
alter the competitive structure of the industry. OSHA has concluded 
this because these costs substantially exceed the average nominal price 
increases in the industry, and the reasons for these nominal price 
increases--increases in the cost of labor and energy, for example--will 
continue. Thus a price increase that would assure continued 
profitability for the entire industry would require almost tripling the 
annual nominal price increase. (The long term average price increase 
for plating, as shown in Table V-9, is 1.6 percent per year. Assuming 
this continues to be needed, an increase that would leave profits 
unchanged would require a cost increase of 4.2 percent (1.6 plus 2.6), 
almost three times as much.) That would represent a significant real 
price increase that might not be passed forward, particularly by older 
and less profitable segments of the industry.
    Welding (Stainless Steel) in Construction: OSHA calculated that the 
costs of the standard could equal 22.3 percent of profits in this 
industry, but only 0.92 percent of revenues. The maximum price 
increases required to fully restore profits (0.92 percent) is unlikely 
to significantly alter the demand for construction welding services 
which are essential for many projects and not subject to foreign 
competition. Further, costs of using stainless steel (the chief source 
of welding exposure) already vary significantly from year to year, and 
often from month to month. Table V-10 shows the producer price index 
for steel prices. Prices of steel have changed by more than 10 percent 
within a single year a number of times in the past ten years without 
affecting the viability of the use of stainless steel in construction.
    Welding in General Industry: There are a significant number of 
establishments engaged in welding in repair and maintenance (NAICS 811) 
and in personal and laundry services (NAICS 812). For repair and 
maintenance services, the costs as a percentage of revenues are 0.40 
percent and the costs as a percentage of profits are 10.5 percent. For 
personal and laundry services the costs as a percentage of revenues are 
0.67 percent and costs as a percentage of profits are 13 percent. (All 
costs include the costs of any respirators welders will need to use.) 
These two sectors conduct maintenance and repair welding. Even if costs 
cannot be passed on, the resulting declines in profits are unlikely to 
affect the viability of an otherwise viable employer. Further, 
businesses of this kind are more likely to be able to increase costs 
because of the absence of foreign competition. While some loss of 
revenue is possible with a price increase, it is unlikely that the 
quantity of routine repairs would be significantly affected by price 
increases of this magnitude.
    Painting and Corrosion Protection: Four sectors in the painting 
application groups have costs as a percentage of revenues in excess of 
one percent or costs as a percentage of profits in excess of 10 
percent. These are motor vehicle body and trailer manufacturing (NAICS 
3362) with costs of 0.51 percent and 20 percent; military armored 
vehicle and tank manufacturers (NAICS 336992) with costs of 0.25 
percent and 10 percent; used car dealers (NAICS 44112) with costs of 
0.41 percent and 34 percent; and automotive body, paint and interior 
repair (NAICS 81121) with costs of 1.5 percent and 39 percent. These 
costs are incurred in part for the use of hexavalent chromium pigments, 
but largely for using hexavalent chromium coating (applied like paint) 
as undercoats for corrosion protection. In the case of the first two 
NAICS codes, these are part of manufacturing processes. For both of 
these manufacturing industries, while the costs of hexavalent chromium 
coatings may be significant in the establishments where they are 
applied, the costs of Hexavalent chromium coatings represent an 
insignificant percentage of the costs of a car or a tank. While 
manufacturers may seek substitutes for hexavalent chromium coatings, 
additional expenses for such coatings are unlikely to affect the 
ultimate demand for cars or tanks. The latter two affected industries 
involve repair and refurbishing of existing automobiles. The cost 
analysis assumes all firms who currently use hexavalent chromium in 
these industries will continue to do so. In each case, there are 
choices that would avoid the costs in question. One choice would be to 
use non-hexavalent chromium pigments or non-hexavalent chromium 
corrosion protection. A variety of substitutes have been developed, and 
the use of hexavalent chromium based coatings for these purposes is 
already banned in California. (Tr. 1913) Although these substitutes 
have not yet been subject to long term use and their protectiveness is 
currently less certain than that of hexavalent chromium, it is likely 
that products that are equivalent to hexavalent chromium will be 
developed, particularly if demand for such products increases as a 
result of the standard. In addition, applying hexavalent chromium 
coatings represents a very small portion of the business of either auto 
body repair shops or used car dealers. A firm whose viability was 
seriously threatened as a result of this standard could retain most of 
its core businesses without continuing to use hexavalent chromium.
    In addition, it is also reasonable to suppose that both used cars 
and auto body repair do not have highly elastic demand, such that a 
small change in prices would result in a very large drop in the number 
of cars repaired. As a result, the required increases in price can be 
accommodated without such significant losses as to alter the 
competitive structure of the industries.
    Chromium Catalyst Producers (0.8 percent; 27 percent) and Service 
Companies (0.44 percent; 12 percent): Chromium catalyst production and 
service companies are also unlikely to be affected by costs of the 
relative magnitude found here. Most companies are locked into the use 
of specific catalysts without major new investments. As a result, while 
there may be some small long-term shift away from the use of chromium 
catalysts, a price change of one percent is unlikely to immediately 
prompt such a change. This also means that the market for chrome 
catalyst services is likely to be maintained. Further, faced with a new 
regulation, companies are more rather than less likely to turn to a 
service company to handle chromium products. Based on these 
considerations, OSHA determined that the standard is economically 
feasible in these sectors.
    Iron and Steel Foundries: Iron and steel foundries (NAICS 3315) 
have costs that are 0.42 percent of revenues and 15 percent of profits. 
An oddity of the estimated costs for this industry is that 44 percent 
of the costs are associated with monitoring costs. In this cost 
estimate, OSHA assumes that iron and steel foundries will use scheduled 
periodic monitoring rather than adopting the option of performance-
based monitoring. Adopting a performance-based monitoring approach 
rather than scheduled monitoring might well reduce costs as a 
percentage of profits to less than 10 percent of profits. As noted 
above, cost changes of less than one percent are routinely passed on 
and impacts that are less than 10 percent of profits have not been 
shown to be likely to affect the viability or competitive structure of 
any of the industries affected by this standard.
    Even if costs are not reduced, the industry has demonstrated its 
ability to survive real cost increases by remaining viable in the face 
of a 32 percent increase in the price of its basic input, steel, over 
the last two years. Based on these considerations, OSHA concludes the 
standard is feasible for this sector.

F. Benefits and Net Benefits

    OSHA estimated the benefits associated with alternative PELs for 
Cr(VI) by applying the dose-response relationship developed in the risk 
assessment to current exposure levels. OSHA determined current exposure 
levels by first developing an exposure profile for industries with 
Cr(VI) exposures using OSHA inspection and site visit data, and then 
applying this profile to the total current worker population. The 
industry-by-industry exposure profile was given in Table VIII-2 above.
    By applying the dose-response relationship to estimates of current 
exposure levels across industries, it is possible to project the number 
of lung cancers expected to occur in the worker
population given current exposures (the "baseline"), and the number 
of these cases that would be avoided under alternative, lower PELs. 
OSHA assumed that exposures below the limit of detection (LOD) are 
equivalent to no exposure to Cr(VI), thus assigning no baseline or 
avoided lung cancers (and hence, no benefits) to these exposures. For 
exposures above the current PEL and for purposes of determining the 
benefit of reducing the PEL, OSHA assumed exposure at exactly the PEL.
    Consequently, the benefits computed below are attributable only to 
a change in the PEL. No benefits are assigned to the effect of a new 
standard increasing compliance with the current PEL. OSHA estimates 
that between 3,167 and 12,514 lung cancers attributable to Cr(VI) 
exposure will occur during the working lifetime of the current worker 
population. Table VIII-10 shows the number of avoided lung cancers by 
PEL. At the final PEL of 5 [mu]g/m3, an estimated 1,782 to 
6,546 lung cancers would be prevented over the working lifetime of the 
current worker population.
    Note that the Agency based these estimates on a worker who is 
employed in a Cr(VI)-exposed occupation for his entire working life, 
from age 20 to 65. The calculation also does not allow workers to enter 
or exit Cr(VI) jobs, nor switch to other exposure groups during their 
working lives. While the assumptions of 45 years of exposure and no 
mobility among exposure groups may seem restrictive, these assumptions 
actually are likely to yield somewhat conservative (lower) estimates of 
the number of avoided cancers, given the nature of the risk assessment 
model.
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BILLING CODE 4510-26-C
    For example, consider the case of job covered by five workers, each 
working nine years rather than one worker for 45 years. The former 
situation will likely yield a slightly higher rate of lung cancers, 
since more workers are exposed to the carcinogen (albeit for a shorter 
period of time) and the average age of the workers exposed is likely to 
decrease. This is due to: (1) The linearity of the estimated dose-
response relationship, and (2) once an individual accumulates a dose, the 
increase in relative risk persists for the remainder of his lifetime. 
For example, a worker exposed from age 20 to 30 will have a constant 
increased relative risk for about 50 or so years (from age 30 on, 
assuming no lag between exposure and increased risk and death at age 
80), whereas a person exposed from age 40 to 50 will have only about 30 
years of increased risk (again assuming no lag and death at age 80). 
The persistence of the increased relative risk for a lifetime follows 
directly from the risk assessment and is typical of life table 
analysis.
    For informational purposes only, OSHA has estimated the monetary 
value of the benefits associated with the final rule. These estimates 
are informational because OSHA cannot use benefit-cost analysis as a 
basis for determining the PEL for a health standard. In order to 
estimate monetary values for the benefits associated with the final 
rule, OSHA reviewed the approaches taken by other regulatory agencies 
for similar regulatory actions. OSHA found that occupational illnesses 
are analogous to the types of illnesses targeted by EPA regulations and 
has thus used them in this analysis.
    OSHA is adopting EPA's approach, applying a value of $6.8 million 
to each premature fatality avoided. The $6.8 million value represents 
individuals' willingness-to-pay (WTP) to reduce the risk of premature 
death.
    Nonfatal cases of lung cancer can be valued using a cost of illness 
(COI) approach, using data on associated medical costs. The EPA Cost of 
Illness Handbook (Ex.35-333) reports that the medical costs for a 
nonfatal case of lung cancer are, on average, $136,460. Updating the 
EPA figure to 2003 dollars yields the value of $160,030. Including 
values for lost productivity, the total COI which is applied to the 
OSHA estimate of nonfatal cases of lung cancer is $188,502.
    An important limitation of the COI approach is that it does not 
measure individuals' WTP to avoid the risk of contracting nonfatal 
cancers or illnesses. As an alternative approach, nonfatal cancer 
benefits may be estimated by adjusting the value of lives saved 
estimates. In its Stage 2 Disinfection and Disinfection Byproducts 
water rule, EPA used studies on the WTP to avoid nonfatal lymphoma and 
chronic bronchitis as a basis for valuing nonfatal cancers. In sum, EPA 
valued nonfatal cancers at 58.3 percent of the value of a fatal cancer. 
Using WTP information would yield a higher estimate of the benefits 
associated with the reduction in nonfatal lung cancers, as the nonfatal 
cancers would be valued at $4 million rather than $188,502 per case. 
These values represent the upper and lower bound values for nonfatal 
cases of lung cancer avoided.
    Using these assumptions, latency periods of 15, 20, 25, and 30 
years--and adjustments to the value of statistical life to today--OSHA 
estimated the total annual benefits of the standard at various PELS in 
Table VIII-11, considering the benefits from preventing both fatal and 
non-fatal cases of lung cancer.
    Occupational exposure to Cr(VI) has also been linked to a multitude 
of other health effects, including irritated and perforated nasal 
septum, skin ulceration, asthma, and dermatitis. Current data on Cr(VI) 
exposure and health effects are insufficient to quantify the precise 
extent to which many of these ailments occur. However, it is possible 
to provide an upper bound estimate of the number of cases of dermatitis 
that occur annually and an upper estimate of the number that will be 
prevented by a standard. This estimate is an upper bound because it 
uses data on incidence of dermatitis among cement workers, where 
dermatitis is more common than it would be for other exposures to 
Cr(VI). It is important to note that if OSHA were able to quantify all 
Cr(VI)-related health effects, the quantified benefits would be 
somewhat higher than the benefits presented in this analysis.
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BILLING CODE 4510-26-C

    Using National Institute for Occupational Safety and Health (NIOSH) 
data, Ruttenberg and Associates (Ex. 35-332) estimate that the 
incidence of dermatitis among concrete workers is between 0.2 and 1 
percent. Applying the 0.2 percent-1 percent incidence rate indicates 
that there are presently 418-2,089 cases of dermatitis occurring 
annually. This approach represents an overestimate for cases of 
dermatitis in other application groups, since some dermatitis among 
cement workers is caused by other known factors, such as the high 
alkalinity of cement. If the measures in this final standard are 50 
percent effective in preventing dermatitis, then there would be an 
estimated 209-1,045 cases of Cr(VI) dermatitis avoided annually.
    To assign values to the cases of avoided dermatitis OSHA applied 
the COI approach. Ruttenberg and Associates computed that, on average, 
the medical costs associated with a case of dermatitis are $119 (in 
2003 dollars) and the indirect and lost productivity costs are $1,239 
(Ex. 35-332). These estimates were based on an analysis of BLS data on 
lost time associated with cases of dermatitis, updated to current 
dollars. Based on the Ruttenberg values, OSHA estimates that a Cr(VI) 
standard will yield $0.3 million to $1.4 million in annual benefits due 
to reduced incidence of dermatitis.
    Occupational exposure to Cr(VI) can lead to nasal septum 
ulcerations and nasal septum perforations. As with cases of dermatitis, 
the data were insufficient to conduct a formal quantitative risk 
assessment to relate exposures and incidence. However, previous studies 
provide a basis for developing an approximate estimate of the number of 
nasal perforations expected under the current PEL as well as PELs of 
0.25 [mu]g/m3, 0.5 [mu]g/m3, 1.0 [mu]g/
m3, 5.0 [mu]g/m3, 10.0 [mu]g/m3 and 
20.0 [mu]g/m3. Cases of nasal perforations were computed 
only for workers in electroplating and chrome production. The 
percentage of workers with nasal tissue damage is expected to be over 
50 percent for those regularly exposed above approximately 20 [mu]g/
m3. Less than 25 percent of workers could reasonably be 
expected to experience nasal tissue damage if Cr(VI) exposure was kept 
below an 8-hour TWA of 5 [mu]g/m3 and regular short-term 
exposures (e.g. an hour or so) were below 10 [mu]g/m3. Less 
than 10 percent of workers could reasonably be expected to experience 
nasal tissue damage at a TWA Cr(VI) below 2 [mu]g/m3 [and 
short-term exposures below 10 [mu]g/m3]. It appears likely 
that nasal damage might be avoided completely if all Cr(VI) exposures 
were kept below 1 [mu]g/m3.
    OSHA estimates that 1,728 nasal perforations/ulcerations occur 
annually under current exposure levels. OSHA estimates that 1,140 of 
these would be prevented under the final PEL of 5 [mu]g/m3. 
Due to insufficient data, it was not possible to monetize the benefits. 
Thus, the benefits associated with a reduction in nasal perforations/
ulcerations are excluded from the net benefits analysis presented 
below.
    Finally, for informational purposes, OSHA examined the net benefits 
of the standard, based on the benefits and costs presented above, and 
the costs per case of cancer avoided, as shown in Table VIII-12.
    As noted above, the OSH Act requires OSHA to set standards based on 
eliminating significant risk to the extent feasible. That criterion or 
a criterion of maximizing net (monetary) benefits may result in very 
different regulatory outcomes. Thus, these analyses of net benefits 
cannot be used as the basis for a decision concerning the choice of a 
PEL for a Cr(VI) standard.
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BILLING CODE 4510-26-C
    Nevertheless, the Agency agrees that additional information 
concerning the circumstances in which monetary benefits exceed costs 
would be a useful addition to the above table. OSHA found the following 
conditions key to determining whether benefits exceed costs:
     If the risk is at the lowest end of the range considered, 
then benefits do not exceed costs no matter what other variables are 
used.
     If the risk is at the high end of the range, and a 
discount rate of 7 percent is used, then benefits exceed costs for PELs 
of 1 and 20 if the latency period is less than 20 years, and for PELs 
of 5 and 10 if the latency period is less than 25 years.
     If the risk is at the high end of the range, and a 
discount rate of 3 percent is used, then benefits exceed costs for a 
PEL of 0.5 if the latency period is twenty years or less, and benefits 
exceed costs for all latency periods for all higher PELs.
    Incremental costs and benefits are those that are associated with 
increasing stringency of the standard. Comparison of incremental 
benefits and costs provides an indication of the relative efficiency of 
the various PELs. OSHA cannot use this information in selecting a PEL, 
but it has conducted these calculations for informational purposes. 
Incremental costs, benefits, net benefits and cost per cancer avoided 
are presented in Table VIII-13.
    In addition to examining alternative PELs, OSHA also examined 
alternatives to other provisions of the standard. These alternatives 
are discussed in the summary of the Final Regulatory Flexibility 
Analysis in the next section.

Click here to view table VIII-13

G. Summary of the Final Regulatory Flexibility Analysis

    The full final regulatory flexibility analysis is presented in 
Chapter VII of the FEA. Many of the topics discussed there, such as the 
legal authority for the rule; the reasons OSHA is going forward with 
the rule; and economic impacts on small business have been presented in 
detail elsewhere in the Preamble. As a result, this section focuses on 
two issues: duplicative, overlapping, or conflicting rules; and 
alternatives OSHA considered.

Federal Rules That May Duplicate, Overlap, or Conflict With the Final 
Rules

    OSHA's SBREFA panel for this rule suggested that OSHA address a 
number of possible overlapping or conflicting rules: EPA's Maximum 
Achievable Control Technology (MACT) standard for chromium 
electroplaters; EPA's standards under the Federal Insecticide, 
Fungicide, and Rodenticide Act (FIFRA) for Chromium Copper Arsenate 
(CCA) applicators; and state use of OSHA PELs for setting fence line 
air quality standards. The Panel was also concerned that, in some 
cases, other OSHA standards might overlap and be sufficient to assure 
that a new final standard would not be needed, or that some of the 
final standard's provisions might not be needed.
    OSHA has thoroughly studied the provisions of EPA's MACT standard 
and has also consulted with EPA. The standards are neither duplicative 
nor conflicting. The rules are not duplicative because they have 
different goals--environmental protection and protection against 
occupation exposure. It is quite possible, as many electroplaters are 
now doing, to achieve environmental protection goals without achieving 
occupational protection goals. The regulations are not conflicting 
because there exist controls that can achieve both goals without 
interfering with one another. However, it is possible that meeting the 
final OSHA standard would cause someone to incur additional costs for 
the MACT standard. If an employer has to make major changes to install 
LEV, this could result in significant expenses to meet EPA requirements 
not accounted for in OSHA's cost analysis. In its final cost estimates, 
OSHA has included costs for additional MACT testing in cases where it 
may be needed. OSHA has also allowed all facilities four years to 
install engineering controls, with the result that electroplaters can 
better coordinate their EPA and OSHA requirements and avoid the need 
for extra testing.
    OSHA examined the potential problem of overlapping jurisdiction for 
CCA applicators, and found that there would indeed be overlapping 
jurisdiction. As a result, OSHA had excluded CCA applicators from the 
scope of the coverage of the rule. OSHA has been unable to find a case 
where a state, as a matter of law, bases fence line standards on OSHA 
PELs. OSHA notes that the OSHA PEL is designed to address the risks 
associated with life long occupational exposure only.
    OSHA has also examined other OSHA standards, and where standards 
are overlapping, referred to them by reference in the final standard in 
order to eliminate the possibility of overlapping, duplicative or conflicting 
standards. Existing OSHA standards that may duplicate the final provisions 
in some respect include the standards addressing respiratory protection (29 CFR 
1910.134); hazard communication (29 CFR 1910.1200); access to medical 
and exposure records (29 CFR 1910.1020); general requirements for 
personal protective equipment in general industry (29 CFR 1910.132), 
construction (29 CFR 1926.95), and shipyards (29 CFR 1915.152); and 
sanitation in general industry (29 CFR 1910.141), construction (29 CFR 
1926.51), and shipyards (29 CFR 1915.97).

Regulatory Alternatives

    This section discusses various alternatives to the final standard 
that OSHA considered, with an emphasis on those suggested by the SBREFA 
Panel as potentially alleviating impacts on small firms. (A discussion 
on the costs of some of these alternatives to OSHA's final regulatory 
requirements for the hexavalent chromium standard can be found in 
Section III.3 Costs of Regulatory Alternatives in the final report by 
OSHA's contractor, Shaw (Shaw, 2006). In the Shaw report, costs are 
analyzed by regulatory alternative and major industry sector at 
discount rates of 7 percent and 3 percent.)
    Scope: The proposed standard covered exposure to all types of 
Cr(VI) compounds in general industry, construction, and shipyard. 
Cement work in construction was excluded.
    OSHA considered the Panel recommendation that sectors where there 
is little or no known exposure to Cr(VI) be excluded from the scope of 
the standard. OSHA decided against this option. The costs for such 
sectors are relatively small--probably even smaller than OSHA has 
estimated because OSHA did not assume that any industry would use 
objective data to demonstrate that initial assessment was not needed. 
However, it is possible that changes in technology and production 
processes could change the exposure of employees in what are currently 
low exposure industries. If this happens, OSHA would need to issue a 
new standard to address the situation. As a result, OSHA is reluctant 
to exempt industries from the scope of the standard.
    However, OSHA has rewritten the scope of the standard for the final 
rule so that it exempts from the scope of the standard any employer who 
can demonstrate that a material containing Cr(VI) or a specific 
process, operation, or activity involving Cr(VI) will not result in 
concentrations at or above 0.5 [mu]g/m\3\ under any condition of use. 
As a result, industries are exempted from all provisions of the 
standard and all costs if the industry can demonstrate that exposure is 
always at relatively low levels. This approach seems the best way to 
minimize the costs for the standard for industries where exposure is 
currently minimal, but could change in the future.
    As stated above, the final standard does not cover exposures to 
hexavalent chromium resulting solely from exposure to portland cement. 
OSHA's assessment of the data indicates that the primary exposure to 
cement workers is dermal contact that can lead to irritant or contact 
allergic dermatitis. Current information indicates that the exposures 
in cement work are well below 0.25 [mu]g/m\3\. Moreover, unlike other 
exposures in construction, general industry or shipyards, exposures 
from cement are most likely to be solely from dermal contact. There is 
little potential for airborne exposures and unlikely to be any in the 
future, as Cr(VI) appears in cement in only minute quantities 
naturally. Given these factors, the final standard excludes cement from 
the scope of the standard. OSHA has determined that addressing the 
dermal hazards from these exposures to Cr(VI) through guidance 
materials and enforcement of existing personal protective equipment and 
hygiene standards may be a more effective approach. Such guidance 
materials would include recommendations for specific work practices and 
personal protective equipment for cement work in construction.
    OSHA's analysis suggests that there are 2,093 to 10,463 cases of 
dermatitis among cement workers annually. Using a cost of illness (COI) 
approach, avoiding 95 percent of these dermatoses would be valued at 
$2.5 million to $12.6 million annually, and avoiding 50 percent of 
these dermatoses would be valued $1.3 million to $6.6 million annually.
    The costs of including cement would depend on what requirements 
were applied to wet cement workers. OSHA estimates that the costs 
associated with existing standards (e.g., requirements for PPE and 
hygiene practices) could range from $80 million to $300 million per 
year. Placing wet cement within the scope of the standard would cost an 
additional $33 million per year for compliance with such provisions as 
initial monitoring; those costs would be incurred even if the employer 
has no airborne exposures.
    PELS: Section F of this preamble summary presented data on the 
costs and benefits of alternative PELS for all industries. The full FEA 
contains detailed data on the impacts on small firms at each PEL.
    The SBREFA Panel also suggested alternatives to a uniform PEL 
across all industries and exposures. The Panel recommended that OSHA 
consider alternative approaches to industries that are intermittent 
users of Cr(VI). OSHA has adopted the concept of permitting employers 
with intermittent exposures to meet the requirements of the standard 
using respirators rather than engineering controls. This approach has 
been used in other standards and does not require workers to routinely 
wear respirators.
    The SBREFA Panel also recommended considering Separate Engineering 
Control Airborne Limits (SECALs). OSHA has adopted this approach for 
applications in the aerospace industry. OSHA considered a SECAL for 
electroplating when the Agency was considering setting PELs lower than 
5, but found a SECAL would not significantly lower costs because 
respirator use would be almost as expensive as using engineering 
controls. The expense of respirator use would also be a problem with 
SECALs for this sector at any PEL. OSHA's reasons for not using the 
SECAL approach in other sectors are provided in the Summary and 
Explanation. The SBREFA Panel also suggested that OSHA consider 
different PELs for different Cr(VI) compounds leading to exposure to 
Cr(VI). This issue is fully discussed in VI. Quantitative Risk 
Assessment. Here, it will only be noted that this would result in lower 
PELs than OSHA is setting in at least some industries, and thus 
potentially increase impacts on some small businesses.
    Special Approaches to the Shipyard and Construction Industries: The 
SBREFA Panel was concerned that changing work conditions in the 
shipyard and construction industry would make it difficult to apply 
some of the provisions that OSHA suggested at the time of the Panel. 
OSHA has decided to change its approach in these sectors. OSHA is 
proposing three separate standards, one for general industry, one for 
construction, and one for shipyards. OSHA initially proposed that, in 
shipyards and construction, medical surveillance would be required only 
for persons with signs and symptoms, and regulated areas would not be 
required. In the final standard, OSHA has provided for the same medical 
surveillance standard in all sectors. The reasons for doing this are 
discussed in the Summary and Explanation section of the Preamble. 
However, employers must still meet the PEL with engineering controls 
and work practices where feasible. OSHA's proposed rule did not require 
exposure monitoring in the construction and maritime sectors. In light 
of comments, OSHA has shifted from this approach to requiring all sectors 
to conduct exposure monitoring, but allowing a performance-oriented option 
to exposure monitoring.
    Timing of the Standard: The SBREFA Panel also recommended 
considering a multi-year phase-in of the standard. OSHA has solicited 
comment and examined the comments on this issue. OSHA has decided to 
allow employers four years (rather than two years) to comply with the 
engineering control provisions of the standard. This expanded phase-in 
of engineering controls has several advantages from a viewpoint of 
impacts on small businesses. First, it reduces the one-time initial 
costs of the standard by spreading them out over time. This would be 
particularly useful for small businesses that have trouble borrowing 
large amounts of capital in a single year. A phase-in is also useful in 
the electroplating sector by allowing employers to coordinate their 
environmental and occupational safety and health control strategies to 
minimize potential costs. See the Summary and Explanation section of 
this Preamble for further discussion of this issue.

SBREFA Panel

    Table VIII-14 lists all of the SBREFA Panel recommendations and 
notes OSHA responses to these recommendations.

Click here to view table VIII-14

BILLING CODE 5410-26-C

H. Need for Regulation

    Employees in work environments addressed by the final standards are 
exposed to a variety of significant hazards that can and do cause 
serious injury and death. The risks to employees are excessively large 
due to the existence of market failures, and existing and alternative 
methods of alleviating these negative consequences have been shown to 
be insufficient. After carefully weighing the various potential 
advantages and disadvantages of using a regulatory approach to improve 
upon the current situation, OSHA concludes that in this case the final 
mandatory standards represent the best choice for reducing the risks to 
employees. In addition, rulemaking is necessary in this case in order 
to replace older existing standards with updated, clear, and consistent 
health standards.

IX. OMB Review Under the Paperwork Reduction Act of 1995

    The final Cr(VI) rule contains collection of information 
(paperwork) requirements that are subject to review by the Office of 
Management and Budget (OMB) under the Paperwork Reduction Act of 1995 
(PRA-95), 44 U.S.C. 3501 et seq., and OMB's regulations at 5 CFR part 
1320. The Paperwork Reduction Act defines "collection of information" 
as "the obtaining, causing to be obtained, soliciting, or requiring 
the disclosure to third parties or the public of facts or opinions by 
or for an agency regardless of form or format * * * " (44 U.S.C. 
3502(3)(A)). The collection of information requirements (paperwork) 
associated with the proposed Cr(VI) rule were submitted to OMB on 
October 1, 2004. On November 30, 2004 OMB did not approve the Cr(VI) 
paperwork requirements, and instructed OSHA to examine "public comment 
in response to the NPRM, including paperwork requirements," and 
address any public comments on the paperwork in the preamble. OMB 
assigned the control number 1218-0252 for the Agency to use in future 
submissions.
    The major information collection requirements in the Standard 
include conducting employee exposure assessment (Sec. Sec.  1910.1026 
(d)(1)-(3), 1915.1026 (d)(1)-(3), and 1926.1126 (d)(1)-(3)), notifying 
employees of their Cr(VI)exposures when employee exposures exceed the 
PEL (Sec. Sec.  1910.1026 (d)(4), 1915.1026 (d)(4), and 1926.1126 
(d)(4)), providing respiratory protection (Sec. Sec.  1910.1026 (g), 
1915.1026 (f), and 1926.1126 (f)), labeling bags or containers of 
contaminated protective clothing or equipment (Sec. Sec.  1910.1026 
(h)(2), 1915.1026 (g)(2), and 1926.1126 (g)(2)), informing persons who 
launder or cleans protective clothing or equipment contaminated with 
Cr(VI) of the potential harmful effects (Sec. Sec.  1910.1026 (h)(3), 
1915.1026 (g)(3), and 1926.1126 (g)(3)), implementing medical-
surveillance of employees (Sec. Sec.  1910.1026 (k), 1915.1026 (i), and 
1926.1126 (i)), providing physician or other licensed health care 
professional (PLHCP) with information (Sec. Sec.  1910.1026 (k)(4), 
1915.1026 (i)(4), and 1926.1126 (i)(4)), ensuring that employees 
receive a copy of their medical-surveillance results (Sec. Sec.  
1910.1026 (k)(5), 1915.1026 (i)(5), and 1926.1126 (i)(5)), maintaining 
employees' exposure-monitoring and medical-surveillance records for 
specific periods, and maintaining historical monitoring and objective 
data (Sec. Sec.  1910.1026 (m), 1915.1026 (k), and 1926.1126 (k)). The 
collection of information requirements in the rule are needed to assist 
employers in identifying and controlling exposures to Cr(VI) in the 
workplace, and to address Cr(VI)-related adverse health effects. OSHA 
will also use records developed in response to this standard to 
determine compliance.
    The final rule imposes new information collection requirements for 
purposes of the PRA. In response to comments on the proposed rule, OSHA 
has revised provisions of the final rule that affect collection of 
information requirements. These revisions include:
     The final rule exempts exposures to portland cement in 
general industry and shipyards;
     An exemption is included in the final rule where the 
employer can demonstrate that Cr(VI) exposures will not exceed 0.5 
[mu]g/m\3\ under any expected conditions;
     The final PEL of 5 [mu]g/m\3\ has been revised from the 
proposed 1 [mu]g/m\3\;
     Requirements for exposure determination have been added to 
the construction and shipyard standards, and a performance-oriented 
option for exposure determination is included in the standards for each 
sector (general industry, construction, and shipyards);
     Medical surveillance must be provided to employees exposed 
to Cr(VI) above the action level (rather than the PEL) for 30 or more 
days per year in general industry, construction, and shipyards;
     Requirements to maintain records used for exposure 
determination have been added to the construction and shipyard 
standards, while requirements for training records have been removed 
for all sectors.
    OSHA has revised the paperwork package to reflect these changes, 
and estimates the total burden hours associated with the collection of 
information to be approximately 940,000 and estimates the cost for 
maintenance and operation to be approximately $126 million.
    Potential respondents are not required to comply with the 
information collection requirements until they have been approved by 
OMB. OMB is currently reviewing OSHA's request for approval of the 
final rule's paperwork requirements. OSHA will publish a subsequent 
Federal Register document when OMB takes further action on the 
information collection requirements in the Cr(VI) rule.

X. Federalism

    The Agency reviewed the final Cr(VI) standard according to the most 
recent Executive Order on Federalism (Executive Order 13132, 64 FR 
43225, August 10, 1999). This Executive Order requires that federal 
agencies, to the extent possible, refrain from limiting state policy 
options, consult with states before taking actions that restrict their 
policy options, and take such actions only when clear constitutional 
authority exists and the problem is of national scope. The Executive 
Order allows federal agencies to preempt state law only with the 
expressed consent of Congress; in such cases, federal agencies must 
limit preemption of state law to the extent possible. Under section 18 
of the Occupational Safety and Health Act (the "Act" or "OSH Act"), 
Congress expressly provides that OSHA preempt state occupational safety 
and health standards to the extent that the Agency promulgates a 
federal standard under section 6 of the Act. Accordingly, under section 
18 of the Act OSHA preempts state promulgation and enforcement of 
requirements dealing with occupational safety and health issues covered 
by OSHA standards unless the state has an OSHA approved occupational 
safety and health plan (i.e., is a state-plan state) [see Gade v. 
National Solid Wastes Management Association, 112 S. Ct. 2374 (1992)]. 
Therefore, with respect to states that do not have OSHA-approved plans, 
the Agency concludes that this final rule falls under the preemption 
provisions of the Act. Additionally, section 18 of the Act prohibits 
states without approved plans from issuing citations for violations of 
OSHA standards; the Agency finds that this final rulemaking does not 
expand this limitation. OSHA has authority under Executive Order 13132 
to promulgate a Cr(VI) standard because the problems addressed by these 
requirements are national in scope.
    As explained in section VII of this preamble, employees face a 
significant risk from exposure to Cr(VI) in the workplace. These 
employees are exposed to Cr(VI) in general industry, construction, and 
shipyards. Accordingly, the final rule would establish requirements for 
employers in every state to protect their employees from the risks of 
exposure to Cr(VI). However, section 18(c)(2) of the Act permits state-
plan states to develop their own requirements to deal with any special 
workplace problems or conditions, provided these requirements are at 
least as effective as the requirements in this final rule.

XI. State Plans

    The 26 states and territories with their own OSHA-approved 
occupational safety and health plans must adopt comparable provisions 
within six months of the publication date of the final hexavalent 
chromium standard. These states and territories are: Alaska, Arizona, 
California, Hawaii, Indiana, Iowa, Kentucky, Maryland, Michigan, 
Minnesota, Nevada, New Mexico, North Carolina, Oregon, Puerto Rico, 
South Carolina, Tennessee, Utah, Vermont, Virginia, Virgin Islands, 
Washington, and Wyoming. Connecticut, New Jersey and New York have OSHA 
approved State Plans that apply to state and local government employees 
only. Until a state-plan state promulgates its own comparable 
provisions, Federal OSHA will provide the state with interim 
enforcement assistance, as appropriate.

XII. Unfunded Mandates

    The Agency reviewed the final Cr(VI) standard according to the 
Unfunded Mandates Reform Act of 1995 (UMRA) (2 U.S.C. 1501 et seq.) and 
Executive Order 12875. As discussed in section VIII of this preamble, 
OSHA estimates that compliance with this final rule would require 
private-sector employers to expend about $288 million each year. 
However, while this final rule establishes a federal mandate in the 
private sector, it is not a significant regulatory action within the 
meaning of section 202 of the UMRA (2 U.S.C. 1532). OSHA standards do 
not apply to state and local governments, except in states that have 
voluntarily elected to adopt an OSHA-approved state occupational safety 
and health plan. Consequently, the provisions of the final rule do not 
meet the definition of a "Federal intergovernmental mandate" [see 
section 421(5) of the UMRA (2 U.S.C. 658(5))]. Therefore, based on a 
review of the rulemaking record, the Agency believes that few, if any, 
of the employers affected by the final rule are state, local, or tribal 
governments. Therefore, the Cr(VI) requirements promulgated herein do 
not impose unfunded mandates on state, local, or tribal governments.

XIII. Protecting Children From Environmental Health and Safety Risks

    Executive Order 13045 requires that Federal agencies submitting 
covered regulatory actions to OMB's Office of Information and 
Regulatory Affairs (OIRA) for review pursuant to Executive Order 12866 
must provide OIRA with (1) an evaluation of the environmental health or 
safety effects that the planned regulation may have on children, and 
(2) an explanation of why the planned regulation is preferable to other 
potentially effective and reasonably feasible alternatives considered 
by the agency. Executive Order 13045 defines "covered regulatory 
actions" as rules that may (1) be economically significant under 
Executive Order 12866 (i.e., a rulemaking that has an annual effect on 
the economy of $100 million or more, or would adversely affect in a 
material way the economy, a sector of the economy, productivity, 
competition, jobs, the environment, public health or safety, or state, 
local, or tribal governments or communities, and (2) concern an 
environmental health risk or safety risk that an agency has reason to 
believe may disproportionately affect children. In this context, the 
term "environmental health risks and safety risks" means risks to 
health or safety that are attributable to products or substances that 
children are likely to come in contact with or ingest (e.g., through 
air, food, water, soil, product use). The final Cr(VI) standard is 
economically significant under Executive Order 12866 (see section VIII 
of this preamble). However, after reviewing the final
Cr(VI) standard, OSHA has determined that the standard would not impose 
environmental health or safety risks to children as set forth in 
Executive Order 13045. The final standard requires employers to limit 
employee exposure to Cr(VI) and take other precautions to protect 
employees from adverse health effects associated with exposure to 
Cr(VI). To the best of OSHA's knowledge, no employees under 18 years of 
age work under conditions that involve exposure to Cr(VI). However, if 
such conditions exist, children who are exposed to Cr(VI) in the 
workplace would be better protected from exposure to Cr(VI) under the 
final rule than they are currently. Based on this determination, OSHA 
believes that the final Cr(VI) standard does not constitute a covered 
regulatory action as defined by Executive Order 13045.

XIV. Environmental Impacts

    The Agency reviewed the final Cr(VI) standard according to the 
National Environmental Policy Act (NEPA) of 1969 (42 U.S.C. 4321 et 
seq.), the regulations of the Council on Environmental Quality (40 CFR 
part 1500), and the Department of Labor's NEPA procedures (29 CFR part 
11).
    As a result of this review, OSHA has made a final determination 
that the final Cr(VI) standard will have no impact on air, water, or 
soil quality; plant or animal life; the use of land or aspects of the 
external environment. Therefore, OSHA concludes that the final Cr(VI) 
standard will have no significant environmental impacts.

XV. Summary and Explanation of the Standards

(a) Scope
    OSHA is issuing separate standards addressing hexavalent chromium 
(also referred to as chromium (VI) or Cr(VI)) exposure in general 
industry, construction, and shipyards. The standard for shipyards also 
applies to marine terminals and longshoring. The standards for 
construction and shipyards are very similar to each other, but differ 
in some respects from the standard for general industry. OSHA believes 
that certain conditions in these two sectors warrant requirements that 
are somewhat different than those that apply to general industry. This 
summary and explanation will describe the final rule for general 
industry and will note differences between it and the standards for 
construction and shipyards.
    Commenters were generally supportive of OSHA's decision to propose 
separate standards for general industry, construction, and shipyards 
(e.g., Exs. 38-199-1; 38-212; 38-214; 38-220-1; 38-236; 38-244; 39-19), 
although one commenter believed that a single standard should apply to 
all sectors (Ex. 39-51). Where concerns were expressed about the 
establishment of separate standards, they focused on the provisions of 
the standards and their application, rather than the concept of 
establishing separate standards. Some commenters argued that certain 
activities or industries should be covered by the construction standard 
rather than the general industry standard (e.g., Exs. 38-203; 38-228-1, 
p. 18; 39-52-2; 39-56); others considered the proposed construction and 
shipyard standards to be less protective than the proposed general 
industry standard (Exs. 38-222; 39-71; 47-23, pp. 16-17; 47-28).
    OSHA has long recognized a distinction between the construction and 
general industry sectors, and has issued standards specifically 
applicable to construction work under 29 CFR Part 1926. The Agency has 
provided a definition of the term "construction work" at 29 CFR 
1910.12(b), has explained the terms used in that definition at 29 CFR 
1926.13, and has issued numerous interpretations over the years 
explaining the classification of activities as either general industry 
or construction. OSHA recognizes that in some circumstances, general 
industry activities and conditions in workplaces where general industry 
tasks are performed may be comparable to those found in construction. 
However, the Agency believes the longstanding delineation between 
sectors is appropriate. The distinction between sectors is generally 
well understood by both OSHA enforcement personnel and the regulated 
community, and any attempt to create exceptions or to provide different 
criteria in this final rule would not improve upon the current criteria 
but would rather cause confusion.
    OSHA is issuing the construction and shipyard standards to account 
for the particular conditions found in those sectors. The Agency 
intends to ensure that Cr(VI)-exposed workers in construction and 
shipyards are provided protection that, to the extent feasible, is 
comparable to the protection afforded workers in general industry. OSHA 
believes that concerns raised about differences between the Cr(VI) 
proposed standard for general industry and the proposed standards for 
construction and shipyards will be lessened because the final standards 
are more consistent with one another than as originally proposed. 
Specifically, OSHA proposed explicit exposure assessment requirements 
for general industry, but not for construction and shipyard workplaces. 
The requirements of the final rule for exposure determination are 
nearly identical for all sectors (see discussion of exposure 
determination under paragraph (d) of this section). In addition, OSHA 
proposed a requirement for periodic medical examinations in general 
industry, but not in construction and shipyards. The final rule 
includes requirements for periodic medical examinations in all sectors 
(see discussion of medical surveillance requirements under paragraph 
(k) of this section). The final standards for construction and 
shipyards provide the most adequate protection within the constraints 
of feasibility.
    The final rule applies to occupational exposures to Cr(VI), that 
is, any chromium species with a valence of positive six, regardless of 
form or compound. Examples of Cr(VI) compounds include chromium oxide 
(CrO2), ammonium dichromate 
((NH4)2Cr2O7), calcium 
chromate (CaCrO4), chromium trioxide (CrO3), lead 
chromate (PbCrO4), potassium chromate 
(K2CrO4), potassium dichromate 
(K2Cr2O7), sodium chromate 
(Na2CrO4), strontium chromate 
(SrCrO4), and zinc chromate (ZnCrO4).
    Some commenters supported the proposal to include all chromium 
compounds within the scope of the new rule. (See, e.g., Exs. 38-214; 
39-60). Other commenters, however, contended that specific Cr(VI) 
compounds should be excluded from the scope of the final rule. Notably, 
the Color Pigments Manufacturers Association and Dominion Colour 
Corporation argued that differences in the bioavailability and toxicity 
of lead chromate pigments when compared to other Cr(VI) compounds 
warrant unique treatment (Exs. 38-201; 38-205). The Boeing Company also 
argued that OSHA should consider the bioavailability of different 
Cr(VI) compounds (Ex. 38-106). Boeing indicated that exposures to 
strontium chromate and zinc chromate used in aerospace manufacturing 
are not equivalent to Cr(VI) exposures in other industries.
    OSHA considers all Cr(VI) compounds to be carcinogenic. This 
conclusion is based upon careful consideration of the epidemiological, 
animal, and mechanistic evidence in the rulemaking record, and is 
discussed in section V, "Health Effects," of this preamble. OSHA's 
conclusion that all Cr(VI) compounds are carcinogenic is consistent 
with the findings of IARC, NTP, and NIOSH. These organizations have 
each found Cr(VI) compounds to be carcinogenic, without exception. 
OSHA therefore sees no reason to exempt any Cr(VI) compounds from the final rule.
    Several commenters argued that existing standards provide adequate 
protection for employees exposed to Cr(VI), citing in particular OSHA's 
current welding and lead standards (Exs. 38-203; 38-254; 38-124; 39-19; 
39-47; 39-48; 39-52, p. 22; 39-54; 39-56). However, none of these 
standards provide the full range of protections afforded by the Cr(VI) 
rule. For example, OSHA's welding requirements (29 CFR Subpart Q for 
general industry; 1926 Subpart J for construction; 1915 Subpart D for 
shipyards) include provisions for ventilation, but do not address other 
aspects of worker protection included in the Cr(VI) rule such as 
exposure determination or medical surveillance. OSHA's lead standards 
(29 CFR 1910.1025 for general industry; 29 CFR 1926.62 for 
construction) have a PEL of 50 [mu]g/m\3\, which effectively limits 
Cr(VI) exposure from lead chromate to 12.5 [mu]g/m\3\; however, this 
value is more than double the PEL in the Cr(VI) rule. Other standards 
therefore do not provide protection equivalent to the final Cr(VI) 
rule. Moreover, even though other requirements may affect Cr(VI) 
occupational exposure, Cr(VI) exposure in the current workplace still 
results in a significant risk that can be substantially reduced in a 
feasible manner by the requirements of this final rule.

Portland Cement

    The final rule does not cover exposure to Cr(VI) in portland 
cement. OSHA proposed to exclude exposure to portland cement in 
construction; the final rule extends this exclusion to all sectors. In 
the proposal, OSHA identified two general industry application groups 
where all employee exposure to Cr(VI) is from portland cement: Portland 
Cement Producers and Precast Concrete Products. (A third application 
group, Ready-Mixed Concrete, was later identified.) OSHA proposed to 
cover exposures to portland cement in general industry because the 
Agency's preliminary exposure profile indicated that some employees in 
these application groups were exposed to Cr(VI) levels associated with 
a significant risk of lung cancer. However, evidence in the record 
indicating the low Cr(VI) content of portland cement has led OSHA to 
conclude that the current PEL for portland cement effectively limits 
inhalation exposures from work with portland cement.
    Cement ingredients (clay, gypsum, and chalk), chrome steel grinders 
used to crush ingredients, refractory bricks lining the cement kiln, 
and ash may serve as sources of chromium that may be converted to 
Cr(VI) during kiln heating, leaving trace amounts of Cr(VI) in the 
finished product (Ex. 35-317, p. 148). The amount of Cr(VI) in American 
portland cement is generally less than 20 g Cr(VI)/g cement (Exs. 9-57; 
9-22; 35-417). Because the Cr(VI) concentration in portland cement is 
so low, OSHA's current PEL for portland cement (15 mg/m\3\ for total 
dust, 29 CFR 1910.1000) effectively limits the Cr(VI) inhalation 
exposure from cement to levels below the new Cr(VI) PEL and Action 
Level (i.e., if an employee is exposed at the PEL for portland cement 
and the Cr(VI) concentration in that cement is below 20 [mu]g/g, the 
employee's exposure to Cr(VI) will be below 0.3 [mu]g/m\3\ ). Because 
the evidence in the record demonstrates that current requirements for 
portland cement are as protective as the new PEL with regard to Cr(VI) 
inhalation exposures, OSHA considers it reasonable to exclude portland 
cement from the scope of the final rule. This position was supported by 
a number of commenters (e.g., Exs. 38-127; 38-217; 38-227; 38-229; 38-
235).
    A number of other commenters, including over 200 laborers, 
requested that portland cement be covered under the scope of the final 
rule (e.g., Exs. 38-10; 38-35; 38-50; 38-110; 38-222). These comments 
generally, but not exclusively, focused on dermal hazards associated 
with exposure to portland cement. For example, the Building and 
Construction Trades Department, AFL-CIO (BCTD) stated:

    To provide construction employees with protection from 
predictable exposures to hexavalent chromium, the construction 
standard must include portland cement within its scope. Portland 
cement represents both a dermal and inhalation hazard in 
construction, and reduction of exposures would greatly benefit 
construction employees (Ex. 38-219).

    Commenters favoring coverage of portland cement in the final rule 
argued that a number of the proposal's provisions would serve to 
protect cement workers, such as requirements for appropriate protective 
clothing (Exs. 47-26, pp. 26-27; 35-332, pp. 22-23; 40-4-2, p. 20), 
hygiene facilities (particularly washing facilities)(Exs. 38-219-1, p. 
14; 47-26, pp. 26-27; 35-332, p. 19; 40-4-2, p. 19), and training and 
education (Exs. 47-26, pp. 26-27; 35-332, p. 19; 40-4-2, p. 19). Some 
commenters also favored medical surveillance requirements for workers 
exposed to portland cement (38-219-1, p. 18; 47-26, pp. 26-27) and 
requirements to reduce the Cr(VI) content of portland cement through 
the addition of ferrous sulfate (Exs. 38-199-1, p. 43; 38-219-1, p. 14-
15; 38-222; 35-332, p. 23-24). Some noted that OSHA's Advisory 
Committee on Construction Safety and Health had recommended that the 
Agency apply certain provisions of the Cr(VI) rule to portland cement 
exposures in construction (Ex. 38-199-1, p. 30).
    The primary intent of this rule is to protect workers from lung 
cancer resulting from inhalation of Cr(VI). The Agency has established 
that exposure to Cr(VI) at the previous PEL results in a significant 
risk of lung cancer among exposed workers, and compliance with the new 
PEL will substantially reduce that risk. As indicated previously, the 
existing PEL for portland cement protects employees against inhalation 
of Cr(VI) that is present in portland cement as a trace contaminant. 
Therefore, OSHA does not believe further requirements addressing 
inhalation exposure to Cr(VI) in portland cement are warranted.
    The Agency does recognize, however, that in addition to respiratory 
effects resulting from Cr(VI) inhalation, Cr(VI) is also capable of 
causing serious dermal effects (see discussion in section V of this 
preamble). In previous chemical-specific health standards, OSHA 
typically has addressed serious health effects associated with exposure 
to a chemical, even if those effects are not the focus of the rule. For 
example, OSHA issued a standard for cadmium primarily based on lung 
cancer and kidney damage associated with inhalation exposures to 
cadmium; however, contact with cadmium can also cause irritation of the 
skin and OSHA included a provision in the final cadmium rule addressing 
protective clothing and equipment to prevent skin irritation. OSHA has 
followed a similar approach in the Cr(VI) rule, incorporating 
provisions for protective clothing and equipment that will address 
potential dermal hazards, and including consideration of dermal effects 
in medical surveillance requirements. The Agency believes this is a 
reasonable approach to protecting workers when a chemical causes a 
variety of adverse health effects.
    The dermal hazards from contact with portland cement, however, are 
not related solely to the Cr(VI) content of cement. Portland cement is 
alkaline, abrasive, and hygroscopic (water-absorbing). Cement 
dermatitis may be irritant contact dermatitis induced by these 
properties, allergic contact dermatitis elicited by an immunological 
reaction to Cr(VI), or a combination of the two (Exs. 35-317; 46-74). 
Although reports vary, the weight of the evidence indicates that the vast 
majority of cement dermatitis cases do not involve Cr(VI) sensitization 
(Ex. 46-74). Dermatitis associated with exposure to portland cement is 
thus substantially, perhaps even primarily, related to factors other 
than Cr(VI) exposure.
    Moreover, OSHA believes that appropriate requirements are already 
in place elsewhere in OSHA standards, to protect workers from dermal 
effects associated with exposure to portland cement. The Agency has 
existing requirements for the provision and use of personal protective 
equipment (PPE) (29 CFR 1910.132 for general industry; 29 CFR 1915.152 
for shipyards; 29 CFR 1926.95 for construction). These requirements are 
essentially equivalent to the requirements of the final Cr(VI) rule 
with respect to provision of protective clothing and equipment.
    OSHA also has existing requirements for washing facilities that are 
comparable to those found in the final Cr(VI) rule (29 CFR 1910.141(d) 
for general industry and shipyards; 29 CFR 1926.51(f) for 
construction). For example, in operations where contaminants may be 
harmful to employees, the Sanitation standard for construction requires 
employers to provide adequate washing facilities in near proximity to 
the worksite. With only limited exceptions for mobile crews and 
normally unattended worksites, lavatories with running water, hand soap 
or similar cleansing agents, and towels or warm air blowers must be 
made available in all places of employment covered by the standard. The 
Sanitation requirements that apply to general industry and shipyards 
provide equivalent protections.
    OSHA's Hazard Communication standard (29 CFR 1910.1200) requires 
training for all employees potentially exposed to hazardous chemicals, 
including mixtures such as portland cement. This training must cover 
the physical and health hazards of the chemicals and measures employees 
can take to protect themselves from these hazards, such as appropriate 
work practices, emergency procedures, and personal protective equipment 
to be used.
    Concerns raised in the record with regard to protective clothing, 
washing facilities, and training on cement dermatitis hazards appear to 
relate to lack of compliance with these existing requirements, rather 
than any inadequacy in the requirements themselves. For example, BCTD 
representatives indicated that in spite of current requirements, 
washing facilities are rarely provided on construction sites (Tr. 1464, 
1470-1471, 1474, 1479-1480). By covering portland cement in the final 
Cr(VI) rule, BCTD argued that compliance would improve (Tr. 1519-1522).
    OSHA recognizes that reiterating the requirements of generic rules 
such as the Sanitation standard in a chemical-specific standard like 
the Cr(VI) rule can be useful in some instances by providing employers 
with a comprehensive reference of applicable requirements. However, the 
Agency does not consider the Code of Federal Regulations to be the best 
tool for raising awareness about existing standards. Rather, OSHA 
believes guidance documents, compliance assistance efforts, and 
enforcement of existing requirements are the best mechanisms for 
accomplishing this objective.
    Some commenters argued that requirements not included in the 
generic standards were needed to protect employees working with 
portland cement. The International Brotherhood of Teamsters (IBT) 
stated that absent coverage under the standard, portland cement workers 
would be responsible for purchasing and maintaining their own PPE. If 
there is no requirement for an employer to purchase and provide 
required PPE, IBT argued, most employees would elect not to purchase it 
(Ex. 38-199-1, p. 30). Of course many employers choose to pay for the 
PPE so that they can be sure of its effectiveness. The important 
factors are that the PPE must be suitable for the job and must be used 
correctly. Moreover, even when employees provide their own protective 
equipment, OSHA's PPE standards specify that the employer is 
responsible for ensuring its adequacy, including proper maintenance and 
sanitation (see 29 CFR 1910.132(b); 29 CFR 1926.95(b)).
    Other commenters believed that medical surveillance was needed for 
employees exposed to portland cement (Exs. 38-219-1, p. 18; 47-26, pp. 
26-27). However, irritant contact dermatitis and allergic contact 
dermatitis present the same clinical appearance, and it is difficult to 
determine if an employee with dermatitis is sensitized to Cr(VI). 
Because cement dermatitis is often related to the irritant properties 
of cement rather than Cr(VI), medical surveillance requirements for 
portland cement would necessarily involve covering health effects not 
solely, or even primarily, attributable to Cr(VI) exposure. OSHA 
therefore does not consider a requirement for medical surveillance for 
portland cement workers to be appropriate within the context of the 
Cr(VI) rule.

Ferrous Sulfate

    Finally, some commenters suggested it would be appropriate to 
require the addition of ferrous sulfate to portland cement (Exs. 38-
199-1, p. 43; 38-219-1, pp. 14-15; 38-222; 35-332, pp. 23-24; 47-26, p. 
8). Cr(VI) concentrations in portland cement can be lowered by the 
addition of ferrous sulfate, which reduces Cr(VI) to Cr(III). Residual 
Cr(VI) concentrations of less than 2 ppm are typical. As discussed in 
section V of this preamble, reports from two researchers suggest that 
the addition of ferrous sulfate to cement in Scandinavian countries 
reduces the incidence of Cr(VI)-related allergic contact dermatitis in 
cement workers (Exs. 9-131; 48-8).
    It is reasonable to believe that a reduction in the Cr(VI) 
concentration of portland cement would reduce the potential for Cr(VI)-
induced allergic contact dermatitis. However, the lack of available 
information regarding a dose-response relationship between Cr(VI) 
exposure and allergic contact dermatitis makes it impossible to 
estimate how substantial that reduction might be. For instance, a 
portion of cement samples already have relatively low Cr(VI) 
concentrations. Analyses of 42 samples of American portland cement 
reported by Perone et al. indicated that 33 of the samples had Cr(VI) 
concentrations below 2 ppm (Ex. 9-57); the benefit of adding ferrous 
sulfate to cement with already low Cr(VI) concentrations is unclear.
    Moreover, it is not clear that the addition of ferrous sulfate to 
cement would be successful in reducing Cr(VI) to Cr(III) under 
conditions found in the U.S. Attempts in the U.S. to reduce Cr(VI) in 
cement to Cr(III) with ferrous sulfate have been unsuccessful, due to 
oxidation of the ferrous sulfate in the production process (Ex. 35-
417). Methods used to handle and store cement have also been shown to 
influence the effectiveness of ferrous sulfate in reducing Cr(VI). When 
cement is exposed to moisture during storage, the ferrous sulfate in it 
is likely to be oxidized, and as a result, the Cr(VI) will not be 
reduced to Cr(III) when the cement is mixed with water (Ex. 9-91). 
Handling and storage of cement in silos can have this effect (Tr. 
1363). Because a substantial amount of cement in the U.S. is produced 
in winter and stored for use during warmer weather, ferrous sulfate 
added to the cement at the time of production could be oxidized during 
that time, rendering it ineffective (Tr. 1363).
    Considering this evidence, OSHA does not believe the record 
demonstrates that the addition of ferrous sulfate to portland cement in 
the U.S. would necessarily result in a reduction in the incidence of 
Cr(VI)-induced allergic contact dermatitis. Therefore, OSHA does not 
believe that requiring the addition of ferrous sulfate to cement is warranted.
    In any event, even if ferrous sulfate was completely effective in 
eliminating the potential for Cr(VI)-induced allergic contact 
dermatitis from portland cement, the potential for portland cement to 
induce irritant contact dermatitis would not be affected. (See section 
V(D) of this preamble for additional discussion.) Therefore, 
appropriate protective clothing, good hygiene practices, and training 
on hazards and control methods would still be necessary and these are 
adequately covered by OSHA's generic standards.

Pesticides

    The final rule does not cover exposures to Cr(VI) that occur in the 
application of pesticides. Some Cr(VI)-containing chemicals, such as 
chromated copper arsenate (CCA) and acid copper chromate (ACC), are 
used for wood treatment and are regulated by EPA as pesticides. Section 
4(b)(1) of the OSH Act precludes OSHA from regulating working 
conditions of employees where other Federal agencies exercise statutory 
authority to prescribe or enforce standards or regulations affecting 
occupational safety or health. Therefore, OSHA specifically excludes 
those exposures to Cr(VI) resulting from the application of a pesticide 
regulated by EPA from coverage under the final rule.
    The exception for exposures that occur in the application of 
pesticides was limited to the proposed standard for general industry. 
At the time, OSHA was not aware of exposures to Cr(VI) from application 
of pesticides in other sectors. Exposures to Cr(VI) from pesticide 
application outside of general industry were brought to OSHA's 
attention during the public comment period (Exs. 39-47, p. 9; 39-48, p. 
4; 39-52). This provision excluding coverage or exposures occurring in 
the application of pesticides has therefore been added to the standards 
for construction and shipyards as well.
    The exemption pertains to the application of pesticides only. The 
manufacture of pesticides containing Cr(VI) is not considered pesticide 
application, and is covered under the final rule. The use of wood 
treated with pesticides containing Cr(VI) is also covered. In this 
respect, the Cr(VI) standard differs from OSHA's Inorganic Arsenic 
standard (29 CFR 1910.1018). The Inorganic Arsenic standard explicitly 
exempts the use of wood treated with arsenic. When the Inorganic 
Arsenic standard was issued in 1978, OSHA found that the evidence in 
the record indicated "the arsenic in the preserved wood is bound 
tightly to the wood sugars, exhibits substantial chemical differences 
from other pentavalent arsenicals after reaction, and appears not to 
leach out in substantial amounts" (43 FR 19584, 19613 (5/5/78)). Based 
on the record in that rulemaking, OSHA did not consider it appropriate 
to regulate the use of preserved wood. A number of commenters argued 
that a similar exception should be included in the final rule for use 
of wood preserved with Cr(VI) compounds (Exs. 38-208; 38-231; 38-244; 
43-28). However, OSHA's exposure profile indicates that work with wood 
treated with pesticides containing Cr(VI) can involve Cr(VI) exposures 
above the new PEL (see FEA, Chapter III). OSHA therefore considers a 
blanket exception from the scope of the final rule for use of wood 
treated with Cr(VI) to be unjustified.

Other Requested Exemptions

    In addition to those who maintained that Cr(VI)-treated wood should 
be exempted from the final rule, a number of commenters requested 
exemptions from the final rule for other operations or industries 
(e.g., welding, electric utilities, Cr(VI) pigment production, 
residential construction, and telecommunications (Exs. 38-124; 38-203; 
38-205; 38-211; 38-230; 38-244; 38-254; 39-14; 39-15; 39-47; 47-25; 47-
37). OSHA does not believe that the evidence in the record supports a 
blanket exception from the final rule for these operations and 
industries. In no case have commenters submitted data demonstrating 
that the operations or industries for which an exception was requested 
do not involve exposures to Cr(VI) that present significant risk to the 
health of employees. Rather, the data presented in Chapter III of the 
FEA indicate that exposures in these sectors can and do involve 
exposures at levels that entail significant risk to workers, and may 
exceed the new PEL. OSHA therefore has not included exceptions for 
these operations or industries in the final rule.
    One commenter argued that the provisions of the standard, including 
the new PEL, should apply only where Cr(VI) exposures occur on more 
than 30 days per year (Ex. 38-233, pp. 43-44). However, exposures of 30 
or fewer days per year may involve cumulative exposures associated with 
significant risk of lung cancer. For example, if an employee was 
exposed to 50 [mu]g/m3 Cr(VI) for 30 days during a year, 
that employee s cumulative exposure for the year would exceed that of 
an employee exposed at the new PEL of 5 [mu]g/m3 working 
five days a week through the entire year. Therefore, OSHA does not 
believe such an exemption is appropriate because it would deny workers 
exposed to relatively high levels of Cr(VI) for 30 or fewer days per 
year the protections afforded by the Cr(VI) rule. The Agency does 
include exceptions from certain requirements of the rule for exposures 
occurring on fewer than 30 days per year (e.g., with regard to 
requirements for engineering controls and periodic medical 
surveillance). However, these exceptions are related to the practical 
aspects of implementing protective measures, and not to an absence of 
risk for exposures occurring on fewer than 30 days per year.
    Other commenters suggested that materials or substances containing 
trace amounts of Cr(VI) (e.g., less than 0.1% or 1%) be exempted from 
the final rule (Exs. 38-203; 38-254; 39-19; 39-47; 39-48; 39-52; 39-54; 
39-56). In particular, some utilities argued that fly ash produced by 
the incineration of coal contains trace amounts of Cr(VI) that are so 
low as to be insignificant, and that an exclusion from the final rule 
for coal ash was warranted (Ex. 39-40). Edison Electric Institute 
supported this argument by submitting sampling data and material safety 
data sheets that indicated the Cr(VI) concentrations in ash by-products 
of the coal combustion process (Exs. 47-25-1; 47-25-2; 47-25-3; 47-25-
4; 47-25-5; 47-25-6; 47-25-7).
    OSHA does not believe that it would be appropriate to establish a 
threshold Cr(VI) concentration for coverage of substances under the 
scope of this final rule. The evidence in the rulemaking record is not 
sufficient to lead OSHA to conclude that the suggested concentration 
thresholds would be protective of employee health. While OSHA has 
recognized that the Cr(VI) content of portland cement is sufficiently 
low to warrant an exception from the standard, a threshold 
concentration of 0.1% for Cr(VI) would be more than 50-fold higher than 
Cr(VI) levels typically found in portland cement (< 0.002%). See above 
discussion of the extremely low Cr(VI) concentration in portland cement 
(< 20 [mu]g/g).
    Although evidence submitted to the record indicates that Cr(VI) 
levels in coal ash may be comparable to levels in portland cement, OSHA 
does not believe that the evidence is sufficient to establish that all 
coal ash from allsources will necessarily have comparable Cr(VI) content.
    A threshold concentration is also not reasonable because many 
operations where Cr(VI) exposures occur are the result of work with 
materials that do not contain any Cr(VI). Welders, who represent nearly 
half of the workers covered by this final rule, do not ordinarily work 
with materials that contain Cr(VI). Rather, the high temperatures 
created by welding oxidize chromium in steel to the hexavalent state. 
An exception based on a specified Cr(VI) concentration could be 
interpreted to exclude these workers from the scope of the standard. 
This would be particularly inappropriate in view of the fact that data 
in the record show that many welders have significant Cr(VI) exposures.
    OSHA does, however, appreciate the concerns of commenters regarding 
situations where they believe exposures are minimal and represent very 
little threat to the health of workers. The Agency believes that a 
reasonable approach is to have an exception based on Cr(VI) exposure 
level. OSHA is therefore including in the final rule an exception for 
those circumstances where the employer has objective data demonstrating 
that a material containing chromium or a specific process, operation, 
or activity involving chromium cannot release dusts, fumes, or mists of 
chromium (VI) in concentrations at or above 0.5 [mu]g/m3 as 
an 8-hour TWA under any expected conditions of use.
    OSHA believes this approach is sensible because it provides an 
exception for situations where airborne exposures are not likely to 
present significant risk and thus allows employers to focus resources 
on the exposures of greatest occupational health concern. The Agency 
has added a definition for "objective data" (discussed with regard to 
paragraph (b) of the final rule) to clarify what information and data 
can be used to satisfy the obligation to demonstrate that Cr(VI) 
exposures will be below 0.5 [mu]g/m3.
    Other standards which have included similar exceptions (e.g., 
Acryolitrile, 29 CFR 1019.1045; Ethylene Oxide, 29 CFR 1910.1047; 1,3-
Butadiene, 29 CFR 1910.1051) have generally relied upon the action 
level as an exposure threshold. A threshold lower than the action level 
has been selected for the Cr(VI) rule because OSHA believes this to be 
more protective of worker health given the existing significant risk at 
the action level. Although OSHA understands the difficulties of 
developing objective data to demonstrate that exposures will be below a 
given level, the Agency believes that the 0.5 [mu]g/m3 
coverage threshold represents an exposure level where it is still 
reasonably possible to develop objective data to take advantage of this 
exception if Cr(VI) exposure levels are minimal. For instance, 
variation in exposures even in well controlled workplaces requires that 
typical exposures be below 0.25 [mu]g/m3 in order for an 
employer to be reasonably sure that exposures will consistently be 
below 0.5 [mu]g/m3 (see Exs. 46-79; 46-80; 46-81). Where 
typical exposures are below 0.25 [mu]g/m3, an industry 
survey might be used to show that exposures for a given operation would 
be below 0.5 [mu]g/m3 under any expected conditions of use.
    When using the phrase "any expected conditions of use" OSHA is 
referring to situations that can reasonably be foreseen. The criteria 
are not intended to be so circumscribed that it is impossible to meet 
them. OSHA acknowledges that a constellation of unforeseen 
circumstances can occur that might lead to exposures above 0.5 [mu]g/
m3 even when the objective data demonstration has been 
correctly made, but believes that such occurrences will be extremely 
rare.
(b) Definitions
    "Action level" is defined as an airborne concentration of Cr(VI) 
of 2.5 micrograms per cubic meter of air (2.5 [mu]g/m3) 
calculated as an eight-hour time-weighted average (TWA). The action 
level triggers requirements for exposure monitoring and medical 
surveillance.
    Because employee exposures to airborne concentrations of Cr(VI) are 
variable, workers may sometimes be exposed above the PEL even if 
exposure samples (which are not conducted on a daily basis) are 
generally below the PEL. Maintaining exposures below the action level 
provides increased assurance that employees will not be exposed to 
Cr(VI) at levels above the PEL on days when no exposure measurements 
are made in the workplace. Periodic exposure measurements made when the 
action level is exceeded provide the employer with a degree of 
confidence in the results of the exposure monitoring. The importance of 
the action level is explained in greater detail in the exposure 
determination and medical surveillance discussions of this section 
(paragraphs (d) and (k) respectively).
    As in other standards, the action level has been set at one-half of 
the PEL. The Agency has had successful experience with an action level 
of one-half the PEL in other standards, including those for inorganic 
arsenic (29 CFR 1910.1018), ethylene oxide (29 CFR 1910.1047), benzene 
(29 CFR 1910.1028), and methylene chloride (29 CFR 1910.1052).
    Following the publication of the proposed rule, which included a 
proposed action level of 0.5 [mu]g/m3 (\1/2\ the proposed 
PEL of 1 [mu]g/m3), OSHA received several comments 
pertaining to the definition of the action level. Commenters such as 
the International Brotherhood of Teamsters (IBT) supported OSHA s 
preliminary determination that the action level should be set at one-
half the permissible exposure limit (Exs. 38-199-1, p. 9; 38-219, p. 
16-17; 38-228-1; 40-10-2). The IBT stated that the action level set at 
one-half the PEL has been successful historically in OSHA's standards 
such as inorganic arsenic, cadmium, benzene, ethylene oxide, 
methylenedianiline, and methylene chloride (Ex. 38-199-1, pp. 9, 44). 
NIOSH also supported OSHA's approach, stating that the action level of 
one-half the PEL is the appropriate level to indicate sufficient 
probability that an employee's exposure does not exceed the PEL on 
other days (Ex. 40-10-2, p. 17). The North American Insulation 
Manufacturer's Association (NAIMA) agreed that an action level of one-
half the PEL is appropriate (in conjunction with a higher PEL than that 
proposed) (Ex. 38-228-1, pp. 23-24).
    Previous standards have recognized a statistical basis for using an 
action level of one-half the PEL (see, e.g., acrylonitrile, 29 CFR 
1910.1045; ethylene oxide, 29 CFR 1910.1047). In brief, OSHA previously 
determined (based in part on research conducted by Leidel et al.) that 
where exposure measurements are above one-half the PEL, the employer 
cannot be reasonably confident that the employee is not exposed above 
the PEL on days when no measurements are taken (Ex. 46-80).
    Following the publication of the proposed rule, the United 
Automobile, Aerospace, and Agricultural Implement Workers of America 
(UAW) requested an action level of one-tenth of the permissible 
exposure limit (PEL) (Tr. 791; Exs. 39-73; 39-73-2, pp. 3, 10; 40-19-
1). The UAW argued that the lower action level is appropriate because 
variability in exposures is greater than was previously believed in 
some occupational settings. While OSHA previously assumed a geometric 
standard deviation (GSD) of 1.4, the UAW stated that a GSD of 2 should 
be assumed as a matter of policy. They concluded that this GSD implies 
an action level of one-tenth the PEL to minimize the frequency of 
exposures above the PEL on days when measurements are not taken (Ex. 
39-73-2, p. 12).
    If the variability of workplace exposures is typically as high as 
the UAW suggests, an action level less than one-half the PEL would be 
required to give employers a high degree of confidence that employees' 
exposures are below the PEL on most workdays. Leidel et al., calculated 
that for exposures with a GSD of 2.0, an action level of 0.115 times 
the PEL would be required to limit to 5% the probability that 5% or 
more of an employee's unmeasured daily exposure averages will exceed 
the PEL (Ex. 46-80, p. 29). However, the evidence in the record is 
insufficient to permit OSHA to conclude that a GSD of 2.0 is typical of 
workplace Cr(VI) exposures. Furthermore, while OSHA recognizes the 
value of high (95%) confidence that exposures exceed the PEL very 
infrequently (<  5%), the Agency believes that the action level should 
be set at a value that effectively encourages employers to reduce 
exposures below the action level while still providing reasonable 
(though possibly <  95%) assurance that workers' exposures are typically 
below the PEL. OSHA's experience with past rules and the comments and 
testimony of NIOSH and other union representatives indicate that 
reasonable assurance of day-to-day compliance with the PEL is achieved 
with an action level of one-half the PEL (Exs. 40-10-2, p. 17; 199-1, 
pp. 9, 44).
    The Agency's experience with previous standards also indicates that 
an action limit of one-half the PEL effectively encourages employers, 
where feasible, to reduce exposures below the action level to avoid the 
added costs of required compliance with provisions triggered by the 
action level. Where there is continuing significant risk at the PEL, 
the decision in the Asbestos case (Building and Construction Trades 
Department, AFL-CIO v. Brock, 838 F. 2d 1258 (D.C. Cir 1988)) indicates 
that OSHA should use its legal authority to impose additional 
requirements on employers to further reduce risk when those 
requirements will result in a greater than de minimus incremental 
benefit to workers' health. OSHA believes that the action level will 
result in a very real and necessary further reduction in risk beyond 
that provided by the PEL alone.
    The action level improves employee protection while increasing the 
cost-effectiveness and performance orientation of the standard. The 
action level will encourage employers who can, in a cost-effective 
manner, identify approaches or innovative methods to reduce their 
employees' exposures to levels below the action level, because this 
will eliminate the costs associated with exposure monitoring and 
medical surveillance. The employees of such employers will have greater 
protection against adverse health effects because their exposures to 
Cr(VI) will be less than half of those permitted by the permissible 
exposure limit. Employees of those employers who are not able to lower 
exposures below the action level will have the additional protection 
provided by medical surveillance, exposure monitoring, and the other 
provisions of the standard that are triggered by the action level.
    "Chromium (VI) [hexavalent chromium or Cr(VI)]" means chromium 
with a valence of positive six, in any form or chemical compound in 
which it occurs. This term includes Cr(VI) in all states of matter, in 
any solution or other mixture, even if encapsulated by another or 
several other substances. The term also includes Cr(VI) when created by 
an industrial process, such as when welding of stainless steel 
generates Cr(VI) fume.
    For regulatory purposes, OSHA is treating Cr(VI) generically, 
instead of addressing specific compounds individually. This is based on 
OSHA's determination that the toxicological effect on the human body is 
similar from Cr(VI) in any of the substances covered under the scope of 
this standard, regardless of the form or compound in which it occurs. 
As discussed in Section V of this preamble, some variation in potency 
may result due to differences in the solubility of compounds. Other 
factors, such as encapsulation, may have some effect on the 
bioavailability of Cr(VI). However, OSHA believes that these factors do 
not result in differences that merit separate provisions for different 
Cr(VI) compounds. OSHA considers it appropriate to apply the 
requirements of the standard uniformly to all Cr(VI) compounds.
    "Emergency" means any occurrence that results, or is likely to 
result, in an uncontrolled release of Cr(VI), such as, but not limited 
to, equipment failure, rupture of containers, or failure of control 
equipment. To constitute an emergency, the exposure to Cr(VI) must be 
unexpected and significant. If an incidental release of chromium (VI) 
can be controlled at the time of release by employees in the immediate 
release area, or by maintenance personnel, it is not an emergency. 
Similarly, if an incidental release of Cr(VI) may be safely cleaned up 
by employees at the time of release, it is not considered to be an 
emergency situation for the purposes of this section. Those instances 
that constitute an emergency trigger certain requirements in this 
standard (e.g., medical surveillance) that are discussed later in this 
section.
    In comments submitted to OSHA following the publication of the 
proposed Cr(VI) rule, the International Brotherhood of Teamsters (IBT) 
disagreed with OSHA's definition of "emergency". IBT stated that all 
spills and leaks involving Cr(VI) are unexpected and significant, and 
should be considered emergencies (Ex. 38-199-1, pp. 20-21).
    OSHA does not agree with the IBT's position that every spill or 
leak should be considered an emergency. Not all spills and leaks are 
significant; the particular circumstances of the release, such as the 
quantity involved, confined space considerations, and the adequacy of 
ventilation will have an impact on the amount of Cr(VI) to which 
employees are exposed when a spill or leak occurs. For example, a minor 
spill that can be quickly cleaned up by an employee with minimal 
airborne or dermal exposure to Cr(VI) is clearly not an emergency. In 
addition, factors such as the personal protective equipment available, 
pre-established standard operating procedures for responding to 
releases, and engineering controls that employees can activate to 
assist them in controlling and stopping the release are all factors 
that must be considered in determining whether a release is incidental 
or an emergency.
    The IBT also stated that the person who determines whether a spill 
or leak constitutes an emergency situation should be qualified with 
specific training, knowledge, and experience regarding the hazards 
associated with exposure to Cr(VI) and the appropriate response 
measures that must be implemented to prevent Cr(VI) exposures during 
the spill or leak remediation (Ex. 38-199-1, pp. 20-21). OSHA believes 
that the provisions of the Hazard Communication standard adequately 
address the IBT's concern (29 CFR 1910.1200). Paragraph (h)(3) of that 
standard directs employers to provide employees who are exposed or 
potentially exposed to a hazardous chemical (such as Cr(VI)) with 
training on the physical and health hazards of the chemical and

[t]he measures employees can take to protect themselves from these 
hazards, including specific procedures the employer has implemented 
to protect employees from exposure to hazardous chemicals, such as 
appropriate work practices, emergency procedures, and personal 
protective equipment to be used * * * (29 CFR 1910.1200 
(h)(3)(iii)).

The Agency expects that employers and employees equipped with the 
training required by the Hazard Communication
standard will be sufficiently knowledgable to determine whether an 
emergency has occurred, and that it is not necessary to mandate 
additional specialized training for this purpose.
    "Employee exposure" means exposure to airborne Cr(VI) that would 
occur if the employee were not using a respirator. This definition is 
included to clarify the fact that employee exposure is measured outside 
any respiratory protection worn. It is consistent with OSHA's previous 
use of the term in other standards.
    "Historical monitoring data" means data from chromium (VI) 
monitoring conducted prior to May 30, 2006, obtained during work 
operations conducted under workplace conditions closely resembling the 
processes, types of material, control methods, work practices, and 
environmental conditions in the employer's current operations. To 
demonstrate employees' exposures, historical monitoring data must 
satisfy all exposure monitoring requirements of this section (e.g., 
accuracy and confidence requirements).
    "Objective data" means information other than employee monitoring 
that demonstrates the expected employee exposure to chromium (VI) 
associated with a particular product or material or a specific process, 
operation, or activity. Types of information that may serve as 
objective data include, but are not limited to, air monitoring data 
from industry-wide surveys; data collected by a trade association from 
its members; or calculations based on the composition or chemical and 
physical properties of a material.
    "Physician or other licensed health care professional" [PLHCP] is 
an individual whose legally permitted scope of practice (i.e., license, 
registration, or certification) allows him or her to independently 
provide or be delegated the responsibility to provide some or all of 
the particular health care services required by the medical 
surveillance provisions of this final rule. This definition is 
consistent with several recent OSHA standards, including the 
respiratory protection standard (29 CFR 1910.134), the bloodborne 
pathogens standard (29 CFR 1910.1030), and the methylene chloride 
standard (29 CFR 1910.1052). In these standards, the Agency determined 
that any professional licensed by state law to do so may perform the 
medical evaluation procedures required by the standard. OSHA recognizes 
that the personnel qualified to provide the required medical evaluation 
may vary from state to state, depending on state licensing laws.
    At the public hearing, the 3M Company (3M) expressed concern with 
OSHA's interpretation of licensing requirements for PLHCPs. In the 
recent standards discussed above, OSHA has interpreted the requirements 
to mean that PLHCPs must be licensed in the states of residence for the 
employees they evaluate. This interpretation is based on OSHA's 
recognition of state licensing laws that require PHLCP's to be licensed 
in the state in which they practice. 3M encouraged OSHA to adopt an 
expanded definition of PLHCP for the Cr(VI) standard, allowing PLHCPs 
licensed in any U.S. state to evaluate employees residing in that or 
any other state, arguing that other federal agencies such as the 
Department of Transportation permitted similar allowances. 3M argued 
that this arrangement " * * * would permit one medical director to 
oversee the program in several states" where a company has operations 
(Tr. 1592, Ex. 47-36). Moreover, 3M added that OSHA has no authority to 
enforce state licensing requirements.
    Despite the concerns raised by 3M, OSHA continues to believe that 
it is appropriate to establish PLHCP requirements consistent with state 
requirements for medical practice. OSHA's goal is that the medical 
surveillance provisions of the final Cr(VI) rule be conducted by or 
under the supervision of a health care professional who is 
appropriately licensed to perform those provisions and is therefore 
operating under his or her legal scope of practice. OSHA also continues 
to believe that issues regarding a PLCHP's legal scope of practice 
reside most appropriately with state licensing boards. While OSHA does 
not enforce state licensing requirements (e.g., fining an individual 
PHCLP for operating outside their legal state license), OSHA can cite, 
using the Cr(VI) standard, an employer for using a health care 
professional who is not operating under his or her legal scope of 
practice. Thus, the Agency believes that the proposed definition for 
PHLCP is reasonable, and has retained it in the final rule. OSHA's 
experience with other standards using this definition supports the 
Agency's determination in this matter.
    "Regulated area" means an area, demarcated by the employer, where 
an employee's exposure to airborne concentrations of Cr(VI) exceeds, or 
can reasonably be expected to exceed the PEL. This definition is 
consistent with the use of the term in other standards, including those 
for cadmium (29 CFR 1910.1027), butadiene (29 CFR 1910.1051), and 
methylene chloride (29 CFR 1910.1052).
    OSHA has not included a requirement for regulated areas in 
construction and shipyards. This definition is therefore not included 
in the standards for construction and shipyards.
    The definitions for "Assistant Secretary", "Director", "High-
efficiency particulate air [HEPA] filter", and "This section" are 
consistent with OSHA's previous use of these terms found in other 
health standards.
(c) Permissible Exposure Limit (PEL)
Introduction
    Paragraph (c) of the final rule establishes an 8-hour time-weighted 
average (TWA) exposure limit of 5 micrograms of Cr(VI) per cubic meter 
of air (5 [mu]g/m3). This limit means that over the course 
of any 8-hour work shift, the average exposure to Cr(VI) cannot exceed 
5 [mu]g/m3. The new limit applies to Cr(VI), as opposed to 
the previous PEL which was measured as CrO3. The previous 
PEL of 1 milligram per 10 cubic meters of air (1 mg/10m3, or 
100 [mu]g/m3) reported as CrO3 is equivalent to a 
limit of 52 [mu]g/m3 as Cr(VI).
    OSHA proposed a PEL of 1 [mu]g/m\3\ for Cr(VI). This PEL was 
proposed because the Agency made a preliminary determination that 
occupational exposure to Cr(VI) at the previous PEL resulted in a 
significant risk of lung cancer among exposed workers, and compliance 
with the proposed PEL was expected to substantially reduce that risk. 
Based on the information available to OSHA at the time, a PEL of 1 
[mu]g/m\3\ was believed to be economically and technologically feasible 
for affected industries.
    The PEL was a focus of comment in the rulemaking process, revealing 
sharply divided opinion on the justification for a PEL of 1 [mu]g/m\3\. 
Some support was expressed for the proposed PEL (Exs. 38-199-1, p. 42; 
38-219-1, p. 2; 39-73-1). The vast majority of commenters, however, did 
not believe the proposed PEL was appropriate. Some maintained that a 
higher PEL was warranted, arguing that the proposed limit was 
infeasible or was not justified by the health and risk evidence (e.g., 
Exs. 38-205; 38-215; 38-231; 38-228; 38-233). Several commenters 
suggested alternative PELs that they considered appropriate, such as 10 
[mu]g/m\3\ (Exs. 38-134; 38-135; 38-195; 38-203; 38-212; 38-250; 38-
254), 20 [mu]g/m\3\ (Ex. 38-204), 23 [mu]g/m\3\ (e.g., Exs. 38-7; 43-
22; 43-23; 43-25; 43-39), or 26 [mu]g/m\3\ (Ex. 38-263). Others 
maintained that the remaining risk at the proposed PEL was excessive 
and believed OSHA should adopt a lower PEL, suggesting 0.2 or 0.25 
[mu]g/m\3\ (Exs. 39-71; 40-10-2; 47-23; 47-28).
    After careful consideration of the evidence in the rulemaking 
record, OSHA has established a final PEL of 5 [mu]g/m\3\. OSHA s 
examination of the health effects evidence, discussed in section V of 
this preamble, reaffirms the Agency's preliminary conclusion that 
exposure to Cr(VI) causes lung cancer, as well as other serious adverse 
health effects. OSHA's quantitative risk assessment, presented in 
section VI, indicates that the most reliable lifetime estimate of risk 
from exposure to Cr(VI) at the previous PEL is 101 to 351 excess lung 
cancer deaths per 1000 workers. As discussed in section VII, this 
clearly represents a significant risk of material impairment of health. 
OSHA believes that lowering the PEL to 5 [mu]g/m\3\ will substantially 
reduce this risk. OSHA estimates the lifetime excess risk of death from 
lung cancer at the new PEL to be between 10 and 45 per 1000 workers.
    The Agency considers the level of risk remaining at the new PEL to 
be significant. However, based on evidence evaluated during the 
rulemaking process, OSHA has concluded that a uniform PEL of 5 [mu]g/
m\3\ is appropriate. The new PEL is technologically and economically 
feasible for all industry sectors. In only two operations within one of 
those sectors, the painting of aircraft and large aircraft parts in the 
aerospace industry, is a PEL of 5 [mu]g/m\3\ infeasible. In accordance 
with section 6(b)(5) of the OSH Act, OSHA has determined that the new 
PEL is the lowest limit that employers can generally achieve, 
consistent with feasibility constraints. Additional requirements are 
included in the final rule to further reduce any remaining risk. OSHA 
anticipates that these ancillary provisions will reduce the risk beyond 
the reduction that will be achieved by the new PEL alone.
    OSHA's rationale for adopting a uniform PEL of 5 [mu]g/m\3\ is set 
forth in greater detail below. The discussion is organized around the 
issues of primary importance to commenters: (a) Whether a uniform PEL 
is appropriate for all chromium compounds, (b) the technologic and 
economic feasibility of various PELs, (c) the requirement of section 
6(b)(5) to promulgate the most protective standard consistent with 
feasibility, and (d) whether there is a need for a short-term exposure 
limit.
A Uniform PEL Is Appropriate for All Chromium Compounds
    OSHA believes that it is appropriate to establish a single PEL that 
applies to all Cr(VI) compounds. OSHA's preferred estimates of risk are 
derived from two cohorts of chromate production workers that were 
predominantly exposed to sodium chromate and sodium dichromate. A 
number of commenters argued that risk estimates from these cohorts were 
not applicable to certain other Cr(VI) compounds (Exs. 38-106; 38-201-
1; 38-205; 38-215-2).
    After carefully evaluating the epidemiological, animal and 
mechanistic evidence in the rulemaking record, OSHA considers all 
Cr(VI) compounds to be carcinogenic. (For additional discussion see 
section V of this preamble.) OSHA has determined that the risk 
estimates developed from the chromate production cohorts are reasonably 
representative of the risks expected from equivalent exposures to 
different Cr(VI) compounds in other industries. OSHA finds that the 
risks estimated from the Gibb and Luippold cohorts of chrome production 
workers adequately represent the risks to workers in other industries 
who are exposed to equivalent levels of Cr(VI) compounds. (The 
rationale supporting these conclusions is discussed in detail in 
sections V and VI of this preamble. In particular, see Section VI(H) of 
the Quantitative Risk Assessment.) Because OSHA's estimates of risk are 
reasonably representative of all occupational Cr(VI) exposures, the 
Agency considers it appropriate to establish a single PEL applicable to 
all Cr(VI) compounds. A number of rulemaking participants supported 
this approach (Exs. 38-214; 38-220; 39-20; 39-60; 40-10; 40-19). See 
also, e.g., Color Pigments Mfr. Ass'n, Inc. v. OSHA, 16 F.3d 1157, 1161 
(11th Cir. 1994):

    Given the absence of definiteness on the issue, the volume of 
evidence that points at least implicitly to the dangers of cadmium 
pigments, and the serious potential health risks present if cadmium 
exposure is as great in pigment form as in other compounds, we 
believe that OSHA was justified in choosing to include cadmium 
pigments in the PEL * * * ;

Asarco, Inc. v. OSHA, 746 F.2d 483, 495 (9th Cir. 1984) (permissible 
for OSHA to "use trivalent arsenic studies and conclusions to support 
inclusion of pentavalent arsenic in the standard").
The Final PEL of 5 [mu]g/m\3\ Is Technologically and Economically 
Feasible for all Affected Industries; the Proposed PEL Is Not
    OSHA has concluded that a PEL of 5 [mu]g/m\3\ is economically and 
technologically feasible for all the affected industries. OSHA has also 
concluded, based on the comments and evidence submitted to the record, 
that the proposed PEL of 1 [mu]g/m\3\ is not feasible in all 
industries. OSHA's feasibility determinations are explained below.
    Technologic feasibility of the final PEL. In making its 
determination of technological feasibility, OSHA relied upon guidance 
provided by the courts that have reviewed previous standards. In 
particular, the decision of the U.S. Court of Appeals for the District 
of Columbia on OSHA's Lead standard (United Steelworkers of America v. 
Marshall, 647 F.2d 1189 (D.C. Cir. 1981)) established a benchmark that 
the Agency has relied on for evaluating technological feasibility. The 
court explained that OSHA has "great discretion * * * in determining 
the feasibility of a chosen PEL." 647 F.2d at 1309. Both technological 
and economic feasibility are "to be tested industry-by-industry." 647 
F.2d at 1301. In order to establish that a standard is technologically 
feasible, "OSHA must prove a reasonable possibility that the typical 
firm will be able to develop and install engineering and work practice 
controls that can meet the PEL in most of its operations." 647 F.2d at 
1272. The court allowed that "insufficient proof of technological 
feasibility for a few isolated operations within an industry, or even 
OSHA's concession that respirators will be necessary in a few such 
operations, will not undermine" OSHA's finding of technological 
feasibility. Id.
    Applying this definition of feasibility, OSHA has evaluated each 
affected industry and has concluded that a PEL of 5 [mu]g/m\3\ can be 
achieved through engineering and work practice controls, with only 
limited respirator use, in every industry. The primary evidentiary 
support for this conclusion is the report of Shaw Environmental, Inc., 
discussed in depth in the Final Economic and Regulatory Flexibility 
Analysis (FEA). Based on the data collected by Shaw, OSHA concludes 
that engineering controls, such as local exhaust ventilation (LEV), 
process control, and process modification or substitution can be used 
to control exposures in most operations.
    OSHA recognizes that there are certain instances in which 
supplemental respirator use will be required because engineering and 
work practice controls are not always sufficient to reduce airborne 
exposures below the PEL. Summary information regarding the extent of 
respirator usage expected at various potential PELs is presented in 
Table VIII-3 (see section VIII, summary of the FEA). Considering this 
information together with other data and analysis presented in the FEA, 
OSHA has concluded that a PEL of 5 [mu]g/m\3\ is technologically feasible 
in all affected industry sectors and in virtually all operations, with the 
limited exception of some aerospace painting operations discussed more fully 
below. In only three sectors would respirator use be required by more than 
5% of exposed employees. In two of these sectors, chromate pigment producers and 
chromium dye producers, use of respirators will be intermittent. The 
third sector, stainless steel welding, presents technological 
challenges in certain operations. However, the new PEL can clearly be 
achieved in most operations with engineering and work practice 
controls.
    OSHA recognizes that for two distinct operations within the 
aerospace industry, painting aircraft and painting large aircraft 
parts, engineering and work practice controls cannot control exposures 
below 25 [mu]g/m\3\ and respirators would be required for most 
employees performing these operations. (See additional discussion of 
aerospace painting below.) For that reason OSHA is adopting a provision 
for those specific operations requiring employers to use engineering 
and work practice controls to limit employee exposures to 25 [mu]g/
m\3\. Respiratory protection must then be used to achieve the PEL.
    OSHA did not set the PEL at 25 [mu]g/m\3\, a level achievable in 
every operation in every industry with engineering and work practice 
controls alone. That approach is inappropriate because it would leave 
the vast majority of affected employees exposed to Cr(VI) levels above 
those that could feasibly be achieved in most industries and 
operations. As discussed above, the lower PEL of 5 [mu]g/m\3\ is 
feasible within the meaning of the case law, although it will result in 
limited use of respirators in some industries and significant 
respirator use in two painting operations in the aerospace industry. 
The two aerospace painting operations with significant respirator use 
are covered by the provision discussed above. For those operations, 
OSHA weighed the added protection provided by respirators against the 
negative aspects of respiratory protection requirements, and decided 
that the additional respirator use was acceptable.
    Technological feasibility of the proposed PEL. OSHA concludes that 
the proposed PEL of 1 [mu]g/m\3\ is not technologically feasible for 
all industries under the criteria in the D.C. Circuit's Lead decision. 
The court's definition of technological feasibility recognizes that for 
a standard based on a hierarchy of controls, a particular PEL is not 
technologically feasible simply because it can be achieved through the 
widespread use of respirators. 647 F.2d at 1272. This is consistent 
with OSHA's long-held view that it is prudent to avoid requirements 
that will result in extensive respirator use.
    In its post-hearing brief, Public Citizen argued that a PEL should 
be considered technologically feasible if respirator use would be 
necessary to achieve compliance in a significant number of operations 
within an industry, or even if the PEL could only be achieved through 
use of respirators alone (Ex. 47-23, pp. 12-15). That position is 
inconsistent with the established test for feasibility for standards 
based on the hierarchy of controls. Moreover, as discussed in the 
preamble explanation of paragraph (f) on methods of compliance, use of 
respirators in the workplace presents a number of independent safety 
and health concerns. The vision of workers wearing respirators may be 
diminished, and respirators can impair the ability of employees to 
communicate with one another. Respirators can impose physiological 
burdens on employees due to the weight of the respirator and increased 
breathing resistance experienced during operation. The level of 
physical work effort required, the use of protective clothing, and 
environmental factors such as temperature extremes and high humidity 
can interact with respirator use to increase the physiological strain 
on employees. Inability to cope with this strain as a result of medical 
conditions such as cardiovascular and respiratory diseases, reduced 
pulmonary function, neurological or musculoskeletal disorders, impaired 
sensory function, or psychological conditions can place employees at 
increased risk of illness, injury, and even death. Routine use of 
respirators for extended periods of time is regarded by the Agency to 
be of greater significance than intermittent use for short time 
periods.
    OSHA also believes that respirators are inherently less reliable 
than engineering and work practice controls. To consistently provide 
adequate protection, respirators must be appropriately selected and 
fitted, properly used, and properly maintained. Because these 
conditions can be difficult to attain, and are subject to human error, 
OSHA does not believe respirators provide the same degree of protection 
as do engineering and work practice controls.
    Based on evidence and comment submitted in response to the 
proposal, OSHA finds that a PEL of 1 [mu]g/m\3\ is not technologically 
feasible for a substantial number of industries and operations 
employing a large number of the workers covered by the standard. The 
record shows that a PEL of 1 [mu]g/m\3\ is technologically infeasible 
for welding and aerospace painting because engineering and work 
practice controls cannot reduce exposures below 1 [mu]g/m\3\ for many 
operations. OSHA also finds that the record contains insufficient 
evidence to establish the technologic feasibility of the proposed PEL 
for four other industries: chromate pigment producers, chromium 
catalyst producers, chromium dye producers and some hard chrome 
electroplaters. OSHA's findings on the technologic feasibility of the 
proposed PEL are summarized below, and are discussed more extensively 
in Chapter III of the FEA (in particular, see section titled: 
"Technological Feasibility of the Proposed 1 [mu]g/m\3\ 8-Hour TWA 
PEL.").
    Welding. OSHA has concluded that a PEL of 1 [mu]g/m\3\ is not 
technologically feasible for shielded metal arc welding (SMAW) on 
stainless steel because engineering and work practice controls cannot 
generally reduce employee exposures to below 1 [mu]g/m\3\. Almost one 
third (29%) of all stainless steel SMAW operations would need to use 
respirators at a PEL of 1 [mu]g/m\3\. In general industry alone, more 
than half (52%) of stainless steel SMAW processes would be unable to 
use engineering or work practice controls to reduce Cr(VI) exposures 
below 1 [mu]g/m\3\. Notably, stainless steel welding is widespread 
throughout the economy; it occurs in over 20,000 establishments 
employing approximately 127,000 workers in over sixty-five 3-digit 
NAICS codes. SMAW is the most common type of stainless steel welding 
and is performed by more than 67,000 employees--more than half of the 
total number of stainless steel welders and one quarter of all welders 
covered by the standard.
    OSHA initially recommended the substitution of gas metal arc 
welding (GMAW) for SMAW as the cheapest and most effective method to 
reduce Cr(VI) exposures. GMAW, like SMAW, is a common type of welding, 
but GMAW tends to produce lower exposures than SMAW. However, based on 
hearing testimony and evidence submitted to the record, OSHA now 
believes that only 60% of SMAW operations can switch to GMAW (Exs. 38-
220-1, p. 8; 39-60, p. 3; 39-70, p. 2; 35-410, p. 4). Moreover, even 
among the SMAW operations with current exposures above 1 [mu]g/m\3\ 
that can switch to GMAW, only a portion (40% in general industry and 
59% in construction and maritime)
would be able to achieve a PEL of 1 [mu]g/m\3\ without respirators.
    OSHA has also determined that a PEL of 1 [mu]g/m\3\ is 
technologically infeasible for stainless steel welding that is 
performed in confined or enclosed spaces due to limitations on the 
availability of ventilation. Because engineering and work practice 
controls cannot consistently reduce exposures to below 1 [mu]g/m\3\, a 
large percentage of stainless steel welding operations in confined or 
enclosed spaces would require respirators at a PEL of 1 [mu]g/m\3\. In 
general industry, for example, 60% of welding tasks done on stainless 
steel in confined spaces would be unable to comply with the proposed 
PEL by using engineering or work practice controls.
    In sum, OSHA has concluded that it is infeasible for some of the 
most common welding operations to achieve a PEL of 1 [mu]g/m\3\. For a 
more detailed explanation of OSHA's technological feasibility analysis 
for welding operations, see Chapter III of the FEA. OSHA has also 
decided that although it may be feasible for some of the less common 
types of welding operations to achieve a PEL of 1 [mu]g/m\3\ with 
engineering and work practice controls, the ubiquitous nature of 
welding necessitates a finding that a PEL of 1 [mu]g/m\3\ is generally 
infeasible for all welding operations. In particular, OSHA believes 
that the proposed PEL is infeasible for welding operations generally 
because welding is not easily separated into high and low exposure 
operations. Welders may perform different types of welding in the same 
day, making it difficult or impossible for employers to monitor them on 
an operation by operation basis. See, e.g., Ex. 39-22. In addition, 
because workers doing different types of welding often work alongside 
one another, what is technologically feasible for a welding operation 
considered in isolation may not be technologically feasible for that 
operation when it is performed next to SMAW on stainless steel or 
another operation for which a PEL of 1 [mu]g/m\3\ is technologically 
infeasible.
    Welding occurs in over 40,000 establishments spanning sixty-five 
different 3-digit NAICS codes. Welding is done in a variety of sites 
throughout many diverse workplaces (Ex. 38-8, p. 5). Stainless steel 
SMAW is commonly done in close proximity to other welding or cutting 
operations, which could expose nearby workers to the higher exposures 
generated by the SMAW welder (Ex. 38-214, p. 7). The Specialty Steel 
Industry of North America commented that, "workers in job categories 
other than those evaluated by OSHA may spend significant time in areas 
of potential exposure" (Ex. 38-233, p. 10). The Integrated Waste 
Services Association similarly indicated that inspectors, scaffold 
workers, laborers, pipe fitters, and refractory workers may pass 
through areas with potential Cr(VI) exposure during nickel chrome alloy 
overlay (Ex. 38-258, p. 2). The Building and Construction Trades 
Department of the AFL-CIO also stated that "workers may be exposed to 
hazards even if they are not directly performing tasks associated with 
Cr VI exposure via close proximity exposure" (Ex. 31-6-1).
    Moreover, OSHA is aware that welders sometimes weld in many 
different environments on a variety of types of base metal using 
different welding methods in the course of a project or even during a 
single work shift (Exs. 34-10, 38-235). In those situations, the 
employee's overall exposure levels are inevitably influenced by the 
variety of exposures present during the various welding tasks he or she 
performs. Therefore, depending on how much time the employee spends 
doing welding operations for which a PEL of 5 [mu]g/m\3\ is the lowest 
feasible level, even the use of engineering and work practice controls 
to comply with a PEL of 1 [mu]g/m\3\ in the other welding operations 
would not necessarily reduce the employee's overall exposure levels 
below that mark.
    Because of these factors, welding is not easily separated into high 
and low exposure operations in the real work site. For these reasons, 
OSHA believes the record demonstrates that the proposed PEL of 1 [mu]g/
m\3\ is infeasible for welding operations generally. Almost 270,000 of 
the employees covered by the new standard engage in these welding 
operations (Table VIII-2).
    Aerospace painting. There are approximately 8300 exposed employees 
in aerospace painting (Table VIII-2). A PEL of 1 [mu]g/m\3\ is not 
feasible for approximately two thirds of all aerospace painting 
operations. At a PEL of 5 [mu]g/m\3\, only \1/3\ of aerospace painting 
operations would require substantial respirator use.
    Exposures in aerospace painting are controlled by enclosing the 
operations in painting booths or dedicated rooms with LEV. This is 
feasible for small parts, but as the size of the parts increases it 
becomes more difficult to control exposures. For example, when painting 
most small parts, exposures below 1 [mu]g/m\3\ are achievable, but for 
larger parts exposures can only be reduced to between 1 [mu]g/m\3\ and 
5 [mu]g/m\3\ using engineering and work practice controls. This group 
that can achieve levels between 1 [mu]g/m\3\ and 5 [mu]g/m\3\ 
(approximately \1/3\ of total aerospace painting operations) can use 
LEV, but as the size of the part increases it becomes increasingly 
difficult to provide good air flow around the entire part, such as 
underneath large horizontal structures. Moreover, as the size of the 
part increases, it becomes increasingly difficult for the painter to 
position him or herself to avoid being downstream of the paint 
overspray due to the geometry of the parts.
    When painting even larger parts, such as fuselages, wings or the 
entire aircraft, exposures below 5 [mu]g/m\3\ are no longer achievable 
without supplementary respiratory protection. Because these large parts 
do not fit into enclosures or painting rooms, they must be painted in 
oversized workspaces, typically hangers that can reach the size of a 
football field (Ex. 38-106-2, p. 2). In oversized workspaces the 
ventilation system becomes less effective and generally, the larger the 
space, the more difficult it is to ventilate.
    Moreover, when ventilation is put into such areas, the simple 
solution of increasing air flow is not feasible because the amount of 
air that is needed to dilute or diffuse the contaminated air can 
adversely affect the quality of the job to the point where the paint or 
coating is unacceptable for its purpose of protecting the part or plane 
(Ex. 38-106, p. 38). Thus, simply increasing the air flow in these 
sites and situations is not a viable alternative. As discussed above, 
OSHA has established a provision to address the situation where 
exposures cannot be brought below 25 [mu]g/m\3\ through engineering and 
work practice controls alone. However, a PEL of 5 [mu]g/m\3\ can be 
achieved using respiratory protection for these operations.
    In short, OSHA believes a PEL of 5 [mu]g/m\3\ is feasible for 
aerospace painting operations. Although one-third of those operations 
will need to use respiratory protection to achieve the PEL, the 
remainder can do so with engineering and work practice controls alone. 
Half of that remaining group cannot achieve a PEL of 1 [mu]g/m\3\ 
because, even though they can take advantage of enclosures such as 
paint rooms with LEV, the LEV becomes less effective as the part 
becomes larger. For this reason lowering the PEL from 5 [mu]g/m\3\ to 1 
[mu]g/m\3\ would result in the above-described substantial increase in 
the number of employees required to wear respirators. OSHA has 
therefore concluded that a PEL of 1 is not generally feasible for 
aerospace painting. For a more detailed explanation of OSHA's 
technological feasibility analysis for aerospace
painting operations, see Chapter III of the FEA.
    Other industries. There are other major industries or applications 
where OSHA is confident the PEL of 5 [mu]g/m\3\ can be met with 
engineering and work practice controls, but the record does not 
establish that a PEL of 1 [mu]g/m\3\ would be technologically feasible. 
In particular, chromate pigment producers, chromium catalyst producers, 
and chromium dye producers would have difficulty meeting the proposed 
PEL. A significant portion of operations in these industries are 
conducted in open and often large areas that are very dusty, making 
exposures hard to control. Just as in aerospace painting above, the 
primary control is to enclose the operation and then ventilate. 
However, some of the operations cannot be enclosed because of the 
physical configuration of the plant, especially in older facilities 
(Ex. 47-3, p. 55). Moreover, because the medium containing the Cr(VI) 
tends to be a fine powder, additional LEV in any worksite potentially 
can result in significant and intolerable product loss. In other words, 
the product could be drawn up through the ventilation system (Ex. 38-
12, pp. 12-14).
    Thus, depending in large part on the number of facilities that can 
accommodate enclosures, these operations could potentially require 
extensive respirator use in order to meet a PEL of 1 [mu]g/m\3\; at 1 
[mu]g/m\3\, OSHA expects that 44% of employees in these three 
industries would need to wear respirators on at least an intermittent 
basis. This number could be even higher if there are a large number of 
facilities that cannot enclose troublesome operations.
    To find the proposed PEL technologically feasible for an industry, 
OSHA must "prove a reasonable possibility" that the typical firm can 
meet it with engineering and work practice controls in most operations. 
United Steelworkers, 647 F.2d at 1272. Table VIII-3 indicates that 
intermittent respirator use would be required to reach the proposed PEL 
of 1 [mu]g/m\3\ for chromate pigment producers, chromium catalyst 
producers, and chromium dye producers. The extent of daily respirator 
usage that would be required to meet the proposed PEL is not clear if 
the recommended controls of enclosures and automation of the key 
operations are not feasible for existing facilities, but could be 
substantial depending upon the variables discussed above. On balance, 
OSHA does not believe that the record establishes the likelihood that 
the typical firm in these industries can meet the proposed PEL with 
engineering and work practice controls. There are a total of 
approximately 469 exposed employees in these three industries (Table 
VIII-2). For a more detailed explanation of OSHA's technological 
feasibility analysis for chromate pigment producers, chromium catalyst 
producers, and chromium dye producers, see Chapter III of the FEA.
    Technological feasibility is also an issue for hard chrome 
electroplating operations where fume suppressants cannot be used to 
control Cr(VI) exposures because they would interfere with the product 
specifications, making the resulting product unusable.
    In conclusion, OSHA has determined that while a PEL of 5 [mu]g/m\3\ 
is technologically feasible for all affected industries, the record 
does not support the feasibility of the proposed PEL of 1 [mu]g/m\3\ 
for welding operations, aerospace painting, chromate pigment producers, 
chromium catalyst producers, chromium dye producers, and some hard 
chrome electroplating operations.
    Economic feasibility of the final and proposed PELs. OSHA has also 
evaluated the economic feasibility of the proposed and final PELs. With 
regard to economic feasibility, OSHA must "provide a reasonable 
assessment of the likely range of costs of its standard, and the likely 
effects of those costs on the industry," so as to "demonstrate a 
reasonable likelihood that these costs will not threaten the existence 
or competitive structure of an industry, even if it does portend 
disaster for some marginal firms." AFL-CIO v. OSHA, 965 F.2d 982 (11th 
Cir. 1992). OSHA believes that the final PEL of 5 [mu]g/m\3\ is 
feasible for all affected industries. (For a more detailed discussion 
of OSHA's economic feasibility analysis, see Chapter VIII, Summary of 
the Final Economic Analysis and Regulatory Flexibility Analysis, 
Sections D and E.) In the majority of industries, costs will be less 
than 1% of revenues. For fewer than 10 of the approximately 250 NAICS 
(North American Industry Classification System) categories affected by 
the rule, costs are estimated to exceed 1% of revenues. OSHA has 
concluded that all affected industries will be able to absorb these 
costs without threatening their existence or competitive structure. 
Accordingly, OSHA has concluded that the new standard is economically 
feasible for all industries.
    By contrast, the proposed PEL of 1 [mu]g/m\3\ would not be 
economically feasible for a significant industry-electroplating job 
shops (NAICS 332813; electroplating, plating, polishing anodizing and 
coloring services). Electroplating establishments can be broadly 
classified into two categories: (1) Job shops and (2) captive shops, 
with roughly half of establishments falling into each category. Job 
shops perform electroplating services for others, while captive shops 
provide plating services to the facility of which they are part.
    A PEL of 1 [mu]g/m\3\ would result in costs exceeding 2.7% of 
revenues and 65% of profits for electroplating job shops. As explained 
further in section VIII of this preamble, and in the FEA, OSHA does not 
believe that options for reducing impacts (e.g., phase-ins or allowing 
use of respirators) would significantly alleviate the burden of the 
proposed PEL. OSHA is concerned that these costs could alter the 
competitive structure of the industry. Approximately 33,400 workers are 
employed in electroplating job shops.
    Summary of the technological and economic feasibility of the final 
and proposed PELs. To summarize, OSHA concludes that the final PEL of 5 
[mu]g/m\3\ is technologically and economically feasible for the 
affected industries. On the other hand, the proposed PEL of 1 [mu]g/
m\3\ would be technologically or economically infeasible or is of 
unproven feasibility in a large number of industries and operations 
covered by the standard, including welding, aerospace painting, 
chromate pigment production, chromium catalyst production, chromium dye 
production, some hard chrome electroplating operations, and 
electroplating job shops. These operations affect approximately 312,170 
exposed employees, or almost 56% of the total number of employees 
occupationally exposed to Cr(VI) (Table VIII-2). This figure includes 
270,000 employees in welding, 8,300 employees in aerospace painting 
operations, 33,400 employees in electroplating job shops, and 469 
employees in the other three industries. (Note that this number does 
not include a separate count for employees performing hard chrome 
electroplating in order to avoid double counting employees performing 
that operation who are employed in the electroplating job shop 
category). OSHA did not receive data or recommendations regarding 
setting the PEL at any levels between 1 and 5 [mu]g/m\3\.
A Uniform PEL of 5 [mu]g/m\3\ Is Consistent With the Feasibility 
Constraint of Section 6(b)(5)
    Section 6(b)(5) of the OSH Act requires OSHA to set the standard 
which most adequately assures, to the extent feasible * * * that no 
employee will suffer material impairment of health." This provision 
requires the agency to eliminate or reduce significant risk, to the 
extent feasible. See American Textile Mfr. Inst., Inc. v. Donovan, 
452 U.S. 490, 506-22(1981). OSHA has always interpreted Section 6(b)(5) 
to accord the agency substantial discretion to set the PEL at the lowest 
level that is feasible for industries and operations as a whole. OSHA has
not interpreted the provision to require setting multiple PELs based on 
the lowest level particular industries or operations could achieve. Because 
Congress did not speak to the precise issue in the statute, OSHA has 
authority to adopt the reasonable interpretation that it judges will 
best carry out the purposes of the Act. Chevron U.S.A. v. Natural 
Resources Defense Council, 467 U.S. 837 (1984).
    The new Cr(VI) standard meets the requirements of Section 6(b)(5) 
because the PEL of 5 [mu]g/m\3\ is the lowest feasible limit for many 
operations and sectors employing a large number of covered employees in 
fact, a majority of affected employees. In addition, the record does 
not afford a basis for any further disaggregation.
    OSHA recognizes that, according to the determination made in 
Section VII of this preamble, significant risk remains at a PEL of 5 
[mu]g/m\3\. As indicated in Table VII-3 in the Significance of Risk 
section, the remaining risk for a worker exposed at the PEL throughout 
a 45-year working lifetime is comparable to or greater than the 
remaining risk in previous OSHA health standards where quantitative 
estimates have been presented. Although OSHA anticipates that the 
ancillary provisions of the standard will reduce this residual risk, 
the Agency realizes that lower PELs might be achievable in some 
industries and operations, which would reduce this risk even further. 
As explained below, however, OSHA concludes that these benefits would 
be offset by the significant disadvantages of attempting to establish 
and apply multiple PELs for the diverse group of industries and 
operations covered by the standard. See Building & Constr. Trades Dep't 
v. U.S. Dep't of Labor, 838 F.2d 1258, 1273 (D.C. Cir. 1988) 
(administrative difficulties, if appropriately spelled out, could 
justify a decision to select a uniform PEL).
    Requiring OSHA to set multiple PELs--taking into account the 
feasibility considerations unique to each industry or operation or 
group of them--would impose an enormous evidentiary burden on OSHA to 
ascertain and establish the specific situations, if any, in which a 
lower PEL could be reached. Such an onerous obligation would inevitably 
delay, if not preclude, the adoption of important health standards. In 
addition, the demanding burden of setting multiple PELs would be 
complicated by the difficulties inherent in precisely defining and 
clearly distinguishing between affected industries and operations where 
the classification determines legal obligations. The definitional and 
line-drawing problem is far less significant when OSHA merely uses a 
unit of industries and operations for analytical but not compliance 
purposes, and when it sets a PEL in the aggregate, i.e., when its 
analysis is limited to determining whether a particular PEL is the 
lowest feasible level for affected industries as a whole. If OSHA had 
to set multiple PELs, and assign industries or operations to those 
PELs, the problem would become much more pronounced as the consequences 
of imprecise classifications would become much more significant.
    The North American Industry Classification System (NAICS), which 
has replaced the Standard Industrial Classification (SIC) system as the 
standard Federal statistical agencies use in classifying business 
establishments, is not an appropriate basis for establishing multiple 
PELs. NAICS classifications are based on generally-worded definitions 
and it is not always clear which definition best fits a particular 
establishment. Moreover, an establishment's NAICS classification is 
based on its primary activity. The establishment may include many other 
activities, however, and what is the lowest feasible level for 
operations in one activity may not be so for other activities. In 
addition, the primary activity in an establishment may change over time 
and the NAICS system itself is subject to revision every five years. 
Definitional uncertainties, the presence of multiple and changing 
business activities, and periodic revisions in individual codes could 
have important consequences for enforcement of the standard over time. 
For these reasons, OSHA has historically been reluctant to disaggregate 
coverage of a standard by SIC classification. See 58 FR 166620-16621 
(March 30, 1993) (discussing disaggregation of coverage of lockout/
tagout standard).
    Similarly, disaggregation by operation has major practical 
disadvantages. In addition to definitional complexities, a significant 
problem with the use of operations for disaggregating the PEL is that 
many firms have exposures in two or more different categories. Welding, 
for example, is widely used in manufacturing operations in general 
industry, maritime and construction. So, for instance, setting the PEL 
at 5 for welding applications and 1 for other applications would mean 
that some firms would have to attain two different PELs for Cr(VI) 
exposures within the same workplace, and possibly even for the same 
employees. As another example, chromium conversion is a process where a 
treated metal surface is converted to a layer containing a complex 
mixture of chromium compounds. Unlike electroplating, chromium 
conversion is an entirely chemical process, and results in lower Cr(VI) 
exposures than are typically associated with chromium electroplating. 
Where chromium conversion is performed along with chromium 
electroplating in a single establishment, it may be virtually 
impossible to distinguish exposures from one source versus the other. 
The same workers may even perform both tasks. Exposures from hard 
chrome electroplating inevitably affect other nearby workers because 
hard chrome plating is often done in the same workplaces or areas and 
even at the same time as other operations involving lower Cr(VI) 
exposures such as decorative plating and chrome conversion. In fact, in 
many circumstances it can be virtually impossible to distinguish the 
different sources that contribute to a particular employee's exposure 
levels.
    These are just a few examples of the many instances reflected in 
the record in which individual employers will have Cr(VI) exposures 
emanating from two or more different operations (Exs. 38-233, pp. 9-10; 
39-52, p. 4; 47-24, p. 2; 39-20, p. 5). If multiple PELs were 
established for different operations, employers would be forced to 
monitor for compliance with two or more PELs within the same 
workplace--a task rendered all the more difficult by the fact that the 
exposure of an employee may not be tied exclusively to a single task; 
different processes may be performed in close proximity to one another 
and each may contribute to the exposure of an individual.
    OSHA also believes that a uniform PEL will ultimately make the 
standard more effective by making it easier for affected employers to 
understand and comply with the standard's requirements. A uniform PEL 
also makes it easier for OSHA to provide clear guidance to the 
regulated community and to identify non-compliant conditions.
    Finally, OSHA is concerned that adopting multiple PELS could result 
in a great number of subcategories that would have to be tracked for 
enforcement purposes. Apart from welding and electroplating, which 
present particularly severe
dissagregation problems, there are over thirty other industry sectors 
with exposure to Cr(VI). None of these sectors individually accounts 
for more than 6% of the total of exposed employees; in fact, several of 
those groups employ fewer than 100 employees.
    For these reasons, OSHA has historically interpreted section 
6(b)(5) to accord the Agency substantial discretion to set the PEL at 
the lowest level feasible for industries or operations as a whole. In 
adopting the arsenic standard, for example, OSHA expressly declined to 
set different PELS, finding that "[s]uch an approach would be 
extremely difficult to implement." 43 FR 19584, 19601 (May 5, 1978). 
In that instance, OSHA explained:

    The approach OSHA believes appropriate and has chosen for this 
and other standards is the lowest level achievable through 
engineering controls and work practices in the majority of 
locations. This approach is intended to provide maximum protection 
without excessively heavy respirator use. Id.

Similarly, when OSHA initially lowered the PEL for benzene from 10 ppm 
to 1 ppm, it considered, but rejected, the idea of establishing 
additional lower PELs, concluding that "different levels for different 
industries would result in serious administrative difficulties." 43 FR 
5918, 5947 (Feb. 10, 1978). And when OSHA subsequently reconsidered the 
benzene standard after it was remanded for a more specific finding of 
significant risk, OSHA considered, but rejected, a PEL of 0.5 ppm, 
noting:

    The unions have pointed out some situations where controls might 
do somewhat better than 1 ppm * * * [but] OSHA believes it has 
chosen the correct balance at 1 ppm as the level it can have a high 
degree of confidence is generally achievable. 52 FR 34460, 34519 
(Sept. 11, 1987).

    In the case of cotton dust, where OSHA did set different PELs for 
certain discrete groups, the groups involved exposures to different 
kinds of cotton dust and different degrees of risk. Even so, OSHA 
declined to adopt a unique PEL for every single affected sector. See 43 
FR 27350, 37360-61 (June 23, 1978) (OSHA set one PEL for textile 
industries and a separate PEL for non-textile industries, but expressly 
rejected the option of adopting different exposure limits for each non-
textile industry).
    In conclusion, the new PEL is the lowest level that can feasibly be 
attained for many industries and operations employing a large number of 
covered workers, in fact a majority of employees exposed to hexavalent 
chromium. Considering all of the factors outlined above, OSHA finds 
that a uniform PEL of 5 [mu]g/m\3\ is consistent with section 6(b)(5) 
and that further dissagregation is not warranted.
    A Short-term Exposure Limit is Unnecessary. Several commenters 
recommended that OSHA establish a short-term exposure limit (STEL) for 
Cr(VI) (Exs. 38-219; 38-222; 39-38; 39-50; 40-19). By restricting 
potential high magnitude exposures of short duration, a STEL is 
intended to protect against health effects associated with relatively 
high exposures, as well as to reduce cumulative exposures. The UAW 
indicated that the high residual risk of cancer justified a STEL (Ex. 
40-19), while NIOSH stated that short-term exposures to high levels of 
Cr(VI) can cause severe respiratory effects (40-10-2, p. 17). Other 
commenters did not believe a STEL was justified, in some cases noting 
that neither NIOSH nor ACGIH recommends a STEL for Cr(VI) (Exs. 38-214; 
38-220; 39-19; 39-20; 39-40; 39-41; 39-47; 39-51; 39-52; 39-60; 43-26).
    OSHA decided not to include a STEL in the final Cr(VI) standard for 
three reasons. First, employers already are required to reduce 
exposures to levels at or below the new PEL, which is expected to limit 
the occurrence of high exposure excursions. Although it will not 
eliminate all risk from peak exposures, the Agency anticipates that 
compliance with the new PEL will substantially reduce the frequency and 
magnitude of high exposure excursions, and thereby minimize the 
likelihood of adverse health effects resulting from peak exposures. 
Second, although in theory imposing a STEL might further lower 
cumulative exposures to Cr(VI), there is little record evidence 
supporting this supposition. Third, in some application groups, such as 
plastic colorant producers, employees are typically exposed to Cr(VI) 
not only for short durations but also intermittently. The industry has 
estimated that only 5% of pigments used contain Cr(VI) (Ex. 47-24-1). 
For these users, compliance with a STEL might require the expenditure 
of considerable resources without providing much additional protection 
to workers. These resources could more effectively be allocated to 
other forms of worker protection.
    Without better justification, OSHA does not consider establishment 
of a STEL to be reasonably necessary or appropriate. OSHA has concluded 
that a STEL would provide at most a de minimis health benefit.
(d) Exposure Determination
    Paragraph (d) of the final rule sets forth requirements for 
determining employee exposures to Cr(VI). The requirements are issued 
pursuant to Section 6(b)(7) of the OSH Act (29 U.S.C. 655) which 
mandates that any standard promulgated under section 6(b) shall, where 
appropriate, "provide for monitoring or measuring of employee exposure 
at such locations and intervals, and in such manner as may be necessary 
for the protection of employees."
    The purpose of requiring an assessment of employee exposures to 
Cr(VI) includes: determination of the extent and degree of exposure at 
the worksite; identification and prevention of employee overexposure; 
identification of the sources of exposure to Cr(VI); collection of 
exposure data so that the employer can select the proper control 
methods to be used; and evaluation of the effectiveness of those 
selected methods. Assessment enables employers to meet their legal 
obligation to ensure that their employees are not exposed to Cr(VI) in 
excess of the permissible exposure level and to notify employees of 
their exposure levels, as required by section 8(c)(3) of the Act. In 
addition, the availability of exposure data enables the PLHCP 
performing medical examinations to be informed of the extent of 
occupational exposures.
    The final requirements have been revised from those proposed in 
response to comments received. In the proposed general industry 
standard, OSHA included a requirement for initial exposure monitoring 
in all workplaces covered by the rule, unless monitoring had been 
performed in the previous 12 months, or the employer had data to 
demonstrate that exposures would be below the action level. Periodic 
monitoring was required at intervals determined by monitoring results 
(i.e., at least every 6 months if exposures were at or above the action 
level, at least every 3 months if exposures were above the PEL), and 
additional monitoring was required when changes in the workplace 
resulted in new or additional exposures to Cr(VI). These requirements 
are similar to requirements for monitoring found in previous OSHA 
substance-specific health standards, such as those for methylene 
chloride (29 CFR 1910.1052) and 1,3-butadiene (29 CFR 1910.1051).
    The proposed standards for construction and shipyards did not 
include provisions for exposure monitoring. OSHA did not propose 
specific exposure monitoring requirements for construction and 
shipyards because operations in these sectors are often of short 
duration, and are performed under varying environmental conditions.
    In omitting exposure monitoring requirements from the proposed
standards for construction and shipyards, OSHA intended to provide 
construction and shipyard employers with the flexibility to assess 
Cr(VI) exposures in any manner they considered appropriate. It was not 
the Agency's intent that employers ignore substantial exposures to 
Cr(VI). Because the obligation to comply with the PEL would remain, the 
employer would have to accurately characterize Cr(VI) exposures in 
order to determine if they were in compliance. At the time of the 
proposal, OSHA considered this performance-oriented approach a 
reasonable way to determine employee exposures to Cr(VI) while avoiding 
the more infeasible requirements of a scheduled monitoring approach 
that might not be useful in construction and shipyard workplaces. This 
performance-based approach was consistent with OSHA's standard for air 
contaminants (29 CFR 1910.1000), which establishes PELs for over 400 
substances but does not include specific requirements for exposure 
monitoring.
    Construction and shipyard employers who expressed an opinion on the 
issue generally supported the absence of specific exposure monitoring 
requirements (e.g., Exs. 38-220; 38-235; 38-244). In addition to those 
operations that involved changing conditions, employers argued that 
periodic monitoring requirements were unnecessary when conditions did 
not change (Exs. 38-124; 38-213, 38-215; 38-189, 38-191). For example, 
the U.S. Navy stated:

    The prescriptive schedule of required air sampling has not 
proved beneficial in assessing risks in shipyards * * * where there 
has been virtually no change in conditions, yet costs for consistent 
air sampling have been incurred on an annual basis without 
informational benefit or added protection for workers. The 
performance-based sampling approach * * * is protective, efficient, 
and logical (Ex. 38-220).

A number of employers also supported a performance oriented approach 
for exposure determination in general industry workplaces (Exs. 38-189; 
38-191; 38-213; 38-215; 39-48). Some of these commenters argued that 
Cr(VI) exposures in their workplaces were intermittent, variable, and 
of short duration, and therefore similar to those found in construction 
and shipyards (Exs. 38-203; 38-254; 39-19; 39-48; 39-56). Other 
comments focused on requirements for periodic monitoring that were 
considered to be excessive (e.g., Exs. 38-124; 38-189; 38-191; 38-213; 
38-215; 38-233). For example, the Color Pigments Manufacturers 
Association stated:

    OSHA continues to require repeated monitoring at great cost in 
general industry under circumstances where no change in procedure, 
process, equipment or exposure has occurred to warrant repeated 
exposure monitoring. This requirement is unnecessary and punitive. 
It forces general industry to expend valuable resources on continual 
monitoring without reason (Ex. 38-205).

Some employers, while maintaining that periodic monitoring requirements 
were not warranted, indicated that initial exposure monitoring or an 
initial hazard assessment would be appropriate (Exs. 38-214; 38-245-1).
    Other commenters, including unions, Public Citizen, and NIOSH, 
supported explicit requirements for exposure assessment (Exs. 38-199-1; 
38-222; 40-10-2; 47-23, p. 16). These parties argued that employers 
will not know whether or not they are in compliance with the standard 
without mandated exposure monitoring. For example, the Building and 
Construction Trades Department, AFL-CIO, stated:

    If OSHA indeed intends construction employers to conduct an 
exposure assessment, this requirement must be explicitly stated in 
the regulation. To suggest that employers will attempt to 
characterize exposure routinely without an explicit requirement in 
the regulation is ludicrous (Ex. 38-219).

Even where controls are implemented, it was argued, exposure assessment 
is still necessary to ensure that those controls are adequately 
protective (Ex. 38-219). NIOSH suggested that OSHA might want to 
consider developing alternative means for assessing exposures, such as 
the use of interim protection provisions in construction for certain 
tasks until exposure monitoring could be done (see the lead standard, 
29 CFR 1926.62(d)) and the use of grouped tasks and grouping job types 
into classes based on exposure potential (see the asbestos standard, 29 
CFR 1926.1101) (Ex. 40-10-2, p. 19).
    After considering the evidence and arguments advanced by rulemaking 
participants, OSHA is convinced that requirements for scheduled initial 
and periodic Cr(VI) exposure monitoring are not appropriate in all 
circumstances. In particular, OSHA believes that the evidence in this 
rulemaking, as discussed earlier in this section in paragraph (c), 
permissible exposure limit, demonstrates the varied nature of Cr(VI) 
exposures across a number of different work operations. However, OSHA 
also believes that valid concerns have been raised regarding the 
adequacy of exposure assessments that would be performed in the absence 
of explicit requirements. The Agency is therefore including in the 
final rule two alternative options for all affected employers to follow 
for determining employee exposures to Cr(VI). The first option, 
referred to as the "scheduled monitoring option", consists of 
requirements for initial monitoring and periodic monitoring at 
intervals based on monitoring results. This approach is similar to that 
proposed for general industry in this rulemaking and with exposure 
assessment requirements in previous OSHA substance-specific standards. 
The second option, referred to as the "performance-oriented option", 
allows employers to use any combination of air monitoring data (i.e., 
data obtained from initial and periodic monitoring performed in 
accordance with the requirements of the Cr(VI) standard), historical 
monitoring data, or objective data to determine employee exposures to 
Cr(VI), as long as the data are sufficient to accurately characterize 
exposures.
    OSHA believes that by including explicit requirements for exposure 
determination in the standards for general industry, construction, and 
shipyards, the Agency makes clear the obligation of employers to 
accurately assess employee exposures to Cr(VI) in all sectors. By 
offering two options for achieving this goal, the final rule provides a 
framework that is familiar to many employers and has been successfully 
applied in the past, as well as flexibility for employers who are able 
to characterize employee exposures through alternative methods.
    OSHA has chosen not to use the task-based approaches suggested by 
NIOSH (Ex. 40-10-2) that the Agency has used in several previous health 
standards covering construction. While OSHA believes that these 
approaches are effective in certain construction settings, there was 
not sufficient information in this rulemaking record for OSHA to 
develop classes of exposures that would apply across the many varied 
work operations with Cr(VI) exposures. While it was not possible to 
develop specific classes of operations to apply across all industries, 
OSHA believes that an individual employer, with specific information 
about the work processes at his worksite, may be able to use such an 
approach in using the performance-based option allowed by this final 
rule.
    Paragraph (d)(2) contains requirements for employers who choose the 
scheduled monitoring option. Employers who select this option must 
conduct initial monitoring to determine employee exposure to Cr(VI). 
OSHA has not established a separate compliance date for initial 
monitoring to allow employers flexibility in scheduling this activity. 
However, employers must allow sufficient time after initial monitoring 
is performed to achieve compliance (e.g., establish regulated areas,
provide appropriate respiratory protection) by the start-up dates specified 
in paragraph (n) (paragraph (l) for construction and shipyards). Monitoring to 
determine employee exposures must represent the employee's time-
weighted average exposure to airborne Cr(VI) over an eight-hour 
workday. Samples must be taken within the employee's breathing zone 
(i.e., "personal breathing zone samples" or "personal samples"), 
and must represent the employee's exposure without regard to the use of 
respiratory protection.
    Employers must accurately characterize the exposure of each 
employee to Cr(VI). In some cases, this will entail monitoring all 
exposed employees. In other cases, monitoring of "representative" 
employees is sufficient. Representative exposure sampling is permitted 
when a number of employees perform essentially the same job under the 
same conditions. For such situations, it may be sufficient to monitor a 
fraction of these employees in order to obtain data that are 
"representative" of the remaining employees. Representative personal 
sampling for employees engaged in similar work with Cr(VI) exposure of 
similar duration and magnitude is achieved by monitoring the 
employee(s) reasonably expected to have the highest Cr(VI) exposures. 
For example, this may involve monitoring the Cr(VI) exposure of the 
employee closest to an exposure source. This exposure result may then 
be attributed to the remaining employees in the group.
    Exposure monitoring should include, at a minimum, one full-shift 
sample taken for each job function in each job classification, in each 
work area, for each shift. These samples must consist of at least one 
sample characteristic of the entire shift or consecutive representative 
samples taken over the length of the shift. Where employees are not 
performing the same job under the same conditions, representative 
sampling will not adequately characterize actual exposures, and 
individual monitoring is necessary.
    Employers who have workplaces covered by the standard must 
determine if any of their employees are exposed to Cr(VI) at or above 
the action level. Further obligations under the standard are based on 
the results of this assessment. These may include obligations for 
periodic monitoring, establishment of regulated areas, implementation 
of control measures, and provision of medical surveillance.
    Requirements for periodic monitoring depend on the results of 
initial monitoring. If the initial monitoring indicates that employee 
exposures are below the action level, no further monitoring is required 
unless changes in the workplace result in new or additional exposures. 
If the initial determination reveals employee exposures to be at or 
above the action level but at or below the PEL, the employer must 
perform periodic monitoring at least every six months. If the initial 
monitoring reveals employee exposures to be above the PEL, the employer 
must repeat monitoring at least every three months.
    The scheduled monitoring option also includes provisions to adjust 
the frequency of periodic monitoring based on monitoring results. If 
periodic monitoring results indicate that employee exposures have 
fallen below the action level, and those results are confirmed by 
consecutive measurements taken at least seven days apart, the employer 
may discontinue monitoring for those employees whose exposures are 
represented by such monitoring. Similarly, if periodic monitoring 
measurements indicate that exposures are at or below the PEL but at or 
above the action level, the employer may reduce the frequency of the 
monitoring to at least every six months.
    OSHA recognizes that exposures in the workplace may fluctuate. 
Periodic monitoring provides the employer with assurance that employees 
are not experiencing higher exposures that may require the use of 
additional control measures. In addition, periodic monitoring reminds 
employees and employers of the continued need to protect against the 
hazards associated with exposure to Cr(VI).
    Because of the fluctuation in exposures, OSHA believes that when 
initial monitoring results equal or exceed the action level but are at 
or below the PEL, employers should continue to monitor employees to 
ensure that exposures remain at or below the PEL. Likewise, when 
initial monitoring results exceed the PEL, periodic monitoring allows 
the employer to maintain an accurate profile of employee exposures. If 
the employer installs or upgrades controls, periodic monitoring will 
demonstrate whether or not controls are working properly. Selection of 
appropriate respiratory protection also depends on adequate knowledge 
of employee exposures.
    In general, the more frequently periodic monitoring is performed, 
the more accurate the employee exposure profile. Selecting an 
appropriate interval between measurements is a matter of judgment. OSHA 
believes that the frequency of six months for subsequent periodic 
monitoring for exposures at or above the action level but at or below 
the PEL, and three months for exposures above the PEL, provides 
intervals that are both practical for employers and protective for 
employees. This belief is supported by OSHA's experience with 
comparable monitoring intervals in other standards, including those for 
cadmium (29 CFR 1910.1027), methylenedianiline (29 CFR 1910.1050), 
methylene chloride (29 CFR 1910.1052), and formaldehyde (29 CFR 
1910.1048).
    OSHA recognizes that monitoring can be a time-consuming, expensive 
endeavor and therefore offers employers the incentive of discontinuing 
monitoring for employees whose sampling results indicate exposures are 
below the action level. The Agency does not believe that periodic 
monitoring is generally necessary when monitoring results show that 
exposures are below the action level because there is a low probability 
that the results of future samples would exceed the PEL. Therefore the 
final rule provides an incentive for employers to control their 
employees' exposures to Cr(VI) below the action level to minimize their 
exposure monitoring obligations while maximizing the protection of 
employees' health.
    Under the scheduled monitoring option, employers are to perform 
additional monitoring when there is a change in production process, raw 
materials, equipment, personnel, work practices, or control methods, 
that may result in new or additional exposures to Cr(VI). For example, 
if an employer has conducted monitoring for an electroplating operation 
while using fume suppressants, and the use of fume suppressants is 
discontinued, then additional monitoring would be necessary to 
determine employee exposures under the modified conditions. In 
addition, there may be other situations which can result in new or 
additional exposures to Cr(VI) which are unique to an employer's work 
situation. For instance, a welder may move from an open, outdoor 
location to an enclosed or confined space. Even though the task 
performed and materials used may remain constant, the changed 
environment could reasonably be expected to result in higher exposures 
to Cr(VI). In order to cover those special situations, OSHA requires 
the employer to perform additional monitoring whenever the employer has 
any reason to believe that a change has occurred which may result in 
new or additional exposures. This additional monitoring is necessary to 
ensure that monitoring results accurately represent existing exposure 
conditions. This information will enable the employer to take appropriate 
action to protect exposed employees, such as instituting additional engineering 
controls or providing appropriate respiratory protection. On the other 
hand, additional monitoring is not required simply because a change has 
been made, if the change is not reasonably expected to result in new or 
additional exposures to Cr(VI). For example, monitoring may be 
conducted in an establishment when welding was performed on steel with 
15% Cr content. If the establishment switches to a steel with 10% Cr 
content without changing any other aspect of the work operation, then 
additional exposures to Cr(VI) would not reasonably be expected, and 
additional monitoring would not be required.
    The performance-oriented option allows the employer to determine 
the 8-hour TWA exposure for each employee on the basis of any 
combination of air monitoring data, historical monitoring data, or 
objective data sufficient to accurately characterize employee exposure 
to Cr(VI). This option is intended to allow employers flexibility in 
assessing the Cr(VI) exposures of their employees. Where the employer 
elects to follow this option, the exposure determination must be 
performed prior to the time the work operation commences, and must 
provide the same degree of assurance that employee exposures have been 
correctly characterized as air monitoring would. The employer is 
expected to reevaluate employee exposures when there is any change in 
the production process, raw materials, equipment, personnel, work 
practices, or control methods that may result in new or additional 
exposures to Cr(VI).
    When using the term "air monitoring data" in this paragraph, OSHA 
refers to initial and periodic Cr(VI) monitoring conducted to comply 
with the requirements of this standard, including the prescribed 
accuracy and confidence requirements. Historical monitoring data refers 
to Cr(VI) monitoring data that was obtained prior to the effective date 
of the final rule, where the data were obtained during work operations 
conducted under workplace conditions closely resembling the processes, 
types of material, control methods, work practices, and environmental 
conditions in the employer's current operations, and where that 
monitoring satisfies all other requirements of this section, including 
the accuracy and confidence requirements described below.
    Objective data means information such as air monitoring data from 
industry-wide surveys or calculations based on the composition or 
chemical and physical properties of a substance demonstrating employee 
exposure to Cr(VI) associated with a particular product or material or 
a specific process, operation, or activity. The data must reflect 
workplace conditions closely resembling the processes, types of 
material, control methods, work practices, and environmental conditions 
in the employer's current operations. Objective data demonstrate the 
Cr(VI) exposures associated with a work operation or product under the 
range of expected conditions of use. For example, data collected by a 
trade association from its members may be used to determine exposures 
to Cr(VI) provided the data meet the definition of objective data in 
the standard.
    Previous OSHA substance-specific health standards have usually 
allowed employers to use objective data to characterize employee 
exposures, but have generally limited its use to demonstrating that 
exposures would be below the action level (e.g., the Cadmium standard, 
29 CFR 1910.1027(d)(2)(iii)). Likewise, use of historical monitoring 
data has typically been allowed, but has usually been limited to data 
obtained within the previous 12 months (e.g., the Methylene Chloride 
standard, 29 CFR 1910.1052(d)(2)(ii)). In this instance, OSHA does not 
place these limitations on the use of historical monitoring data or 
objective data. However, the burden is on the employer to show that the 
data comply with the requirements of this section. For example, 
historical monitoring data obtained 18 months prior to the effective 
date of the standard could be used to determine employee exposures, but 
only if the employer could show that the data were obtained during work 
operations conducted under workplace conditions closely resembling the 
processes, types of material, control methods, work practices, and 
environmental conditions in the employer's current operations, and that 
the monitoring satisfies all other requirements of this section, 
including the accuracy and confidence requirements. OSHA's intent is to 
allow employers the greatest possible flexibility in methods used to 
determine employee exposures to Cr(VI), but to ensure that the methods 
used are accurate in characterizing employee exposures.
    Under paragraph (d)(4) of the final rule, employers covered by the 
general industry standard must notify each affected employee within 15 
working days if the exposure determination indicates that employee 
exposure exceeds the PEL. In construction and shipyards, employers must 
notify each affected employee as soon as possible but not more than 5 
working days after the exposure determination indicates that employee 
exposure exceeds the PEL. A shorter time period for notification is 
provided in construction and shipyards in recognition of the often 
short duration of operations and employment in particular locations in 
these sectors. The time allowed for notification is consistent with the 
harmonized notification times established for these sectors in Phase II 
of OSHA's Standards Improvement Project (70 FR 1112 (1/5/05)). Where 
the employer follows the scheduled monitoring option, the 15 (or 5) 
working day period commences when monitoring results are received. For 
employers following the performance-oriented option, the 15 (or 5) 
working day period commences when the determination is made (i.e., 
prior to the time the work operation commences, and when exposures are 
reevaluated).
    When using the term "affected employees" in this provision, OSHA 
is referring to all employees considered to be above the PEL. This 
would include employees who are not actually subject to personal 
monitoring, but are represented by an employee who is sampled. Affected 
employees also include employees whose exposures have been deemed to be 
above the PEL on the basis of historical or objective data. The 
employer shall either notify each affected employee in writing or post 
the monitoring results in an appropriate location accessible to all 
affected employees. In addition, whenever the PEL has been exceeded, 
the written notification must contain a description of the corrective 
action(s) being taken by the employer to reduce the employee's exposure 
to or below the PEL. The requirement to inform employees of the 
corrective actions the employer is taking to reduce the exposure level 
to or below the PEL is necessary to assure employees that the employer 
is making efforts to furnish them with a safe and healthful work 
environment, and is required under section 8(c)(3) of the Act.
    Paragraph (d)(5) of the final rule requires the employer to use 
monitoring and analytical methods that can measure airborne levels of 
Cr(VI) to within an accuracy of plus or minus 25% (25%) and 
can produce accurate measurements to within a statistical confidence 
level of 95% for airborne concentrations at or above the action level. 
Many laboratories presently have methods to measure Cr(VI) at the action 
level with at least the required degree of accuracy. One example of an 
acceptable method of monitoring and analysis is OSHA method ID215, which 
is a fully validated analytical method used by the Agency. (See Chapter III 
of the FEA for a discussion of issues regarding methods of sampling and 
analysis). Rather than specifying a particular method that must be 
used, OSHA allows the employer to use any method as long as the chosen 
method meets the accuracy specifications. This is consistent with the 
general performance approach favored in the OSH Act.
    Paragraph (d)(6) requires the employer to provide affected 
employees or their designated representatives an opportunity to observe 
any monitoring of employee exposure to Cr(VI), whether the employer 
uses the scheduled monitoring option or the performance-oriented 
option. When observation of monitoring requires entry into an area 
where the use of protective clothing or equipment is required, the 
employer must provide the observer with that protective clothing or 
equipment, and assure that the observer uses such clothing or equipment 
and complies with all other required safety and health procedures.
    The requirement for employers to provide employees or their 
representatives the opportunity to observe monitoring is consistent 
with the OSH Act. Section 8(c)(3) of the OSH Act mandates that 
regulations developed under Section 6 provide employees or their 
representatives with the opportunity to observe monitoring or 
measurements. Also, Section 6(b)(7) of the OSH Act states that where 
appropriate, OSHA standards are to prescribe suitable protective 
equipment to be used in dealing with hazards. The provision for 
observation of monitoring and protection of the observers is also 
consistent with OSHA's other substance-specific health standards such 
as those for cadmium (29 CFR 1910.1027) and methylene chloride (29 CFR 
1910.1052).
(e) Regulated Areas
    Paragraph (e) of the final rule requires general industry employers 
to establish regulated areas wherever an employee's exposure to 
airborne concentrations of Cr(VI) is, or can reasonably be expected to 
be, in excess of the PEL. Regulated areas are to be demarcated from the 
rest of the workplace in a manner that adequately establishes and 
alerts employees to the boundaries of these areas. Access to regulated 
areas is to be limited to persons authorized by the employer and 
required by work duties to be present in the regulated area; any person 
entering the regulated area to observe monitoring procedures; or any 
person authorized by the OSH Act or regulations issued under it to be 
in a regulated area.
    The purpose of a regulated area is to ensure that the employer 
makes employees aware of the presence of Cr(VI) at levels above the 
PEL, and to limit Cr(VI) exposure to as few employees as possible. The 
establishment of a regulated area is an effective means of limiting the 
risk of exposure to substances known to have carcinogenic effects. 
Because of the potentially serious results of exposure and the need for 
persons exposed above the PEL to be properly protected, the number of 
persons given access to the area must be limited to those employees 
needed to perform the job. Limiting access to regulated areas also has 
the benefit of reducing the employer's obligation to implement 
provisions of this standard to as few employees as possible.
    In keeping with the performance orientation of this standard, OSHA 
has not specified how employers are to demarcate regulated areas. OSHA 
proposed that warning signs be posted at all approaches to regulated 
areas, and set forth specific language in paragraph (1) of the proposed 
standard to be included on the warning signs. However, OSHA has 
determined that other means of demarcation such as barricades, lines 
and textured flooring, or signs using other language can be equally 
effective in identifying the boundaries of regulated areas and 
notifying employees of associated hazards, the need to restrict access 
to such areas, and protective measures to be implemented. The specific 
language for warning signs included in paragraph (1) of the proposal, 
and the reference to that language in this provision, have therefore 
been deleted from the final rule.
    In the final rule, OSHA thus has provided employers with the 
flexibility to use the methods of demarcation that are most appropriate 
for identifying regulated areas in their workplace. Factors that the 
Agency believes are appropriate for employers to consider in 
determining how to mark their areas include the configuration of the 
area, whether the regulated area is permanent, the airborne Cr(VI) 
concentration, the number of employees in adjacent areas, and the 
period of time the area is expected to have exposure levels above the 
PEL. Permitting employers to choose how best to identify and limit 
access to regulated areas is consistent with OSHA's belief that 
employers are in the best position to make such determinations, based 
on their knowledge of the specific conditions of their workplaces. 
Whatever methods are chosen, the demarcation must effectively warn 
employees not to enter the area unless they are authorized, and then 
only if they are using the proper personal protective equipment. 
Allowing employers to demarcate and limit access to the regulated areas 
as they choose is consistent with OSHA's two most recent substance-
specific health standards, addressing occupational exposure to 
methylene chloride (29 CFR 1910.1052(e)) and 1,3-butadiene (29 CFR 
1910.1051(e)).
    Access to the regulated area is restricted to "authorized 
persons." For the purposes of this standard, these are persons 
required by their job duties to be present in the area, as authorized 
by the employer. This may include maintenance and repair personnel, 
management, quality control engineers, or other personnel if job duties 
require their presence in the regulated area. In addition, persons 
exercising the right to observe monitoring procedures are allowed to 
enter regulated areas when exposure monitoring is being conducted. 
Persons authorized under the OSH Act, such as OSHA compliance officers, 
are also allowed access to regulated areas.
    In the final rule, OSHA has not included a requirement for 
regulated areas in construction and shipyard workplaces, due to the 
expected practical difficulties of establishing regulated areas for 
operations in these sectors. OSHA raised the issue of requiring 
regulated areas for these workplaces and received comments and 
testimony from a variety of sources. A number of commenters supported 
not requiring regulated areas in construction and shipyards (Exs. 38-
214; 38-220; 38-235; 38-236; 38-244; 39-37; 39-20; 39-40; 39-48; 39-64; 
39-65). The National Association of Home Builders, for example, 
indicated that regulated areas are not feasible on residential 
construction jobsites because the area where exposures would exceed the 
PEL could not be accurately determined, stating:

    Because of the fluid nature of construction work and the ever-
changing work environment, a regulated area could never be 
accurately determined due to the fact that construction areas are 
mostly exposed to the ambient environment. Factors such as shifting 
winds, tight work areas and multiple operations adjacent to the 
regulated area would create changes in air movement and would make 
establishment of a regulated area unattainable (Ex. 38-244).

Associated Builders and Contractors concurred with this assessment, and 
maintained that establishment of regulated areas could interfere with 
construction operations:

    The nature of construction sites makes it extremely difficult to 
close off certain areas from others without shutting down or 
interfering with significant construction activities (Ex. 39-65).

    Some commenters maintained that certain activities should not be 
subject to requirements for regulated areas (Exs. 38-7, p. 5; 38-124; 
38-203; 38-205; 38-228; 38-233; 38-238; 38-254; 39-19; 39-56; 39-62). 
The Office of Advocacy of the Small Business Administration, for 
example, stated that requirements for regulated areas should be limited 
to industries and processes where they would likely reduce exposures, 
arguing that establishment of regulated areas would have the effect of 
requiring respirators or other controls for more employees than 
necessary (Ex. 38-7). Because regulated areas are required only where 
exposures exceed the PEL, OSHA considers that these requirements are 
limited to situations where they can reduce exposures. As mentioned 
previously, making employees aware of potential exposures in excess of 
the PEL and limiting the number of employees present in regulated areas 
will effectively reduce exposures to Cr(VI). Moreover, establishment of 
regulated areas will not result in additional requirements for 
respirators or other controls, because requirements for these other 
control measures are not directly related to the establishment of 
regulated areas. Simply entering a regulated area, for example, does 
not trigger a requirement for use of respiratory protection.
    Other commenters maintained that certain general industry 
activities, or general industry as a whole, should not be subject to 
the proposed requirements for regulated areas. Alabama Power, for 
example, indicated that the same rationale used to justify the absence 
of regulated area requirements in construction and shipyards also 
applied to general industry environments such as power plants (Exs. 38-
254; 38-203). Others argued that regulated areas were not appropriate 
for specific activities such as welding (Ex. 38-124), job shop 
fabrication (Exs. 38-238; 39-62), or glass manufacturing (Ex. 38-228).
    Other commenters expressed support for regulated area requirements, 
arguing that they were a feasible and useful means of protecting 
workers, and should apply to construction and shipyards as well as 
general industry workplaces (Exs. 38-199-1; 38-219; 38-222; 39-38; 39-
71; 40-10-2; 47-28). For example, NIOSH indicated that regulated areas 
help minimize exposures to bystanders in construction and shipyard 
worksites:

    * * * regulated areas are important on construction and shipyard 
worksites because of the potential for "bystander" exposures given 
that it is common for employees from different trades to work in 
close proximity. For construction, bystander employees may work for 
different employers, thus complicating control efforts (Ex. 40-10-
2).

Regulated areas, it was argued, are not unduly burdensome. Dr. Franklin 
Mirer of the United Auto Workers, when asked if he foresaw problems 
with requirements for regulated areas, stated:

    * * * you put a sign [up] and you tell people who don't have to 
be there not to be there * * * what's burdensome about that? It's 
like * * * putting up a sign on the ladies room. Certain people 
can't go in that regulated area (Tr. 837).

    OSHA believes, however, that Dr. Mirer oversimplifies the 
situation. The difficulty is not with the mere physical act of putting 
up a sign at a regulated area, but rather with determining where, when, 
and for how long a duration to establish a regulated area. Making these 
determinations is very problematic given the varied and changing nature 
of the operations involving Cr(VI) exposures at construction and 
shipyard worksites. Moreover, areas where employees are exposed above 
the PEL might change on a daily or even hourly basis and may occur at 
different sites on the worksite than they did the day before, making it 
unreasonably difficult to keep up with the posting (and removal) of 
signs, barricades or other warning in a manner that would effectively 
let employees know about the hazard.
    OSHA has concluded that requirements for regulated areas are 
appropriate for general industry, but not for construction and 
shipyards, because the work sites and conditions and other factors, 
such as environmental variability normally present in construction and 
shipyard employment, differ substantially from those typically found in 
general industry. Construction and shipyard tasks are often of 
relatively short duration; are commonly performed outdoors, sometimes 
under adverse environmental conditions (e.g., wind, rain); and are 
often performed at non-fixed workstations or work sites. Collectively, 
these factors make establishment of regulated areas impracticable for 
many construction and shipyard operations.
    These difficulties are particularly evident with regard to welding 
operations in construction and shipyard workplaces. Welding is the 
predominant source of Cr(VI) exposures in these sectors, accounting for 
over 82% of employees exposed above the PEL in construction and over 
73% of employees exposed above the PEL in shipyards. Welding operations 
in construction and shipyards often involve movement to different 
locations during the workday, and welding fumes are highly subject to 
changes in air currents, meaning the exposure patterns can shift 
rapidly.
    In the typical shipyard and construction project involving 
exposure, it is difficult to determine appropriate boundaries for 
regulated areas because the work and worksite are varied and subject to 
environmental influences. Moreover, workers are often moving from place 
to place throughout the site on a regular basis. While each employer 
has the obligation under the requirements of paragraph (d) of this 
final rule to determine Cr(VI) exposures for all employees, accurately 
demarcating all areas where Cr(VI) exposures could potentially exceed 
the PEL is a separate and potentially much more difficult undertaking. 
In general industry environments, which are typically more stable, 
likely to be indoors, and usually at a fixed location, this can 
generally be accomplished with minimal difficulty. In construction and 
shipyard workplaces, for the reasons described above, OSHA has 
determined that establishing regulated areas to control exposures to 
Cr(VI) can not reasonably be accomplished, and has therefore not 
included a requirement for regulated areas for these sectors in the 
final rule.
    The Agency realizes that in some cases general industry work 
operations and work environments may be comparable to those found in 
construction and shipyards, and where the general industry employer can 
show compliance is not feasible, regulated areas will not have to be 
established. However, OSHA believes its longstanding distinction 
between these sectors provides an appropriate line for delineating 
between those operations where the employer generally is reasonably 
able to establish regulated areas where exposures to Cr(VI) exceed the 
PEL versus operations where regulated areas are generally not 
practicable.
    OSHA recognizes that the determination not to include requirements 
for regulated areas for construction and shipyards in this final rule 
differs from the determinations made in previous rulemakings. The AFL-
CIO pointed out that a number of previous standards including those for 
asbestos, cadmium, benzene, 1,2-dibromo-3-chloropropane, ethylene oxide, 
methylenedianiline, formaldehyde, and 1,3 butadiene, included provisions 
for regulated areas in construction (Exs. 38-222; 47-28-1). It is important 
to note, however, that many of these standards such as benzene, 1,2-dibromo-3-
chloropropane, ethylene oxide, methylenedianiline, and formaldehyde 
involved relatively few exposures in construction operations. For 
example, in the preamble to the final benzene standard OSHA concluded 
that while the standard would cover construction, "The standard has 
virtually no impact on construction" (52 FR at 34527). Similarly, 
requirements for regulated areas in the standard for cadmium in 
construction did not pose major problems for employers, because few 
workers were expected to be exposed above the PEL and thus subject to 
requirements for regulated areas. More importantly, in the cadmium 
rulemaking as in others discussed below, regulated areas for 
construction were not at issue because so few employees were 
potentially exposed above the PEL. Thus, the Agency did not address the 
factors that were presented in this rulemaking.
    OSHA's standards for lead in construction and asbestos in 
construction, on the other hand, affect relatively large numbers of 
employers and employees. The standard for lead in construction is a 
notable exception to the AFL-CIO's list. OSHA did not include 
requirements for regulated areas in that standard (see 29 CFR 1926.62). 
While the asbestos construction standard does include requirements for 
regulated areas, the classification scheme for asbestos construction 
operations (i.e., Class I, II, III and IV) and requirements for 
enclosing many work operations makes establishment of regulated areas 
easier for employers. (see 29 CFR 1926.1101). The Agency believes that 
the broad scope of the Cr(VI) final rule for construction, similar to 
the standard covering lead construction operations, would make 
application of regulated area requirements substantially more difficult 
than is the case for a standard with a much more limited scope, such as 
the standards for cadmium or benzene in construction.
    Finally, in none of the previous health standards were the 
particular difficulties of implementing regulated areas for shipyard 
and construction work specifically considered as they have been in this 
rulemaking. In this rulemaking, the establishment of regulated areas 
was a major issue with a significant volume of comments and testimony, 
allowing OSHA to fully consider the matter in light of the specific 
nature of Cr(VI) exposures. First, OSHA's proposal did not include 
regulated areas in construction and shipyard employment. Secondly, in 
the proposal, OSHA included two general questions, numbers 31 and 32, 
on modifying the requirements for construction and shipyard employment 
and one very specific question, number 47, on whether regulated areas 
should be included for construction and shipyard employment (69 FR 
59452, 59310). Thus, the public had sufficient notice and OSHA was able 
to weigh the evidence, ultimately finding the reasons for excluding 
regulated areas from construction and shipyard employment persuasive.
(f) Methods of Compliance
    Paragraph (f) of the final rule (paragraph (e) for construction and 
shipyards) establishes which methods must be used by employers to 
comply with the PEL. It requires that employers institute effective 
engineering and work practice controls as the primary means to reduce 
and maintain employee exposures to Cr(VI) to levels that are at or 
below the PEL unless the employer can demonstrate that such controls 
are not feasible. Where the employer demonstrates that such controls 
are not feasible, the final rule requires the employer to institute 
engineering and work practice controls to reduce exposures to the 
lowest feasible level. The employer is then required to supplement 
these controls with respiratory protection to achieve the PEL.
    A number of commenters supported OSHA's inclusion of the hierarchy 
of controls in the final Cr(VI) rule (e.g., Tr. 826, Exs. 38-232; 38-
235; 38-238; 39-20; 39-47; 40-10-2; 47-23; 47-26). For example, NIOSH 
endorsed the use of engineering and work practice controls as primary 
methods of controlling exposures to Cr(VI) (Ex. 40-10-2). Personal 
protective equipment such as respirators was regarded by NIOSH as the 
last line of defense, to be used only when engineering controls are not 
feasible. Other commenters objected to OSHA's proposed application of 
the hierarchy of controls in the Cr(VI) rule, arguing that use of 
respiratory protection instead of engineering controls should be 
allowed in a variety of different situations (e.g., Exs. 38-204; 38-
215; 38-216-1; 38-218; 38-233; 39-51; 39-66; 43-14; 47-30; 47-31; 47-
32). For example, the National Paint and Coatings Association contended 
that respirator use should be permitted in paint and coatings 
manufacture:

    * * * exposures to hexavalent chromium compounds are limited in 
time and place, and their handling is seldom encountered by 
other[sic] than a relatively small number of workers, whose use of 
respirators would not pose most of the problems OSHA associates with 
respirators * * * (Ex. 39-66).

    OSHA is requiring primary reliance on engineering controls and work 
practices because reliance on these methods is consistent with good 
industrial hygiene practice, with the Agency's experience in assuring 
that workers have a healthy workplace, and with the Agency's 
traditional adherence to a hierarchy of preferred controls. Engineering 
controls are reliable, provide consistent levels of protection to a 
large number of workers, can be monitored, allow for predictable 
performance levels, and can efficiently remove a toxic substance from 
the workplace. Once removed, the toxic substance no longer poses a 
threat to employees. The effectiveness of engineering controls does not 
generally depend to any substantial degree on human behavior, and the 
operation of equipment is not as vulnerable to human error as is 
personal protective equipment.
    Engineering controls can be grouped into three main categories: (1) 
Substitution; (2) isolation; and (3) ventilation, both general and 
localized. Quite often a combination of these controls can be applied 
to an industrial hygiene control problem to achieve satisfactory air 
quality. It may not be necessary to apply all these measures to any 
specific potential hazard.
    Substitution can be an ideal control measure. One of the best ways 
to prevent workers from being exposed to a toxic substance is to stop 
using it entirely. Although substitution is not always possible, 
replacement of a toxic material with a less hazardous alternative 
should always be considered.
    In those cases where substitution of a less toxic material is not 
possible, substituting one type of process for another process may 
provide effective control of an air contaminant. For example, process 
changes from batch operations to continuous operations will usually 
reduce exposures. This is true primarily because the frequency and 
duration of workers' potential contact with process materials is 
reduced in continuous operations. Similarly, automation of a process 
can further reduce the potential hazard.
    In addition to substitution, isolation should be considered as an 
option for controlling employee exposures to
Cr(VI). Isolation can involve containment of the source of a hazard, 
thereby separating it from most workers. Workers can be isolated from 
Cr(VI) by working in a clean room or booth, or by placing some other 
type of barrier between the source of exposure and the employee. 
Employees can also be protected by being placed at a greater distance 
from the source of Cr(VI) emissions.
    Frequently, isolation enhances the benefits of other control 
methods. For example, Cr(VI) compounds may be used in the formulation 
of certain paints. If the mixing operation is conducted in a small, 
enclosed room the airborne Cr(VI) potentially generated by the 
operation could be confined to a small area. By ensuring containment, 
local exhaust ventilation is more effective.
    Ventilation is a method of controlling airborne concentrations of a 
contaminant by supplying or exhausting air. A local exhaust system is 
used to remove an air contaminant by capturing the contaminant at or 
near its source before it spreads throughout the workplace. General 
ventilation (dilution ventilation), on the other hand, allows the 
contaminant to spread throughout the work area but dilutes it by 
circulating large quantities of air into and out of the area. A local 
exhaust system is generally preferred to dilution ventilation because 
it provides a cleaner and healthier work environment.
    Work practice controls involve adjustments in the way a task is 
performed. In many cases, work practice controls complement engineering 
controls in providing worker protection. For example, periodic 
inspection and maintenance of process equipment and control equipment 
such as ventilation systems is an important work practice control. 
Frequently, equipment which is in disrepair or near failure will not 
perform normally. Regular inspections can detect abnormal conditions so 
that timely maintenance can then be performed. If equipment is 
routinely inspected, maintained, and repaired or replaced before 
failure is likely, there is less chance that hazardous exposures will 
occur.
    Workers must know the proper way to perform their job tasks in 
order to minimize their exposure to Cr(VI) and to maximize the 
effectiveness of control measures. For example, if an exhaust hood is 
designed to provide local ventilation and a worker performs a task that 
generates a contaminant away from the exhaust hood, the control measure 
will be of no use. Workers can be informed of proper operating 
procedures through information and training. Good supervision further 
ensures that proper work practices are carried out by workers. By 
persuading a worker to follow proper procedures, such as positioning 
the exhaust hood in the correct location to capture the contaminant, a 
supervisor can do much to minimize unnecessary exposure.
    Employees' exposures can also be controlled by scheduling 
operations with the highest exposures at a time when the fewest 
employees are present. For example, routine clean-up operations that 
involve Cr(VI) releases might be performed at night or at times when 
the usual production staff is not present.
    Respirators are another important, although less preferred, method 
of compliance. However, to be effective, respirators must be 
individually selected; fitted and periodically refitted; 
conscientiously and properly worn; regularly maintained; and replaced 
as necessary. In many workplaces, these conditions for effective 
respirator use are difficult to achieve. The absence of any of these 
conditions can reduce or eliminate the protection the respirator 
provides to some of all of the employees.
    Respirator effectiveness ultimately relies on the good work 
practices of individual employees. In contrast, the effectiveness of 
engineering controls does not rely so routinely on actions of 
individual employees. Engineering and work practice controls are 
capable of reducing or eliminating a hazard from the workplace as a 
whole, while respirators protect only the employees who are wearing 
them correctly. Furthermore, engineering and work practice controls 
permit the employer to evaluate their effectiveness directly through 
air monitoring and other means. It is considerably more difficult to 
directly measure the effectiveness of respirators on a regular basis to 
ensure that employees are not unknowingly being overexposed. OSHA 
therefore considers the use of respirators to be the least satisfactory 
approach to exposure control.
    In addition, use of respirators in the workplace presents other 
safety and health concerns. Respirators can impose substantial 
physiological burdens on employees, including the burden imposed by the 
weight of the respirator; increased breathing resistance during 
operation; limitations on auditory, visual, and odor sensations; and 
isolation from the workplace environment. Job and workplace factors 
such as the level of physical work effort, the use of protective 
clothing, and temperature extremes or high humidity can also impose 
physiological burdens on workers wearing respirators. These stressors 
may interact with respirator use to increase the physiological strain 
experienced by employees.
    Certain medical conditions can compromise an employee's ability to 
tolerate the physiological burdens imposed by respirator use, thereby 
placing the employee wearing the respirator at an increased risk of 
illness, injury, and even death. These medical conditions include 
cardiovascular and respiratory diseases (e.g., a history of high blood 
pressure, angina, heart attack, cardiac arrhythmias, stroke, asthma, 
chronic bronchitis, emphysema), reduced pulmonary function caused by 
other factors (e.g., smoking or prior exposure to respiratory hazards), 
neurological or musculoskeletal disorders (e.g., epilepsy, lower back 
pain), and impaired sensory function (e.g., a perforated ear drum, 
reduced olfactory function). Psychological conditions, such as 
claustrophobia, can also impair the effective use of respirators by 
employees and may also cause, independent of physiological burdens, 
significant elevations in heart rate, blood pressure, and respiratory 
rate that can jeopardize the health of employees who are at high risk 
for cardiopulmonary disease.
    These concerns about the burdens placed on workers by the use of 
respirators were acknowledged in OSHA's revision of its Respiratory 
Protection standard, and are the basis for the requirement that 
employers provide a medical evaluation to determine the employee's 
ability to wear a respirator before the employee is fit tested or 
required to use a respirator in the workplace (63 FR 1152, 1/8/98). 
Although experience in industry shows that most healthy workers do not 
have physiological problems wearing properly chosen and fitted 
respirators, nonetheless common health problems can cause difficulty in 
breathing while an employee is wearing a respirator.
    In addition, safety problems created by respirators that limit 
vision and communication must always be considered. In some difficult 
or dangerous jobs, effective vision or communication is vital. Voice 
transmission through a respirator can be difficult, annoying, and 
fatiguing. In addition, movement of the jaw in speaking can cause 
leakage, thereby reducing the efficiency of the respirator and 
decreasing the protection afforded the employee. Skin irritation can 
result from wearing a respirator in hot, humid conditions. Such 
irritation can cause considerable distress to workers and can cause 
workers to refrain from wearing the respirator, thereby rendering it 
ineffective.
    Because respirators are less reliable than engineering and work 
practice controls and may create additional problems, OSHA believes 
that primary reliance on respirators to protect workers is generally 
inappropriate when feasible engineering and work practice controls are 
available. All OSHA substance-specific health standards have recognized 
and required employers to observe the hierarchy of controls, favoring 
engineering and work practice controls over respirators. Moreover, 
OSHA's enforcement experience with these standards has reinforced the 
importance of this concept in the protection of employee health.
    The Color Pigment Manufacturers Association suggested that supplied 
air respirators provide an acceptable alternative to engineering 
controls in many circumstances (Ex. 38-205, p. 44). The American 
Foundry Society concurred with this opinion (Ex. 43-14). They claimed 
that supplied air hoods do not present the problems and limitations 
associated with the use of other respirators and are more reliable and 
effective than most engineering controls (Tr. 1713-1717, Exs. 38-205; 
43-14). The National Paint and Coatings Association (NPCA) indicated 
that Cr(VI) exposures in paint and coatings manufacturing are sporadic 
and are limited to a small number of processes and a few workers (Ex. 
39-66). NPCA believed these exposures could be effectively controlled 
with modern air purifying or supplied air respirators (Ex. 39-66).
    While OSHA acknowledges that certain types of respirators may 
lessen problems associated with breathing resistance and skin 
discomfort, these respirators may still present safety concerns of 
their own. OSHA does not believe that respirators provide employees 
with a level of protection that is equivalent to engineering controls, 
regardless of the type of respirator used. To summarize: engineering 
and work practice controls are capable of reducing or eliminating a 
hazard from the workplace; respirators only protect the employees who 
are wearing them. In addition, the effectiveness of respiratory 
protection always depends on the actions of employees, while the 
efficacy of engineering controls is generally independent of the 
individual.
    It is well-recognized that certain types of respirators are 
superior to other types of respirators with regard to the level of 
protection offered, or impart other advantages. OSHA is currently 
evaluating the level of protection offered by different types of 
respirators in the Agency's Assigned Protection Factors rulemaking (68 
FR 34036, 6/6/03). However, OSHA believes that engineering controls 
offer more reliable and consistent protection to a greater number of 
workers, and are therefore preferable to any type of respiratory 
protection.
    Collier Shannon Scott, on behalf of various steel industry groups, 
maintained that OSHA should allow use of respiratory protection as a 
primary control to achieve the PEL where respiratory protection is 
currently used to comply with another OSHA standard (Exs. 38-233; 40-
12). Without such an allowance, it was claimed, employers would have to 
add additional controls where employees are already wearing 
respirators, which would impose "significant burden and expense on the 
employer with no attendant benefit to the employee" (Ex. 38-233, p. 
34). If an employer has adopted all feasible engineering controls to 
address other workplace exposures (e.g., lead, cadmium), and no other 
feasible engineering controls are available to limit Cr(VI) exposures, 
the final Cr(VI) rule would not require additional engineering controls 
to meet the new Cr(VI) PEL. On the other hand, if additional feasible 
engineering controls are available that would reduce Cr(VI) exposures 
that exceed the PEL, then these controls would justifiably be required. 
OSHA believes these additional engineering controls would better 
protect employees. As discussed previously, OSHA considers engineering 
controls to be the most effective method of protecting employees and 
allows respiratory protection only where such controls have been found 
infeasible.
    A number of responses to the proposal commented on the possibility 
of including separate engineering control air limits, or SECALs, in the 
final Cr(VI) rule. Several commenters maintained that SECALs were 
unnecessary (Exs. 38-214; 38-220; 39-20). The majority of respondents 
who expressed an opinion on this issue supported the use of SECALs (Tr. 
373, 1701, 1732, Exs. 38-205; 38-215; 38-216; 38-218; 38-231; 39-43; 
47-30). However, it was apparent that these commenters did not have a 
common understanding of the basis for establishing SECALs or their 
application in the workplace.
    SECALs were included in one previous OSHA rule, the Cadmium 
standard for general industry (29 CFR 1910.1027). In that rule, SECALs 
were based on a two tiered approach to controlling worker exposures. As 
described in the preamble to the final rule:

    The first tier would be a PEL, set at the level required by the 
health science data to protect workers' health. The PEL, in the case 
of industries where compliance by means of engineering and work 
practice controls was infeasible, could be achieved by any allowable 
(e.g., not worker rotation) combination of work practice and 
engineering controls and respirators. The second tier would be set 
above the PEL at the lowest feasible level that could be achieved by 
engineering and work practice controls (57 FR 42389, 9/14/92).

Thus, employers in all industries covered by the cadmium standard were 
required to use engineering and work practice controls to the extent 
feasible to achieve the PEL. For specified processes in particular 
industries, SECALs provided explicit recognition of the lowest exposure 
level that could feasibly be achieved with engineering and work 
practice controls. Respirators could then be used as supplementary 
controls to reduce exposures to the PEL.
    While the cadmium standard is the only standard to use the term 
"SECAL" other standards have adopted the same approach. For example, 
although the PEL in the lead standard is set at 50 [mu]g/m\3\ (29 CFR 
1910.1025(c)) the brass and bronze ingot manufacture industry sector is 
only required to achieve a lead in air concentration of 75 [mu]g/m\3\ 
through engineering and work practice controls (29 CFR 1910.1025(e)(1) 
Table I, n.3). As with all industry sectors, brass and bronze ingot 
manufacture must provide respiratory protection to supplement 
engineering and work practice controls if they cannot achieve the PEL. 
Similarly, the asbestos standard exempts certain specified operations 
from meeting the PEL of 0.1 fiber per cubic centimeter of air (0.1 
fiber/cm\3\) through engineering controls, but requires such operations 
to use such controls to get down to 0.5 fiber/cm\3\ or 2.5 fibers/cm\3\ 
for short term exposures and to provide supplemental respiratory 
protection (29 CFR 1910.1001(f)(1)(iii)).
    Public Citizen maintained that SECALs could be used to provide a 
more protective PEL. According to Public Citizen, technological 
feasibility considerations applicable to a relatively small number of 
workers should not form the basis for establishing a PEL. They said 
that if OSHA determines that a lower PEL is not feasible in limited 
applications through use of engineering and work practice controls, the 
Agency should use SECALs to allow for use of respirators in those 
applications (Tr. 721, Ex. 47-23). However, SECALs (or equivalent 
provisions) can only be applied to discrete operations that can
be distinguished from other sources of Cr(VI) exposure. As discussed 
with regard to the PEL in paragraph (c) of this Summary and 
Explanation, this is not the case for most operations involving Cr(VI) 
exposure. Moreover, and also as discussed with regard to paragraph (c), 
the established test for technological feasibility for standards 
requires that the PEL be achieved in most operations with engineering 
and work practice controls.
    On the other hand, a number of commenters supported SECALs in the 
belief that they would lessen the burdens imposed on employers. These 
parties appeared to believe that SECALs would allow them to circumvent 
the hierarchy of controls and use respiratory protection to achieve the 
PEL, even when feasible engineering controls were available. This 
approach was advocated by Elementis Chromium and the Chrome Coalition 
(Exs. 38-216; 38-231).
    As discussed previously, OSHA considers engineering and work 
practice controls to be superior to respiratory protection for 
controlling workplace exposures to Cr(VI). The Agency, therefore, does 
not consider it appropriate to allow regular use of respirators to 
achieve the PEL when feasible engineering and work practice controls 
are available. The scenario envisioned by some commenters, which 
apparently involves a SECAL established at some point higher than the 
lowest level achievable with engineering and work practice controls, 
would therefore compromise worker safety by allowing an inferior method 
of control to substitute for a superior and feasible method.
    OSHA does recognize, however, that an administrative burden can be 
relieved by providing explicit recognition in the final rule of 
operations where the PEL cannot be achieved through use of engineering 
and work practice controls alone. In these instances, absent 
recognition of infeasibility in the standard, the employer would need 
to be able to demonstrate that feasible engineering and work practice 
controls could not achieve the PEL.
    As discussed in Chapter III of the Final Economic Analysis, OSHA 
has determined that during certain painting operations in the aerospace 
industry, the PEL of 5 [mu]g/m\3\ cannot be achieved with engineering 
and work practice controls (Ex. 49). In these operations, the evidence 
indicates that employee exposure to Cr(VI) can feasibly be reduced to 
25 [mu]g/m\3\ using engineering and work practice controls; respiratory 
protection is necessary to supplement these controls to achieve the 
PEL. Accordingly, a provision has been added to the final rule 
recognizing the limitations of engineering and work practice controls 
in controlling Cr(VI) exposures where painting of aircraft or large 
aircraft parts is performed in the aerospace industry. In using the 
term "aircraft or large aircraft parts" OSHA is referring to the 
interior or exterior of whole aircraft, aircraft wings, tail sections, 
wing panels and rocket sections, large aircraft body sections, control 
surfaces such as rudders, elevators, and ailerons, or comparably sized 
aircraft parts. Thus, in these operations employee exposures must be 
reduced to 25 [mu]g/m\3\ or less using engineering and work practice 
controls. Respiratory protection will then need to be used to achieve 
the PEL.
    There may even be some situations where the engineering and work 
practice controls cannot achieve exposures of 25 [mu]g/m\3\. The final 
rule recognizes this and addresses this by permitting the employer to 
demonstrate the infeasibility of achieving 25 [mu]g/m\3\ with these 
controls. In these limited circumstances the employer would be 
permitted to further rely on respirators to protect employees.
    OSHA acknowledges that engineering and work practice controls 
cannot feasibly achieve the PEL in some specific operations. In 
particular, OSHA is aware that the use of engineering and work practice 
controls to comply with the PEL is infeasible for some maintenance and 
repair operations and during emergency situations. These situations are 
recognized in paragraph (g) of the final rule (paragraph (f) for 
construction and shipyards), which addresses use of respiratory 
protection where employers can demonstrate that engineering and work 
practice controls are not feasible. In such situations, the burden of 
proof is appropriately placed on the employer to make and support a 
claim of infeasibility because the employer has better access to 
information specific to the particular operation that is relevant to 
the issue of feasibility.
    An exception to the general requirement for primary reliance on 
engineering and work practice controls is included in the final rule 
for employers who do not have employee exposures above the PEL for 30 
or more days per year (during 12 consecutive months) in a particular 
process or task. Thus, if a particular process or task causes employee 
exposures to Cr(VI) that exceed the PEL on 29 or fewer days during any 
12 consecutive months, the employer is allowed to use any combination 
of controls, including respirators alone, to achieve the PEL. The 
obligation to implement engineering and work practice controls to 
comply with the PEL is not triggered until a process or task causes 
employees to be exposed above the PEL on 30 or more working days during 
a year.
    The employer may use this exception if he or she can demonstrate 
that a process or task will not cause employee exposures above the PEL 
for 30 or more days per year (12 consecutive months). The burden of 
proof is on the employer to show that exposures do not exceed the PEL 
on 30 or more days per year. OSHA believes this provision provides 
needed flexibility to employers, while still providing adequate 
protection for workers.
    Under current exposure conditions, the primary adverse health 
effect addressed by this final rule (i.e., lung cancer) is associated 
with cumulative exposure to Cr(VI). Thus, assuming stable exposure 
levels, the fewer number of days that a worker is exposed, the lower 
the risk incurred. Consequently, some exception based on the number of 
days of exposure is justified.
    OSHA realizes that in some industries (e.g., color pigment 
manufacturing), exposure to Cr(VI) is typically infrequent (i.e., fewer 
than 30 days, over 12 consecutive months). For example, certain Cr(VI) 
processes may occur only several days a year when production of a 
particular product is needed. Under such conditions, it may not be cost 
effective or very beneficial to workers' health for employers to invest 
the monies needed to install engineering controls to control Cr(VI) to 
the PEL. Without this exception, employers would be required to 
implement feasible engineering controls and work practice controls 
wherever employees are exposed to Cr(VI) above the PEL, even if they 
are only exposed on one or several days a year. OSHA believes that the 
expense of implementing engineering controls in such circumstances is 
not reasonable.
    A number of commenters expressed general support for this exception 
(e.g., Tr. 1426-1427, 1730; Exs.