[Federal Register: October 4, 2004 (Volume 69, Number 191)]
[Proposed Rules]
[Page 59305-59474]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr04oc04-28]
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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, 1917, 1918, and 1926
Occupational Exposure to Hexavalent Chromium; Proposed 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: Proposed rule; request for comments and scheduling of informal
public hearings.
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SUMMARY: The Occupational Safety and Health Administration (OSHA)
proposes to amend its existing standard for employee exposure to
hexavalent chromium (Cr(VI)). The basis for issuance of this proposal
is a preliminary determination by the Assistant Secretary that
employees exposed to Cr(VI) face a significant risk to their health at
the current permissible exposure limit and that promulgating this
proposed standard will substantially reduce that risk. The information
gathered so far in this rulemaking indicates that employees exposed to
Cr(VI) well below the current permissible exposure limit are at
increased risk of developing lung cancer. Occupational exposures to
Cr(VI) may also result in asthma, and damage to the nasal epithelia and
skin.
This document proposes an 8-hour time-weighted average permissible
exposure limit of one microgram of Cr(VI) per cubic meter of air (1 mg/
m3) for all Cr(VI) compounds. OSHA also proposes other
ancillary provisions for employee protection such as preferred methods
for controlling exposure, respiratory protection, protective work
clothing and equipment, hygiene areas and practices, medical
surveillance, hazard communication, and recordkeeping. OSHA is
proposing separate regulatory texts for general industry, construction,
and shipyards in order to tailor requirements to the circumstances
found in each of these sectors.
DATES: Written comments. The Agency invites interested persons to
submit written comments regarding the proposed rule, including comments
on the information collection determination described in Section X of
the preamble (OMB Review under the Paperwork Reduction Act of 1995), by
mail, facsimile, or electronically. All comments, whether submitted by
mail, facsimile, or electronically through the Internet, must be sent
by January 3, 2005.
Informal public hearings. The Agency plans to hold an informal
public hearing in Washington, DC, beginning on February 1, 2005. OSHA
expects the hearing to last from 9:30 a.m. to 5:30 p.m.; however, the
exact daily schedule is at the discretion of the presiding
administrative law judge.
Notice of intention to appear to provide testimony at the informal
public hearing. Interested persons who intend to present testimony at
the informal public hearing in Washington, DC, must notify OSHA of
their intention to do so no later than December 3, 2004.
Hearing testimony and documentary evidence. Interested persons who
request more than 10 minutes to present their testimony, or who will be
submitting documentary evidence at the hearing, must provide the Agency
with copies of their full testimony and all documentary evidence they
plan to present by January 3, 2005. See Section XVI below for details
on the format and how to file a notice of intention to appear, submit
documentary evidence at the hearing, and request an appropriate amount
of time to present testimony.
ADDRESSES: Written comments. Interested persons may submit three copies
of written comments to the Docket Office, Docket H054A, Room N-2625,
OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW.,
Washington, DC 20210; telephone (202) 693-2350. If written comments are
10 pages or fewer, they may be faxed to the OSHA Docket Office,
facsimile number (202) 693-1648. Comments may also be submitted
electronically through the Internet at http://ecomments.osha.gov.
Supplemental information such as studies and journal articles cannot be
attached to electronic submissions. Instead, three copies of each
study, article, or other supplemental document must be sent to the OSHA
Docket Office at the address above. These materials must clearly
identify the associated electronic comments to which they will be
attached in the docket by the following information: Name of person
submitting comments; date of comment submission; subject of comments;
and docket number to which comments belong.
Informal public hearings. The informal public hearing to be held in
Washington, DC, will be held in the Frances Perkins Building, U.S.
Department of Labor, 200 Constitution Avenue, NW., Washington, DC
20210.
Notice of intention to appear to provide testimony at the informal
public hearing. Interested persons who intend to present testimony at
the informal public hearing in Washington, DC, may submit three copies
of their notice of intention to appear to the Docket Office, Docket
H054A, Room N-2625, OSHA, U.S. Department of Labor, 200 Constitution
Avenue, NW., Washington, DC 20210. Notices may also be submitted
electronically through the Internet at http://ecomments.osha.gov. OSHA
Docket Office and Department of Labor hours of operation are 8:15 a.m.
to 4:45 p.m.
Hearing testimony and documentary evidence. Interested persons who
request more than 10 minutes in which to present their testimony, or
who will be submitting documentary evidence at the informal public
hearing must submit three copies of the testimony and the documentary
evidence to the Docket Office, Docket H054A, Room N-2625, OSHA, U.S.
Department of Labor, 200 Constitution Avenue, NW., Washington, DC
20210. Written testimony may also be submitted electronically through
the Internet at http://ecomments.osha.gov.
Please note that security-related problems may result in
significant delays in receiving comments and other materials by regular
mail. Telephone the OSHA Docket Office at (202) 693-2350 for
information regarding security procedures concerning delivery of
materials by express delivery, hand delivery, and messenger service.
All comments and submissions will be available for inspection and
copying in the OSHA Docket Office at the address above. Most comments
and submissions will be posted on OSHA's Web page (http://www.osha.gov
). Contact the OSHA Docket Office at (202) 693-2350 for
information about materials not available on the OSHA Web page and for
assistance in using this Web page to locate docket submissions. Because
comments sent to the docket or to OSHA's Web page are available for
public inspection, the Agency cautions interested parties against
including in these comments personal information such as social
security numbers and birth dates.
FOR FURTHER INFORMATION CONTACT: For general information and press
inquiries, contact Mr. George Shaw, Office of Communications, Room N-
3647, OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW.,
Washington, DC 20210; telephone (202) 693-1999. For technical
inquiries, contact Ms. Amanda Edens, Directorate of Standards and
Guidance, Room N-3718, OSHA, U.S. Department of Labor, 200 Constitution
Avenue, NW., Washington, DC 20210; telephone (202) 693-2093 or
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fax (202) 693-1678. For hearing information contact Ms. Veneta Chatmon,
Office of Communications, Room N-3647, OSHA, U.S. Department of Labor,
200 Constitution Avenue, NW., Washington, DC 20210; telephone (202)
693-1999.
SUPPLEMENTARY INFORMATION: For additional copies of this Federal
Register document, contact the Office of Publications, Room N-3101,
OSHA, U.S. Department of Labor, 200 Constitution Avenue, NW.,
Washington, DC 20210; telephone (202) 693-1888. Electronic copies of
this Federal Register, as well as news releases and other relevant
documents, are available at OSHA's Home page at http://www.osha.gov.
I. General
The preamble to the proposed standard on occupational exposure to
chromium (VI) discusses events leading to the proposal, health effects
of exposure, the degree and significance of the risk presented, a
summary of the analysis of technological and economic feasibility,
regulatory impact, and regulatory flexibility, and the rationale behind
the specific provisions set forth in the proposed standard. The
discussion follows this outline:
I. General
II. Issues
III. Pertinent Legal Authority
IV. Events Leading to the Proposed Standards
V. Chemical Properties and Industrial Uses
VI. Health Effects
VII. Preliminary Quantitative Risk Assessment
VIII. Significance of Risk
IX. Summary of the Preliminary Economic Analysis and Initial
Regulatory Flexibility Analysis
X. OMB Review under the Paperwork Reduction Act of 1995
XI. Federalism
XII. State Plans
XIII. Unfunded Mandates
XIV. Protecting Children from Environmental Health and Safety Risks
XV. Environmental Impacts
XVI. Public Participation--Notice of Hearing
XVII. Summary and Explanation of the Standards
XVIII. Authority and Signature
XIX. Proposed Standards
II. Issues
OSHA requests comment on all relevant issues, including health
effects, risk assessment, significance of risk determination,
technological and economic feasibility, and the provisions of the
proposed regulatory text. OSHA is especially interested in responses,
supported by evidence and reasons, to the following questions:
Health Effects
1. OSHA has described a variety of studies addressing the major
adverse health effects that have been associated with exposure to
Cr(VI). Has OSHA adequately identified and documented all critical
health impairments associated with occupational exposure to Cr(VI)? Are
there any additional studies or other data that would controvert the
information discussed or significantly enhance the determination of
material health impairment or the assessment of exposure-response
relationships? Submit any relevant information, and explain your
reasoning for recommending the inclusion of any studies you suggest.
2. Using currently available epidemiologic and experimental
studies, OSHA has made a preliminary determination that all Cr(VI)
compounds (e.g., water soluble, insoluble and slightly soluble) possess
carcinogenic potential and thus present a lung cancer risk to exposed
workers. Is this determination correct? Are there additional data OSHA
should consider in evaluating the carcinogenicity or relative
carcinogenic potencies of different Cr(VI) compounds?
Risk Assessment
3. In its preliminary assessment of risk, OSHA has relied primarily
on two epidemiologic cohort studies of chromate production workers to
estimate the lung cancer risk to workers exposed to Cr(VI) (Exs. 31-22-
11; 33-10). Are there any other studies that you believe are better
suited to estimating the risk to exposed workers; if so, please provide
the studies and explain why you believe they are better.
4. OSHA is aware of two cohorts (i.e., Alexander cohort, Ex. 31-16-
3, and Pastides cohort, Ex. 35-279) in which a sizable number of
workers were probably exposed to low Cr(VI) air levels (e.g., < 10
[mu]g/m3) more consistent with concentrations found in the
workplace today. However, OSHA believes the period of follow-up
observation (median < 10 yr), the young age (< 45 yr at end of follow-up)
and the low number of observed lung cancers (< =15 lung cancers)
severely limits these cohorts as primary data sets for quantitative
risk analysis. Other limitations to the Alexander study include a lack
of data on workers who were employed between 1940 and 1974, but whose
employment ended prior to 1974, and on exposures prior to 1974. Are
there updated analyses available for the Alexander and Pastides
cohorts? How many years do these cohorts need to be followed and how
many lung cancers need to be observed in order for these data sets to
provide insight into the shape of the exposure-response curve at lower
levels of Cr(VI) exposure (e.g., 0.5 to 5 [mu]g/m3)? In the
case of the Alexander cohort, is there additional information on cohort
members' exposures prior to 1974 or workers who left prior to 1974 that
could improve the analysis? Are there other cohorts available to look
at low exposures?
5. OSHA has relied upon a linear relative risk model and cumulative
Cr(VI) exposure for estimating the lifetime occupational lung cancer
risk among Cr(VI)-exposed workers. In particular, OSHA has made a
preliminary determination that a threshold model is not appropriate for
estimating the lung cancer risk associated with Cr(VI). However, there
is some evidence that pathways (e.g., extracellular reduction, DNA
repair, cell apoptosis, etc.) may exist within the lung that protect
against Cr(VI)-induced respiratory carcinogenesis, and may potentially
introduce non-linearities into the Cr(VI) exposure-cancer response. Is
there convincing scientific evidence of a non-linear exposure-response
relationship in the range of occupational exposures of interest to
OSHA? If so, are there sufficient data to define a non-linear approach
that would provide more reliable predictions of risk than the linear
relative risk model used by OSHA?
6. OSHA's estimates of lung cancer risk are based on workers
primarily exposed to highly water-soluble sodium chromate and sodium
dichromate. OSHA has preliminarily concluded that the risk for workers
exposed to equivalent levels of other Cr(VI) compounds will be of a
similar magnitude or, in the case of some Cr(VI) compounds, possibly
greater than the risks projected in the OSHA quantitative risk
assessment. Is this determination appropriate? Are there sufficient
data to reliably quantify the risk from occupational exposure to
specific Cr(VI) compounds? If so, explain how the risk could be
estimated.
7. The preliminary quantitative risk assessment relies on two (Gibb
and Luippold) cohort studies in which most workers were exposed higher
Cr(VI) levels than the PEL proposed by OSHA, for shorter durations than
a working lifetime exposure. The risks estimated by OSHA for lifetime
exposure to the proposed PEL, therefore, carry the assumption that a
cumulative exposure achieved by short duration exposure to higher
Cr(VI) air levels (e.g., exposed 3 years to 15 [mu]g/m3)
leads to the same risk as an equivalent cumulative exposure achieved by
longer duration exposure to
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lower Cr(VI) exposure (e.g, exposed 45 years to 1 [mu]g/m3).
OSHA preliminarily finds this assumed exposure equivalency to represent
an uncertainty in the estimates of risk but does not have information
that indicates this uncertainty introduces serious error in its
predictions of risk. Does the OSHA exposure-response assessment based
on the higher Cr(VI) air levels and/or shorter durations experienced by
the Gibb and Luippold cohorts lead to a serious underprediction or
overprediction in estimated risks for the occupational exposure
scenarios of interest to OSHA? Please provide any data to support your
rationale.
8. OSHA has made a preliminary determination that suitable data are
not available for making quantitative risk estimates for the non-cancer
adverse health effects associated with exposure to Cr(VI) (e.g., nasal
septum ulcerations and perforations, asthma, irritant and allergic
contact dermatitis). Are there suitable data for a quantitative
estimation of risk for non-cancer adverse effects that OSHA should
include in its final quantitative risk assessment? If so, what models
or approaches should be used?
9. Are there other factors OSHA should take into consideration in
its final quantitative risk assessment to better characterize the risks
associated with exposure to Cr(VI)?
Technologic and Economic Feasibility
10. In its Preliminary Economic Analysis of the proposed standard,
OSHA presents a profile of the affected worker population. In that
profile are estimates of the number of affected workers by application
group and job category and the distribution of exposures by job
category. Are there additional data that will enable the Agency to
refine its profile of the worker population exposed to Cr(VI)? If so,
how should OSHA use these data in making such revisions?
11. What are the job categories in which employees are potentially
exposed to Cr(VI) in your company or industry? For each job category,
provide a brief description of the operation and describe the job
activities that may lead to Cr(VI) exposure. How many employees are
exposed, or have the potential for exposure, to Cr(VI) in each job
category in your company or industry? What are the frequency, duration
and levels of exposures to Cr(VI) at each job category in your company
or industry? Where commenters are able to provide exposure data, OSHA
requests that, where possible, exposure data be personal samples with
clear descriptions of the length of the sample and analytical method.
Exposure data that provide information concerning the controls in place
are more valuable than exposure data without such information.
12. Have there been technological changes within your industry that
have influenced the magnitude, frequency, or duration of exposure to
Cr(VI) or the means by which employers attempt to control exposures?
Describe in detail these technological changes and their effects on
Cr(VI) exposures and methods of control.
13. Has there been a trend within your industry to eliminate Cr(VI)
from production processes, products and services? If so, comments are
requested on the success of substitution efforts. Commenters should
estimate the percentage reduction in Cr(VI), and the extent to which
Cr(VI) is still necessary in their processes within product lines or
production activities. OSHA also requests that commenters describe any
technical, economic or other deterrents to substitution.
14. Does any job category or employee in your workplace have
exposures to Cr(VI) that raw air monitoring data do not adequately
portray due to the short duration, intermittent or non-routine nature,
or other unique characteristics of the exposure? Please explain your
response and indicate peak levels, duration and frequency of exposures
for employees in these job categories.
15. OSHA requests the following information regarding engineering
and work practice controls in your workplace or industry:
a. Describe the operations in which the proposed PEL is being
achieved most of the time by means of engineering and work practice
controls.
b. What engineering and work practice controls have been
implemented in these operations?
c. For all operations in facilities where Cr(VI) is used, what
engineering and work practice controls have been implemented? If you
have installed engineering controls or adopted work practices to reduce
exposure to Cr(VI), describe the exposure reduction achieved and the
cost of these controls. Where current work practices include the use of
regulated areas and hygiene facilities, provide data on the
implementation of these controls, including data on the costs of
installation, operation, and maintenance associated with these
controls.
d. Describe additional engineering and work practice controls which
could be implemented in each operation where exposure levels are
currently above the proposed PEL to further reduce exposure levels.
e. When these additional controls are implemented, to what levels
can exposure be expected to be reduced, or what per cent reduction is
expected to be achieved?
f. What are the costs and amount of time needed to develop, install
and implement these additional controls? Will the added controls affect
productivity?
g. Are there any processes or operations for which it is not
reasonably possible to implement engineering and work practice controls
within two years to achieve the proposed PEL? If so, would allowing
additional time for employers to implement engineering and work
practice controls make compliance possible? How much additional time
would be necessary?
16. OSHA requests information on whether there are any limited or
unique conditions or job tasks in Cr(VI) manufacture or use where
engineering and work practice controls are not available or are not
capable of reducing exposure levels to or below the proposed PEL most
of the time. Provide data and evidence to support your response.
17. In its Preliminary Economic Analysis, OSHA presents estimated
baseline levels of use of personal protective equipment (PPE) and the
incremental costs associated with the proposed standard. Are OSHA's
estimated compliance rates reasonable? Are OSHA's estimates of PPE
costs, and the assumptions underlying these estimates, consistent with
current industry practice? Comments are solicited on OSHA's analysis of
PPE costs.
18. In its Preliminary Economic Analysis, OSHA presents estimated
baseline levels of communication of Cr(VI)-related hazards and the
incremental costs associated with the additional requirements for
communication in the proposed standard. OSHA requests information on
hazard communication programs addressing Cr(VI) that are currently
being implemented by employers and any necessary additions to those
programs that are anticipated in response to the proposed standard. Are
OSHA's baseline estimates and unit costs for training reasonable and
consistent with current industry practice?
Effects on Small Entities
19. Will difficulties be encountered by small entities when
attempting to comply with requirements of the proposed standard? Can
any of the
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proposal's requirements be deleted or simplified for small entities,
while still protecting the health of employees? Would a longer time
allowed for compliance for small entities make a difference to their
ability to comply, and if so, why? (Information submitted in the SBREFA
process is part of the record and need not be resubmitted).
Economic Impacts and Economic Feasibility
20. OSHA, in its Preliminary Economic Analysis, has estimated, by
application group, compliance costs per affected entity and the likely
impacts on revenues and profits under alternative market scenarios.
OSHA requests that affected employers provide comment on OSHA's
estimate of revenue, profit, and the impacts of costs for their
industry or application group. Are there special circumstances--such as
unique cost factors, foreign competition, or pricing constraints--that
OSHA needs to consider when evaluating economic impacts for particular
application groups? Comments are requested on OSHA's analysis of
economic feasibility in the PEA.
Overlapping and Duplicative Regulations
21. Do any federal regulations duplicate, overlap, or conflict with
the proposed Cr(VI) standard?
22. In some facilities, adjustments in ventilation systems to
comply with the proposed PEL may require additional time and expense to
retest these systems to ensure compliance with EPA requirements or
state requirements. OSHA requests information and comment indicating
how frequently retesting would be required, and the time and costs
involved in such retesting.
Environmental Impacts
23. Submit any data, information, or comments pertaining to
possible environmental impacts of adopting this proposal, such as the
following:
a. Any positive or negative environmental effects that could
result;
b. Any irreversible commitments of natural resources which could be
involved; and
c. Estimates of the effect of the proposed standard on the levels
of Cr(VI) in the environment.
In particular, consideration should be given to the potential
direct or indirect impacts of the proposal on water and air pollution,
energy use, solid waste disposal, or land use.
d. Some small entity representatives noted that OSHA PELs are
sometimes used to set ``fence line'' standards for air pollutants. OSHA
is unable to find evidence of states formally using this procedure,
though some states may use such a procedure informally. Do any states
or other air pollution authorities base standards on OSHA PELs? What
effects might this have on the environment and on environmental
compliance?
Provisions of the Standard
24. OSHA's safety and health advisory committees for Construction
and Maritime advised the Agency to take into consideration the unique
nature of their work environments by either settings separate standards
or making accommodations for the differences in work environments in
construction and maritime. To account for differences in the workplace
environment for these different sectors OSHA has proposed separate
standards for general industry, construction, and shipyards. Is this
approach appropriate? What other approaches should the Agency consider?
Please provide a rationale for your response.
25. OSHA has not proposed to cover agriculture, because the Agency
is not aware of significant exposures to Cr(VI) in agriculture. Is this
determination correct?
26. OSHA has proposed to regulate exposures to all Cr(VI)
compounds. As discussed in the health effects section of this preamble,
the Agency has made a preliminary determination that the existing data
support coverage of all Cr(VI) compounds in the scope of the proposed
standard. Is this an appropriate determination or are there additional
data that support the exclusion of certain compounds from the scope of
the final standard? If so, describe specifically how these data would
support a decision to exclude certain compounds from the scope of the
final rule.
27. OSHA has made a preliminary determination to exclude Cr(VI)
exposures due to work with portland cement from the scope of the
construction standard. OSHA believes that guidance efforts by the
Agency may be more suitable for addressing the dermal hazards
associated with portland cement use in construction settings. OSHA's
Advisory Committee for Construction Safety and Health (ACCSH) advised
OSHA to include construction cement work under the proposed standard
because of the known hazards associated with wet cement and the large
number of workers exposed to wet cement in construction work settings.
In particular ACCSH advised OSHA that only certain provisions might be
necessary for workers exposed to wet cement (e.g., protective work
clothing, hygiene areas and practices, medical surveillance for signs
and symptoms of adverse health effects only, communication of hazards
and recordkeeping for medical surveillance and training). Other
provisions, ACCSH advised, might not be necessary (e.g., permissible
exposure levels, exposure assessment, methods of compliance and
respiratory protection). Should OSHA expand the scope of the
construction proposal to include Cr(VI) exposures from portland cement?
If so, what would be the best approach for addressing the dermal
hazards from Cr(VI) faced by these workers? If Cr(VI) exposure from
portland cement work in construction is included in the final standard,
should only certain provisions such as those outlined by ACCSH be
considered?
28. OSHA has proposed to include exposure to Cr(VI) from portland
cement in the scope of the standard for general industry. The Agency
believes that the potential for airborne exposure to Cr(VI) in general
industry due to work with portland cement, as indicated by the profile
of exposed workers presented in Table IX-2 of this preamble, is higher
than in the construction industry. OSHA acknowledges, however, that the
exposure profile indicates that no workers are exposed to Cr(VI) at
levels over the proposed action level. Given the low level of airborne
exposure among cement workers in general industry, should OSHA exclude
exposures to Cr(VI) from portland cement from the scope of the general
industry standard? OSHA seeks data to help inform this issue, and
solicits comments on particular provisions of the general industry and
construction standards that may or may not be appropriate for cement
workers.
29. OSHA has proposed to exempt from coverage Cr(VI) exposures
occurring in the application of pesticides in general industry (such as
the treatment of wood with chromium copper arsenate (CCA)) because
pesticide application is regulated by EPA, and section 4(b)(1) of the
OSH Act precludes OSHA from regulating where other Federal agencies
exercise their statutory authority to do so. OSHA has proposed to cover
exposures resulting from use of treated materials. Is this approach
appropriate? Are there any instances where EPA-regulated pesticide
application occurs in construction or shipyard workplaces?
30. Describe any additional industries, processes, or applications
that should be exempted from the Cr(VI) standard and provide detailed
reasons for any requested exemption. In
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particular, are the epidemiologic and experimental studies sufficient
to support OSHA's the inclusion of various industries or processes
under the scope of the proposed standard? Please provide the rationale
and supporting data for your response.
31. Can the proposed Cr(VI) standard for the construction industry
be modified in any way to better account for the workplace conditions
in that industry, while still providing appropriate protection to
Cr(VI)-exposed workers in that industry? Would an alternative approach
similar to that used in OSHA's asbestos standard, where the application
of specified controls in certain situations would be considered
adequate to meet the requirements of the standard, be useful? Is there
enough information available to define such technology specifications?
32. Can the proposed Cr(VI) standard for shipyards be modified in
any way to better account for the workplace conditions in that
industry, while still providing appropriate protection to Cr(VI)-
exposed workers in that industry?
33. OSHA has proposed a TWA PEL for Cr(VI) of 1.0 [mu]g/
m3. The Agency has made a preliminary determination that
this is the lowest level that is both technologically and economically
feasible and is necessary to reduce significant risks of material
health impairment from exposure to Cr(VI). Is this PEL appropriate and
is it adequately supported by the existing data? If not, what PEL would
be more appropriate or would more adequately protect employees from
Cr(VI)-associated health risks? Provide evidence to support your
response.
34. Should different PELs be established for different Cr(VI)
compounds? If so, how should they be established? Where possible,
provide specific detail about how different PELs could be established
and how the Agency should apply those PELs in instances where workers
may be exposed to more than one Cr(VI) compound.
35. OSHA has proposed an action level for Cr(VI) exposure in
general industry, but not in construction or shipyards. Is this an
appropriate approach? Should OSHA set an action level for exposure to
Cr(VI) in construction and shipyards? Should the proposed action level
in general industry be retained in the final rule?
36. If an action level is included in the final rule, is the
proposed action level for general industry (0.5 [mu]g/m3)
the appropriate level for the PEL under consideration? If not, at what
level should the action level be set?
37. If an action level is included in the final rule, which
provisions should be triggered by exposure above the action level?
Indicate the basis for your position and include any supporting
information.
38. If no action level is included in the final rule, which
provisions should apply to all Cr(VI)-exposed workers? Which provisions
should be triggered by the PEL? Are there any other appropriate
triggers for the requirements of the standard?
39. Should OSHA set a short-term exposure limit (STEL) or ceiling
for exposure to Cr(VI)? If so, please specify the appropriate air
concentration and the rationale for its selection.
40. Do you conduct initial air monitoring or do you rely on
objective data to determine Cr(VI) exposures? Describe any other
approaches you have implemented for assessing an employee's initial
exposure to Cr(VI).
41. Describe any follow-up or subsequent exposure assessments that
you conduct. How often do you conduct such follow-up or subsequent
exposure assessments? Please comment on OSHA's estimate of baseline
industry practice and the projected costs for initial and periodic
exposure assessment. Are OSHA's estimates consistent with current
industry practice?
42. Do shipyard employers presently measure their employees'
exposure to Cr(VI)? If not, do they use some alternative method of
identifying which employees may be over-exposed to Cr(VI)?
43. OSHA has proposed specific requirements for exposure assessment
in general industry, but has not proposed that these requirements apply
to construction or shipyard employers. Should requirements for exposure
assessment in construction or shipyards be included in the final Cr(VI)
standard? Are there any advantages to requiring construction or
shipyard employers to measure their employees' exposures to Cr(VI)? If
so, would the exposure assessment requirements proposed for general
industry be appropriate? Would construction or shipyard employers
encounter situations where monitoring would be infeasible if they were
required to follow the exposure assessment requirements proposed for
employers in general industry? Indicate the basis for your position and
include any supporting information. What types of exposure assessment
strategies are effective for assessing worker exposures at construction
and shipyard worksites?
44. Should requirements for exposure assessment in general industry
be included in the final Cr(VI) standard, or would the performance-
oriented requirement proposed for construction and shipyards be more
appropriate? Indicate the basis for your position and include any
supporting information.
45. OSHA has proposed that exposure monitoring in general industry
be conducted at least every six months if exposures are above the
action level but below the PEL, and at least every three months if
exposures are at or above the PEL. Are these proposed frequencies
appropriate? If not, what frequency of monitoring would be more
appropriate, and why?
46. OSHA has proposed that regulated areas be established in
general industry wherever an employee's exposure to airborne
concentrations of Cr(VI) is, or can reasonably be expected to be, in
excess of the PEL. OSHA seeks comments on this provision and in
particular:
a. Describe any work settings where establishing regulated areas
could be problematic or infeasible. If establishing regulated areas is
problematic, what approaches might be used to warn employees in such
work settings of high risk areas (i.e., areas where the airborne
concentrations of Cr(VI) exceed the PEL?).
b. Should OSHA add hazards from eye or skin contact as a trigger
for establishing regulated areas? Explain the basis for your position,
and include any supporting information. c. Describe any methods
currently used that have been found to be effective in establishing
regulated areas.
47. OSHA has not proposed requirements for establishment of
regulated areas in construction or shipyards. Should requirements for
regulated areas for construction or shipyards be included in the final
Cr(VI) standard? If so, would the requirements for regulated areas
proposed for general industry be appropriate? Are there any particular
problems in construction or shipyard settings that make regulated areas
problematic or infeasible? If requirements for regulated areas for
construction or shipyards are not included in the final Cr(VI)
standard, should OSHA include requirements for warning signs or other
measures to alert employees of the presence of Cr(VI)? If so, what
practical means could be used to determine where and when such labeling
would be required? What potential difficulties might be encountered by
using such an approach? Indicate the basis for your position and
include any supporting information.
48. Under the proposed standard, employers are required to use
engineering and work practice controls
[[Page 59311]]
to reduce and maintain employee exposure to Cr(VI) to or below the PEL
unless the employer can demonstrate that employees are not exposed
above the PEL for 30 or more days per year, or the employer can
demonstrate that such controls are not feasible. Is this approach
appropriate for Cr(VI)? Indicate the basis for your position and
include any supporting information.
49. In OSHA's Cadmium standard (29 CFR 1010.1027), the Agency
established separate engineering control air limits (SECALs) for
certain processes in selected industries. SECALs were established where
compliance with the PEL by means of engineering and work practice
controls was infeasible. For these industries, a SECAL was established
at the lowest feasible level that could be achieved by engineering and
work practice controls. The PEL was set at a lower level, and could be
achieved by any allowable combination of controls. SECALs thus allowed
OSHA to establish a lower PEL for cadmium than would otherwise have
been possible, given technological feasibility constraints. Should OSHA
establish SECALs for Cr(VI) in any industries or processes? If so, in
what industries or processes, and at what levels? Provide rationale to
support your position.
50. The proposed standard prohibits the use of job rotation for the
sole purpose of lowering employee exposures to Cr(VI). Are there any
circumstances where this practice should be allowed in order to meet
the proposed PEL?
51. OSHA is proposing that employers provide appropriate protective
clothing and equipment when a hazard is present or is likely to be
present from skin or eye contact with Cr(VI). OSHA would expect an
employer to exercise common sense and appropriate expertise to
determine if a hazard is present or likely to be present. Is this
approach appropriate? Are there other approaches that would be better
for characterizing eye and skin contact with Cr(VI)? For example, are
there methods to measure dermal exposure that could be used to
routinely monitor worker exposure to Cr(VI) that OSHA should consider
including in the final standard?
52. For employers whose employees are exposed to Cr(VI), what
approaches do you currently use to assess potential hazards from eye or
skin contact with Cr(VI)? What protective clothing and equipment do you
use to protect employees from eye or skin contact with Cr(VI)? What
does this protective clothing and equipment cost? Who pays for the
protective clothing and equipment?
53. Should OSHA require the use of protective clothing and
equipment for those employees who are exposed to airborne
concentrations of Cr(VI) in excess of the PEL? If so, what type of
protective clothing and equipment might be necessary?
54. OSHA has proposed to require that employers pay for protective
clothing and equipment provided to employees. The Agency seeks comment
on this provision, in particular:
a. Should OSHA refrain from requiring employer payment, and follow
the outcome of the rulemaking addressing employer payment for personal
protective equipment (64 FR 15401 (3/31/99))?
b. Are there circumstances where employers should not be required
to pay for clothing and equipment used to protect employees from Cr(VI)
hazards, such as situations where it is customary for employees to
provide their own protective clothing and equipment (i.e., ``tools of
the trade'')?
c. OSHA realizes that there is frequent turnover in the
construction industry, where employees frequently move from jobsite to
jobsite. This is an important factor because an employer with a high-
turnover workplace would have to buy protective clothing and equipment
for more employees if the protective clothing and equipment could only
be used by one employee. The Agency requests comment on whether this
proposal's requirement for employer payment for protective clothing and
equipment is appropriate in the construction industry. Are there any
alternative approaches that would be responsive to the turnover
situation and would also be protective of construction workers? Are
there any other issues specific to the construction industry that OSHA
should be consider in this rulemaking?
d. At some ports, employees are hired for jobs in shipyards,
longshoring, and marine terminals through a labor pool, and a single
employee may work for five different employers in the same week. How do
these factors affect who is required to pay for protective clothing and
equipment? Are there any other issues specific to shipyards,
longshoring, or marine terminals that OSHA should consider in this
rulemaking?
55. OSHA is proposing that washing facilities capable of removing
Cr(VI) from the skin be provided to affected employees, but does not
propose that showers be required. Should OSHA include requirements to
provide showers to employees exposed to Cr(VI)? If so, under what
circumstances should showers be required? Describe work situations
where showers are either unnecessary for employee protection or that
present obstacles to their implementation and describe any such
obstacles.
56. OSHA has not included housekeeping provisions in the proposed
Cr(VI) standard for construction or shipyards. The Agency has made a
preliminary determination that the housekeeping requirements proposed
for general industry are likely to be difficult to implement in the
construction and shipyard environments. Is this an appropriate
determination? If not, what practicable housekeeping measures can
construction and shipyard employers take to reduce employee exposure to
Cr(VI) at the work site? What housekeeping activities are currently
being performed?
57. Is medical surveillance being provided to Cr(VI)-exposed
employees at your worksite? If so,
a. What exposure levels or other factors trigger medical
surveillance?
b. What tests or evaluations are included in the medical
surveillance program?
c. What benefits have been achieved from the medical surveillance
program?
d. What are the costs of the medical surveillance program? How do
your current costs compare with OSHA's estimated unit costs for the
physical examination and employee time involved in the medical
surveillance program? Please comment on OSHA's baseline assumptions and
cost estimates for medical surveillance.
e. How many employees are included in your medical surveillance
program?
f. In what North American Industry Classification System (NAICS)
code does your workplace fall?
58. OSHA has proposed that medical surveillance be triggered in
general industry in the following circumstances: (1) When exposure to
Cr(VI) is above the PEL for 30 days or more per year; (2) after an
employee experiences signs or symptoms of the adverse health effects
associated with Cr(VI) exposure (e.g., dermatitis, asthma); or (3)
after exposure in an emergency. OSHA seeks comments as to whether or
not these are appropriate triggers for offering medical surveillance
and whether there are additional triggers that should be included.
Should OSHA require that medical surveillance be triggered in general
industry only upon an employee experiencing signs and symptoms of
disease or after exposure in an emergency, as in the construction and
maritime standards? OSHA also solicits comment on the optimal frequency
of medical surveillance.
[[Page 59312]]
59. OSHA has proposed that medical surveillance be triggered in
construction and shipyards in the following circumstances: (1) after an
employee experiences signs or symptoms of the adverse health effects
associated with Cr(VI) exposure (e.g., dermatitis, asthma); or (2)
after exposure in an emergency. Should medical surveillance in
construction or shipyards be triggered by exposure to Cr(VI) above the
PEL for 30 days or more per year, as proposed for general industry?
OSHA seeks comments as to whether or not the proposed triggers are
appropriate for offering medical surveillance and whether there are
additional triggers that should be included.
60. OSHA has not included certain biological tests (e.g., blood or
urine monitoring, skin patch testing for sensitization, expiratory flow
measurements for airway restriction) as a part of the medical
evaluations required to be provided to employees offered medical
surveillance under the proposed standard. OSHA has preliminarily
determined that the general application of these tests is of uncertain
value as an early indicator of potential Cr(VI)-related health effects.
However, the proposed standard does allow for the provision of any
tests (which could include urine or blood tests) that are deemed
necessary by the physician or other licensed health care professional.
Are there any tests (e.g., urine tests, blood tests, skin patch tests,
airway flow measurements, or others) that should be included under the
proposed standard's medical surveillance provisions? If there are any
that should be included, explain the rationale for their inclusion,
including the benefit to worker health they might provide, their
utility and ease of use in an occupational health surveillance program,
and associated costs.
61. OSHA has not included requirements for medical removal
protection (MRP) in the proposed standard. OSHA has made a preliminary
determination that there are few instances where temporary worker
removal and MRP will be useful. The Agency seeks comment as to whether
the final Cr(VI) standard should include provisions for the temporary
removal and extension of MRP benefits to employees with certain Cr(VI)-
related health conditions. In particular, what endpoints should be
considered for temporary removal and for what maximum amount of time
should MRP benefits be extended? OSHA also seeks information on whether
or not MRP is currently being used by employers with Cr(VI)-exposed
workers, and the costs of such programs.
62. OSHA has proposed that employers provide hazard information to
employees in accordance with the Agency's Hazard Communication standard
(29 CFR 1910.1200), and has also proposed additional requirements
regarding signs, labels, and additional training specific to work with
Cr(VI). Should OSHA include these additional requirements in the final
rule, or are the requirements of the Hazard Communication standard
sufficient?
63. OSHA has proposed that bags or containers of laundry
contaminated with Cr(VI) bear warning labels. Will this cause you to
alter your current laundry practices? Are there laundries in your area
that would accept such laundry? Would laundering costs increase? If so,
by how much?
64. OSHA requests comment on the time allowed for compliance with
the provisions of the proposed standard. Is the time proposed
sufficient, or is a longer or shorter phase-in of requirements
appropriate? Identify any industries, processes, or operations that
have special needs for additional time, the additional time required
and the reasons for the request.
65. Some other OSHA health standards have included appendices that
address topics such as the hazards associated with the regulated
substance, health screening considerations, occupational disease
questionnaires, and PLHCP obligations. OSHA has not proposed to include
any appendices with the Cr(VI) rule because the Agency has made a
preliminary determination that such topics would be best addressed with
guidance materials. What would be the advantage of including such
appendices in the final rule? If you believe they should be included,
what information should be included? What would be the disadvantage of
including these appendices in the final rule?
III. 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 to
promulgate and enforce occupational safety and health standards. 29
U.S.C. 655(a)(authorizing summary adoption of existing consensus and
federal standards within two years of Act's enactment),
655(b)(authorizing promulgation of standards pursuant to notice and
comment), 654(b)(requiring employers to comply with OSHA standards).
A safety or health standard is a standard ``which requires
conditions or the adoption of or use of one or more practices, means,
methods, operations or processes, reasonably necessary or appropriate
to provide safe or healthful employment or places of employment 29
U.S.C. 652(8).
A standard is reasonably necessary or appropriate within the
meaning of Section 652(8) if it substantially reduces or eliminates
significant risk, and is economically feasible, technologically
feasible, cost effective, consistent with prior Agency action or
supported by a reasoned justification for departing from prior Agency
actions, supported by substantial evidence, and is better able to
effectuate the Act's purpose than any national consensus standard it
supersedes. See 58 Fed. Reg. 16612-16616 (March 30, 1993).
OSHA has generally considered, at minimum, fatality risk of 1/1000
over a 45-year working lifetime to be a significant health risk. See
the Benzene standard, Industrial Union Dep't v. American Petroleum
Institute, 448 U.S. 607, 646 ((1980); the Asbestos standard,
International Union, UAW v. Pendergrass, 878 F.2d 389, 393 (D.C. Cir.
1989).
A standard is technologically feasible if the protective measures
it requires already exist, can be brought into existence with available
technology, or can be created with technology that can reasonably be
expected to be developed. American Textile Mfrs. Institute v. OSHA, 452
U.S. 490, 513 (1981)(``ATMI'') American Iron and Steel Institute v.
OSHA, 939 F.2d 975, 980 (D.C. Cir. 1991)(``AISI'').
A standard is economically feasible if industry can absorb or pass
on the costs of compliance without threatening its long-term
profitability or competitive structure. See ATMI, 452 U.S. at 530 n.
55; AISI, 939 F. 2d at 980.
A standard is cost effective if the protective measures it requires
are the least costly of the available alternatives that achieve the
same level of protection. ATMI, 453, U.S, at 514 n. 32; International
Union, UAW v. OSHA, 37 F.3d 665, 668 (D.C., Cir 1994)(``LOTO III'').
All standards must be highly protective. See 58 FR 16614-16615;
LOTO III, 37 F. 3d at 669. However, health standards must also meet the
``feasibility mandate'' of Section 6(b)(7) of the Act, 29 U.S.C.
655(b)(5). Section 6(b)(5) requires OSHA to select ``The most
protective standard consistent with feasibility'' that is needed to
reduce significant risk when regulating health standards. ATMI, 452
U.S. at 509.
[[Page 59313]]
Section 6(b)(5) also directs OSHA to base health standard on ``the
best available evidence,'' including research, demonstrations, and
experiments. 29 U.S.C. 655(b)(5). OSHA shall consider ``in addition to
the attainment of the highest degree of health and safety protection *
* * feasibility and experience gained under this and other health and
safety laws.'' Id.
Section 6(b)(7) authorizes OSHA to include among a standard's
requirements labeling, monitoring, medical testing and other
information gathering and transmittal provisions. 29 U.S.C. 655(b)(7).
Finally, whenever practical, standards shall ``be expressed in
terms of objective criteria and of the performance desired.'' Id.
IV. Events Leading to the Proposed Standards
OSHA's present standards for workplace exposure to Cr(VI) were
adopted in 1971, pursuant to section 6(a) of the OSH Act, from a 1943
American National Standards Institute (ANSI) recommendation originally
established to control irritation and damage to nasal tissues (Ex. 20-
3). OSHA's general industry standard set a permissible exposure limit
(PEL) of 1 mg chromium trioxide per 10 m3 air in the
workplace (1 mg/10 m3 CrO3) as a ceiling
concentration, which corresponds to a concentration of 52 [mu]g/
m3 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/
m3 Cr(VI), adopted from the American Conference of
Governmental Industrial Hygienists (ACGIH) 1970 Threshold Limit Value
(TLV) (36 FR 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/m3 for
chromic acid and chromates as Cr2O3 (Ex. 5-37),
and 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/m3, 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 ``There 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, p. 8). 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 (HRG), 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, OSHA was sued by HRG for unreasonable delay in issuing a
Cr(VI) standard. The U.S. Court of Appeals for the Third Court ruled in
OSHA's favor and the Agency continued its data collection and analytic
efforts on Cr(VI) (Ex. 35-208, p. 3). OSHA was sued again in 2002 by
HRG for continued unreasonable delay in issuing a Cr(VI) standard (Ex.
31-24-1). In August 2002, OSHA published a Request for Information on
Cr(VI) to solicit additional information on key issues related to
controlling exposures to Cr(VI)(67 FR 54389 (8/22/02)), and on December
4, 2002 announced its intent to proceed with developing a proposed
standard (Ex. 307). The Court ruled in favor of HRG on December 24,
2002, ordering the Agency to proceed expeditiously with a Cr(VI)
standard (Ex. 35-208). On April 2, 2003 the Court set deadlines of
October 4, 2004 for publication of a proposed standard and January 18,
2006 for publication of a final standard (Ex. 35-306).
OSHA initiated Small Business Regulatory Enforcement Act (SBREFA)
proceedings in 2003, 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).
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 in early 2004. OSHA representatives met with ACCSH in February
2004 and May 2004 to discuss the rulemaking and receive their comments
and recommendations. On February 13, ACCSH recommended that portland
cement should be included
[[Page 59314]]
within the scope of the proposed standard (Ex. 35-308, pp. 288-293) and
that identical PELs should be set for the construction, maritime, and
general industries (Ex. 35-308, pp. 293-297). The Committee recommended
on May 18 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, MACOSH decided to collect and forward additional exposure
monitoring data to OSHA to help the Agency better evaluate exposures to
Cr(VI) in shipyards (Ex. 310, 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. 310, p.
227).
V. 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. They range from very
soluble to insoluble in water. 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 potassium chromate
(lemon yellow crystals), sodium chromate (yellow crystals), and sodium
dichromate (reddish to bright orange crystals). Nickel chromate, lead
chromate oxide, and zinc chromate are completely insoluble in water.
The nickel chromate (black crystals) dissolves in nitric acid and
hydrogen peroxide. Lead chromate oxide is a red crystalline powder. The
zinc chromate (lemon yellow crystals) decomposes in hot water and is
soluble in acids and liquid ammonia. Examples of slightly soluble
Cr(VI) compounds are barium (light yellow), calcium (yellow), lead
(yellow to orange-yellow), and strontium (yellow) chromates, and zinc
chromate hydroxide (yellow). They all exist in solid form as crystals
or powder. Potassium zinc chromate hydroxide (greenish-yellow crystals)
is also slightly soluble in water.
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 (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 IX of this preamble.
VI. Health Effects
The studies of adverse health effects resulting from exposure to
hexavalent chromium (Cr(VI)) in humans and experimental animals are
summarized in the section below. Section VI includes 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. This chapter on health effects will not attempt to
describe every study ever conducted on Cr(VI) toxicity. Instead, only
the most important articles and reviews of studies will be evaluated.
A. Absorption, Distribution, Metabolic Reduction and Elimination
Chromium can exist in a number of valence states from -2 to +6
valence. The most common forms are the elemental metal Cr(0), trivalent
Cr(III), and hexavalent Cr(VI). Chromium exists naturally in the
environment in
[[Page 59315]]
chromite ore as Cr(III). Cr(0) and Cr(VI), as well as Cr(III) are
produced during industrial processes. Cr(VI) is the form considered to
be the greatest health risk. A small amount of Cr(III) is needed for
optimal insulin receptor function in human tissues but much larger
amounts may be harmful. Much less is known about the toxicity of Cr(0),
but it is believed to be converted to Cr(III) in the body and is not
considered to be a serious 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.
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. Schlesinger and
Lippman have shown a high degree of correlation between sites of
greatest particle deposition in the tracheobronchial airways and
increased incidence of bronchial tumors (Ex. 35-102). It is possible to
have a buildup of chromium at certain sites in the bronchial tree that
could create areas of very high chromium concentration. This would
especially be true for occupational environments that are particularly
dusty or contain other irritating aerosols.
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 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 anion
(CrO4)2-enter cells via facilitated diffusion
through non-specific anion channels (similar to phosphate and sulfate
anions). Suzuki et al. have demonstrated that Cr(VI) is rapidly and
extensively transported to the bloodstream in rats (Ex. 35-97). They
exposed rats to 7.3-15.9 mg Cr(VI)/m3 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. Bragt and van Dura
demonstrated that more soluble chromates are absorbed faster than less
soluble chromates (Ex. 35-56). Insoluble chromates are poorly absorbed
and therefore have longer resident time in the lungs. They studied the
kinetics of three Cr(VI) compounds: Sodium chromate, zinc chromate and
lead chromate. They instilled 51chromium-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 51chromium 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 due to irritative properties of the zinc chromate used, as it
caused hemorrhages in the lungs which were macroscopically visible as
early as 24 hours after intratracheal administration.
The studies by Langard et al. and Adachi et al. provide further
evidence of absorption of chromates from the lungs (Exs. 35-93; 189).
Rats exposed to 2.1 mg Cr(VI)/m3 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)/m3
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 that are encapsulated in a
paint matrix may be released in the lungs (Ex. 31-15, p. 2). LaPuma et
al. measured the mass of Cr(VI) released from particles into water
originating from three types of paint particles: solvent-borne expoxy
(25% strontium chromate (SrCrO4)), water-borne expoxy (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 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.
A number of questions remain unanswered regarding encapsulated
Cr(VI) and bioavailability from the lung. There is a lack of detailed
information on the encapsulation process. The efficiency of
encapsulation and whether all of the chromate molecules are
[[Page 59316]]
encapsulated is not known. The stability of the encapsulated product in
physiological and environmental conditions has not been demonstrated.
It would be useful to know if any processes can break the encapsulation
during its use. Finally, the fate of inhaled encapsulated and
unencapsulated Cr(VI) in the respiratory tract as well as the systemic
tissues needs to be more 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. 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)/cm2/hour for a 0.01 molar
solution, 6.4 [mu]g Cr(VI)/cm2/hour for a 0.1 molar
solution, and 10 [mu]g Cr(VI)/cm2/hour for a 0.2 molar
solution.
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 exposed to 51
chromium labeled Cr(VI) compounds (Ex. 35-81). In this study
radiolabeled sodium chromate solution was dermally applied to guinea
pigs and 51Cr was monitored by scintillation counting in
tissues. These studies demonstrate that the absorption of Cr(VI)
compounds can take place through the dermal route. Also, the absorption
of Cr(VI) can be facilitated by organic solvents.
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. 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 51chromium
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). The mechanism by which Cr(VI) is carried
across the intestinal wall and the site of absorption are not known and
may well depend upon the efficiency of defense mechanisms (Mertz, 1969
as cited in Ex. 19-1).
Kuykendall et al. studied the absorption of Cr(VI) in human
volunteers after oral administration of potassium dichromate (Ex. 35-
77). They reported the bioavailability based on 14-day urinary
excretion to be 6.9% (range 1.2-18%) for Cr(VI). Other investigators
have also reported absorption of Cr(VI) compounds after oral
administration (Exs. 35-76; 31-22-13; 35-91).
Studies with 51chromium in animals also indicate that
chromium and its compounds are poorly absorbed from the
gastrointestinal tract after oral exposure. When radioactive sodium
chromate (Cr(VI)) was given orally to rats, the amount of chromium in
the feces was greater than that found when sodium chromate was injected
directly into the small intestine. These results are consistent with
evidence that the gastric environment has a capacity to reduce Cr(VI)
to Cr(III) and therefore decrease the amount of Cr(VI) absorbed from
the GI tract.
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. The binding of chromium
compounds by proteins in the blood has been studied in some detail
(Exs. 5-24; 35-41; 35-52). It was found that intravenously injected
anionic Cr(VI) passes through the membrane of red blood cells and binds
to the globin fraction of hemoglobin. It has been hypothesized that
before Cr(VI) is bound by hemoglobin, it is reduced to Cr(III) by an
enzymatic reaction within red blood cells. Once inside the blood cell,
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). According to Aaseth et
al., the intracellular Cr(VI) reduction 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
[[Page 59317]]
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.
The highest lung level reported was 456 mg/10 g tissue in the first
worker, 178 in the second worker, and 1,920 for the third worker. There
were significant chromium levels in the tissue of the second worker
even though he had not been exposed to chromium for 18 years. 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. The distribution of Cr(VI) compared with Cr(III)
was investigated in guinea pigs after intratracheal instillation of
potassium dichromate or chromium trichloride (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. After chromium trichloride instillation, 69%
of the dose remained in the lungs at 20 minutes, while only 4% was
found in the blood and other tissues, with the remaining 27% cleared
from the lungs and swallowed. The only tissue that contained a
significant amount of chromium two days after instillation of chromium
trichloride was the spleen. After 30 and 60 days, 30 and 12%,
respectively, of the Cr(III) was retained in the lungs, while only 2.6
and 1.6%, respectively, of the Cr(VI) dose was retained in the lungs.
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 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.
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). As
discussed earlier, Cr(VI) is also reduced to Cr(III) in the gastric
environment by the gastric juice (Ex. 35-85) and ascorbate after oral
exposure (Ex. 35-82).
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 0.05-
1.7 mg Cr(III)/m \3\ as chromium sulfate and 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) and 92 days for Cr(III) (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 less 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 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
O'Flaherty developed physiologically-based pharmacokinetic (PBPK)
models 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-
[[Page 59318]]
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. Soluble Cr(VI) compounds enter
the bloodstream more readily than highly insoluble Cr(VI) compounds.
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, Maryland and one in Painesville,
Ohio 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, Ohio 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 consistently elevated lung
cancer mortality reported in these cohorts and the significant upward
trends with duration of employment and cumulative exposure provide some
of the strongest evidence that Cr(VI) be regarded as carcinogenic to
workers. A summary of selected human epidemiologic studies in chromate
production workers is presented in Table VI-1.
[[Page 59319]]
Table VI-1.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
Chromate Production
----------------------------------------------------------------------------------------------------------------
Reference Chromium (VI)
Reference/exhibit number Study population population exposure Lung Cancer Risk
----------------------------------------------------------------------------------------------------------------
Hayes et al. (1979, Ex. 7-14)... 1803 male workers Baltimore City Primarily sodium --O/E of 2.0
Braver et al. (1985, Ex. 7-17).. initially mortality. chromate and (p< 0.01) based on
employed 3 or dichromate 59 lung cancer
more months 1945- production. Avg deaths.
1974 at old and Cr(VI) of 21 to --Increased risk
new Baltimore MD 413 [mu]g/m\3\ with duration of
production and avg duration employment.
facility; follow- 1.6 yr to 13 yr
up through 1977. depending on
subcohort, plant,
and year employed.
Gibb et al. (2000, Ex. 31-22-11) 2357 male workers U.S. mortality.... Primarily sodium --O/E of 1.86
initially chromate and (p< 0.01) based on
employed 1950- dichromate. Mean 71 lung cancer
1974 only at new cumulative Cr(VI) deaths.
Baltimore MD of 0.070 mg/m\3\ - --Significant
production yr and work upward mortality
facility; follow- duration of 3.1 trend with
up through 1992. yr. cumulative Cr(VI)
exposure.
Mancuso (1997, Ex. 23).......... 332 male workers Mortality rate Primarily sodium O/E not calculated
Mancuso (1975, Ex. 7-11)........ employed at directly chromate and but significant
Mancuso and Heuper (1951, Ex. 7- Painesville OH calculated using dichromate increase in age-
13).. facility 1931- the distribution production with adjusted lung
Bourne and Yee (1950, Ex. 7-98). 1937; follow-up of person years some calcium cancer death rate
through 1993. by age group for chromate as a with cumulative
the entire result of using chromium exposure
exposed high lime based on 66
population as the process. Most deaths.
standard. cumulative
soluble Cr(VI)
between 0.25 and
4.0 mg/m\3\ - yr
based on 1949
survey.
Luippold et al. (2003, Ex. 31-18- 492 male workers U.S. and Ohio Primarily sodium --O/E of
4). employed one year Mortality Rates. chromate and 2.41(p< 0.01)
between 1940 and dichromate based on Ohio
1972 at production with rates and 51
Painesville OH minor calcium deaths.
facility; follow- chromate. Mean --Significant
up through 1997. cumulative upward mortality
soluble Cr(VI) of trend with
1.58 mg/m\3\ - yr. cumulative Cr(VI)
exposure
Davies et al. (1991, Ex. 7-99).. 2298 male chromate Cancer mortality Principally sodium --O/E of 1.97
Alderson et al. (1981, Ex. 7- production of England, Wales chromate and (p< 0.01) pre-
22).. workers employed and Scotland and dichromate process change
Bistrup and Case (1956, Ex. 7- for one year unexposed local production with based on 175
20).. between 1950 and workers. some calcium deaths.
1976 at three chromate before --SMR of 1.02 (NS)
different UK switch from high post-process
plants; follow-up lime to no lime change based on
through 1989. process. Avg 14 deaths.
soluble Cr(VI) in --Increased risk
early 1950s from for high exposed
2 to 880 [mu]g/ compared with
m\3\ depending on less exposed.
job.
Korallus et al. (1993, Ex. 7- 1417 chromate Mortality rates Principally sodium --O/E of 2.27
91).. production for North Rhine- chromate and (p< 0.01) pre-
Korallus et al. (1982, Ex. 7- workers employed Westphalia region dichromate process change
26).. for one year of Germany where production with based on 66
between 1948 and plants located. some calcium deaths.
1987 at two chromate before --O/E of 1.25 (NS)
different German switch from high post-process
plants; follow-up lime to no lime change based on 9
through 1988. process. Annual deaths.
mean Cr(VI)
between 6.2 and
38 [mu]g/m\3\
after 1977.
Cr(VI) exposure
not reported
before 1977.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E)
Relative Risk (RR)
Not Statistically Significant (NS)
Odds Ratio (OR)
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-
[[Page 59320]]
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 was abstracted from plant records, but was not
utilized in any analyses since the investigators thought it ``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
[[Page 59321]]
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/m\3\.
The usual exposure to Cr(VI) was estimated to be 218 [mu]g/m\3\ 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 x
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/m\3\ and 7.3 years at an exposure of 218
[mu]g/m\3\. For the long-term workers hired 1950-1959, 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 [mu]g/m\3\-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.
In an attempt 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.
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.
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). 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. SMRs were not adjusted for smoking.
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 mgCrO3/m3-yr; 0.0015-0.0089
mgCrO3/m3-yr; 0.009-0.0769 mgCrO3/
m3-yr; and 0.077-5.25 mgCrO3/m3-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
[[Page 59322]]
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 asking 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 are 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 suggests that Gibb's use of U.S. and Maryland mortality
rates for developing expectations for the SMR analysis was
inappropriate and 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 employee's
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 < 1 year and
for those who worked one year or more. Exponent defined short-term
workers as those who worked a minimum of 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/m3-
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 (<07.2 [mu]g CrO3/m3 or
approximately 3.6 [mu]g/m3 of Cr(VI)). The ``majority'' of
the short-term workers had peak exposures of < 100 [mu]g
CrO3/m3. There were five peak Cr(VI) exposure
levels (<7.2 [mu]g CrO3/m3; 7.2<19.3 [mu]g
CrO3/m3; 19.3<48.0 [mu]g CrO3/
m3; 48.0<105 [mu]g CrO3/m3; 105<182
[mu]g CrO3/m3; and 182<806 [mu]g CrO3/
m3) 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
[[Page 59323]]
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 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 is
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 preamble section VII.C of the preliminary quantitative
risk assessment.
The exposure matrix of Gibb et al. does utilize a unique 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 still 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.
Despite the potential methodological limitations of the Gibb study,
this 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 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/m3-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/m3-
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/m3-years to 6.0+ mg/
m3-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/m3 years. For the
highest exposure to insoluble Cr(III) (6.00+ mg/m3 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/
m3 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/m3 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/m3-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
[[Page 59324]]
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 VII on the preliminary quantitative risk assessment.
[[Page 59325]]
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 1989 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. 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 administered 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 age was 42 years and mean duration of employment was 9.5 years.
Two thirds of the workers had accumulated less than 0.01mg/
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.
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
[[Page 59326]]
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
[[Page 59327]]
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. 35-245). 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).
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
[[Page 59328]]
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.
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, and Luippold 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 declined 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 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). 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. However, it should be
noted 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 lime-free process was probably 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 VI-2.
[[Page 59329]]
Table VI-2.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
Chromate Pigment Production
----------------------------------------------------------------------------------------------------------------
Reference Chromium (VI)
Reference/exhibit No. Study population population exposure Lung cancer risk
----------------------------------------------------------------------------------------------------------------
Langard & Vigander (1983, Ex. 7- 133 Norwegian Cancer incidence Lead and zinc -O/E of 44 for
36). chromium pigment from Norwegian chromates with subcohort of 24
Langard & Vigander (1975, Ex. 7- production Cancer Registry some sodium workers based on
33).. workers employed 1955-1976. dichromate as 6 cancer cases.
between 1948 and starting -5 of 6 cases were
1972; 24 workers material; Cr(VI) exposed primarily
with 3+ years levels between 10 to zinc chromate.
exposure to and 30 [mu]g/m3
chromate dust; 1975-1980. No
follow up through reporting < 1975.
1980.
Davies (1984, Ex. 7-42)......... 1152 British Mortality of Factory A: --O/E of 2.2
Davies (1979, Ex. 7-41)......... chromate pigment England and Wales. chromates--primar (p< 0.05) for high
workers from 3 ily lead; some exposed in
plants with a zinc; minor Factory A 1932-
minimum of 1 year barium Factory B: 1954; 21 deaths.
employment mostly lead and --O/E of 4.4
between 1930- zinc chromates; (p< 0.05) for high
June, 1975; minor strontium. exposed in
follow up through Factory C: lead Factory B 1948-
1981. chromate only No 1967; 11 deaths.
Cr(VI) levels --O/E of 1.1 (NS)
reported. for exposed
Factory C 1946-
1967; 7 deaths.
Hayes et al. (1989, Ex. 7-46)... 1,946 male pigment U.S. Mortality.... -Primarily lead --O/E of 1.2 (NS)
Sheffet et al. (1982, Ex. 7-48). workers from New chromate with for entire cohort
Jersey facility some zinc based on 41
employed for a chromate. deaths.
minimum of one -Cr(VI) levels in --O/E of 1.5
month between later years (p< 0.5) for
1940 and 1969; reported to be workers employed
follow up through >500 [mu]g/m3 for >10 yr based on
March, 1982. exposed workers.. 23 deaths.
--Upward trend
(p< 0.01) with
duration of
exposure.
Equitable Environmental Health 574 male chromate U.S. white male West Virginia: --O/E of 1.30 (NS)
(1983, Ex. 2-D-1). workers from mortality rates. lead chromates. for West Virginia
Equitable Environmental Health three plants Kentucky: plant based on 3
(1976, Ex. 2-D-3). (West Virginia, chromates--mostly deaths.
New Jersey or lead, some zinc, --O/E of 2.16 (NS)
Kentucky) with a minor strontium for Kentucky
minimum of 6 and barium.. plant based on 3
months of --New Jersey; deaths.
exposure to lead mostly lead and --O/E of 2.31
chromate prior to some zinc (p< .05) for New
1974. chromate.. Jersey plant
--Median Cr(VI) in based on 9
1975 reported to deaths.
equal or exceed
52 [mu]g/m3.
Deschamps et al. (1995, 35-234). 294 male pigment Death rates from --Mostly lead --O/E of 3.6
Haguenoer et al. (1981, Ex. 7- workers from northern France. chromate with (p< 0.01) based on
44). French facility some zinc 18 deaths.
employed for a chromate. --Upward trend
minimum of six --Cr(VI) levels in (p< 0.01) with
months between 1981 between 2 duration of
1958 and 1987. and 180 [mu]g/m3. exposure.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E).
Relative Risk (RR).
Not Statistically Significant (NS).
Odds Ratio (OR).
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
[[Page 59330]]
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).
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
[[Page 59331]]
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, New Jersey 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 ex- pectations 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 death 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
[[Page 59332]]
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.
In response to OSHA's August 2002 Request for Information, the
Color Pigment Manufacturers Association suggested that OSHA consider
reviewing the Davies (Ex. 7-43), Cooper [Equitable Environmental
Health, Inc.] (Ex. 2-D-1) and Kano (Ex. 14-1-B) epidemiologic studies
with respect to the health effects of lead chromate color pigments. The
Equitable Environmental Health and the Kano et al. studies each report
three deaths from lung cancer among chromate pigment production
workers. The number of lung cancer deaths is too small to be
meaningful. Even if there were a sufficient number of deaths for
analysis, no quantitative exposure data are provided. In the case of
the Davies study, there were seven lung cancer deaths at the one
manufacturing facility that made only lead chromate pigments. When
analyzed by period (early, 1946-1967) and high/medium and low exposure
category, the numbers are too small in any category to be meaningful.
Studies of lead and zinc chromate pigment worker cohorts that
experienced a greater number of lung cancer deaths (e.g., >10 deaths)
consistently found significant elevations in lung cancer risk,
particularly those workers with the longest latency and durations of
exposure (Exs. 234; 7-46; 7-42).
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 VI-3.
Table VI-3.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
Chromium Plating
----------------------------------------------------------------------------------------------------------------
Reference Chromium (VI)
Reference/exhibit No. Study population population exposure Lung cancer risk
----------------------------------------------------------------------------------------------------------------
Sorahan & Harrington (2000, Ex. 920 male platers --Mortality rates --Chromic acid --O/E of 1.85
35-62). employed in 54 for the general mist with some (p=0.001) based
Royle (1975, Ex. 7-49).......... plants in population of nickel and on 60 deaths and
Yorkshire, UK for England and Wales. cadmium co- general pop.
a minimum of --Age-, sex- exposure. --O/E of 1.39
three months matched --Cr(VI) levels in (p=0.06) based on
between 1969 and comparison group 1970 reported to unexposed
1972; follow up unexposed to range from < 30 comparison group.
through 1997. CR(VI).. [mu]g/m\3\ to --No upward trend
>100 [mu]g/m\3\.. w/duration of
exposure.
Sorahan et al. (1998, Ex. 35- 1,762 platers --Mortality rates --Chromic acid --O/E of 1.6
271). employed for a for the general mist with nickel (p< 0.01) for male
Sorahan et al. (1987, Ex. 7-57). minimum of six population of co-exposure. chrome bath
months between England and Wales. --No reported workers based on
1946 and 1975 Cr(VI) exposure 40 deaths.
from a Midlands, levels.. --O/E of 0.66 (NS)
UK plant; follow for other chrome
up through 1995. workers based on
9 deaths.
--Upward trend
(p< 0.05) with
duration of
chrome bath work.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E).
Relative Risk (RR).
Not Statistically Significant (NS).
Odds Ratio (OR).
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.
[[Page 59333]]
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/m3. The two exceptions were large plants, and in
both the chromic acid levels exceeded 100 [mu]g/m3.
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. Poisson 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) that was not the case for 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
[[Page 59334]]
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. 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/m3 (range of 1-50 [mu]g/m3) as
chromic acid near the baths and 3 [mu]g/m3 (range of 0-12
[mu]g/m3) 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 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. Another limitation was the co-
exposures to other potential lung carcinogens, such as nickel,
asbestos, and cigarette smoke. 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 VI-4.
[[Page 59335]]
Table VI-4.- Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
Stainless Steel Welding
----------------------------------------------------------------------------------------------------------------
Reference Chromium (VI)
Reference/Exhibit No. Study population population exposure Lung cancer risk
----------------------------------------------------------------------------------------------------------------
Moulin (1997, Ex. 35-285)....... Meta analysis of Stainless steel Stainless steel --RR of 1.50
epidemiological welding cohort welders exposed (p< 0.05) for
studies of lung studies: Simonato to higher Cr(VI) stainless steel
cancer risk among et al., 1991; than mild steel welders based on
welders in five Polednak et al., welders. combined 114
categories 1981 case control deaths from five
including studies: Hull et studies
stainless steel al., 1989; Gerin --RR of 1.50
welding and mild et al., 1984; (p< 0.05) for mild
steel welding. Kjuus et al. 1986. steel welders
based on combined
137 deaths from
four studies.
Sjogren et al. (1994, Ex. 7-113) Meta analysis of Stainless steel Cr(VI) exposure RR of 1.94
epidemiological welding cohort was not part of (p< 0.05) for
studies of studies: Moulin the analysis. stainless steel
exposure to et al., 1993; welders based on
stainless steel Sjogren et al., combined 70
welding fumes and 1987 case control deaths from five
lung cancer. studies: studies.
Lauritsen et al.,
1996; Gerin et
al., 1984; Kjuus
et al. 1986.
Simonato et al. (1991, Ex.7-114) Cohort of 11,092 Age and sex Avg cumulative --O/E of 1.23 (NS)
Gerin et al. (1993, Ex. 35-220). male welders from specific Cr(VI) exposures for primarily
135 companies in mortality rates estimated between stainless steel
nine European computed using 0.05 to 1.5 mg/ welders based on
countries. Cohort the WHO mortality m\3\-yr based on 20 deaths.
entrance criteria data bank. job process --Upward trend
varied by country. matrix. (p< 0.05) with
time since first
exposure.
--No trend with
cumulative
exposure
Moulin et al. (1993, Ex. 7-92).. Cohort of 2,721 6,683 unexposed --Primarily manual --O/E of 1.03 (NS)
French male manual workers metal arc welding. for primarily
welders from 13 from 13 factories --Cr(VI) exposures stainless steel
factories with a with a minimum of not recorded. welders based on
minimum of one one year of 2 deaths.
year of employment from --No trend with
employment from 1975 to 1988. exposure
1975 to 1988. duration.
Hansen et al. (1996, Ex. 35-247) Cohort of 10,059 National cancer Cr(VI) exposure --O/E of 2.38 (NS)
male welders and incidence rates not recorded. for stainless
other steel from the Danish steel only
workers from 79 Cancer Registry. welders based on
Danish companies 5 deaths.
employed for a No trend with
minimum of one exposure
year between 1964 duration.
and 1984.
Lauritsen et al. (1996, Ex. 35- Nested case- 439 eligible Cr(VI) exposure --OR of 1.3 (NS)
291). control study of controls who were not recorded. for stainless
94 lung cancer not cases and did steel only
deaths from not have welders.
Hansen study. respiratory --No trend with
disease or exposure
unknown duration.
malignancy as
cause of death.
Sjogren et al. (1987, Ex. 795).. Cohort of 234 male Mortality rates Median Cr level --O/E of 2.5 (NS)
stainless steel for Swedish males. for stainless for
welders and 208 steel welding was stainlesssteel
male railway 57 [mu]g/m\3\ and welders based on
track welders. for gas shielded 5 deaths.
Minimum welding [railway --O/E of 0.3 (NS)
employment was 5 welders] was 5 for railway
years between [mu]g/m\3\ in welders based on
1950 and 1965. Sweden during 1 death.
Follow-up through 1975.
1984.
Kjuus et al. (1986, Ex. 7-72)... A hospital-based 186 controls Cr(VI) exposure --OR of 3.0 (p
case-control admitted to the not recorded. < 0.05, adjusted
study of 176 male same hospitals in for smoking) for
incident lung Norway during stainless steel
cancer cases 1979-1983 and welding based on
admitted to two matched to cases 16 deaths.
hospitals in for age +/-5 --Welding not
Norway during years. significant in
1979-1983. logistic model
with smoking,
asbestos.
Hull, et al. (1989, Ex. 35-243). Case-control study Controls were 74 No direct Cr(VI) --OR of 0.9 (NS)
of 85 lung cancer welders with non- exposure for stainless
cases in white pulmonary measurements steel welding
male welders malignancies. recorded. based on 34
identified cases.
through the LA --OR of 1.3 (NS)
County tumor for manual metal
registry (1972- arc welding on
1987). stainless steel
based on 61
cases.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E)
Relative Risk (RR)
Not Statistically Significant (NS)
Odds Ratio (OR)
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 five
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 five 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;
[[Page 59336]]
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 six 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 only mild steel 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 five
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 [mu]g-years/m\3\ Cr(VI) exposure; the lung
cancer SMR for those in the < 0.5 [mu]g-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 are
167 (>0.5 [mu]g-years/m\3\ Cr(VI) exposure) based upon nine cases and
191 (< 0.5 [mu]g-years/m\3\ Cr(VI) exposure) based upon three cases.
Neither SMR is 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 eight 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/m3 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/m3)
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).
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
[[Page 59337]]
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 had
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. 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. 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.
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
[[Page 59338]]
cohort studies and for all the studies combined.
Three case-control studies (Exs. 243; 7-120; 7-72) and two cohort
studies (Exs. 7-114; 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;
243). For the cohort studies, the risk ratio was 1.49 (O=79; 95% CI:
1.15-1.93) (Exs. 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.
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 VI-5.
Table VI-5.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
Ferrochromium Production
----------------------------------------------------------------------------------------------------------------
Reference Chromium (VI)
Reference/Exhibit No. Study population population exposure Lung cancer risk
----------------------------------------------------------------------------------------------------------------
Axelsson et al. (1980, Ex. 7-62) 1932 Swedish males Swedish county ``Recent'' job- --O/E of 0.7 (NS)
employed at least mortality and specific Cr(VI) for ferrochromium
one year in a incidence rates. levels estimated workers based on
ferrochromium at 10 to 250 5 cases.
between 1930 to [mu]g/m3. --No trend with
1975. job-specific
Cr(VI).
Langard et al. (1990, Ex. 7-37). 1235 males --Norwegian Cancer Avg total Cr --O/E of 1.5 (NS)
employed at least Registry. exposure was 50 for ferrochromium
one year who --Subcohort of [mu]g/m3 in 1975 workers based on
started working ferrosilicon with 11 to 33% 10 cases.
prior to 1965 in workers at same soluble Cr(VI). --O/E of 0.3 for
a Norway plant not exposed ferrosilicon
ferrochromium to Cr(VI).. workers based on
plant. Follow-up 2 cases.
was through 1985.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E).
Relative Risk (RR).
Not Statistically Significant (NS).
Odds Ratio (OR).
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 VI.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 VI.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
[[Page 59339]]
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 VI-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.
Table VI-6.--Summary of Selected Epidemiologic Studies of Lung Cancer in Workers Exposed to Hexavalent Chromium--
Aircraft Manufacture
----------------------------------------------------------------------------------------------------------------
Reference Chromium (VI)
Reference/Exhibit No. Study population population exposure Lung Cancer risk
----------------------------------------------------------------------------------------------------------------
Alexander et al. (1996, Ex. 31- 2429 aerospace Incidence rates Painters/sanders --O/E of 0.8 (NS)
16-3). workers with a from regional exposed to zinc for aerospace
minimum six cancer strontium and cohort based on
months employment surveillance lead chromates. 15 deaths.
in Washington system registry. Platers/tank --No clear trend
State from 1974 tenders exposed with chromate
to 1994. Median primarily to exposure.
age at end of chromic acid
study was 42 Median cumulative
years with median chromate exposure
9 years follow-up. between 0.01 and
0.18 mg/m\3\-yr
based on 1974 to
1994 data..
Boice et al. (1999, Ex. 31-16-4) 77,965 workers Mortality rates 8 percent of --O/E of 1.02 (NS)
employed for for white cohort had for workers with
minimum of one population of potential for routine Cr(VI)
year in California and routine Cr(VI) exposures based
California for non-white exposure as on 87 deaths.
aircraft U.S. population. painters and --Upward trend
manufacturing platers. (NS) with
plant on or after No Cr(VI) exposure duration of
1960. Follow-up levels reported.. exposure.
through 1996. --O/E of 0.71
(p< 0.05) for non-
factory workers.
----------------------------------------------------------------------------------------------------------------
Observed/Expected (O/E)
Relative Risk (RR)
Not Statistically Significant (NS)
Odds Ratio (OR)
[[Page 59340]]
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/m3 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. The cohort
was followed for a relatively short 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. Estimates of chromate
exposure were not provided in the study.
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: 0.82-1.26). 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: 0.75-
1.57) 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: 0.80-1.51). For those who worked as a process operator or
plater the SMR for lung cancer was 103 based upon 38 deaths (95% CI:
0.73-1.41).
OSHA believes the Alexander (Ex. 31-16-3) and the Boice et al. (Ex.
31-16-4) studies have several limitations. The Alexander cohort is
small and lacks smoking data. In addition, the study's authors cite the
relatively young age of the population. Considering these three
factors, the authors note, ``limits 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
well conducted study of workers in the aircraft manufacturing industry,
but lacks information on Cr(VI) exposure (Ex. 31-16-4).
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 was 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.
[[Page 59341]]
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) and
by ATSDR in their toxicological profile for chromium (Ex. 35-41). OSHA
reviewed
[[Page 59342]]
the critical studies from both the IARC Monograph and the ATSDR
toxicological profile on chromium and conducted its own literature
search to update and supplement the review.
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 (i.e., compounds that are considered highly
soluble in water, followed by those considered slightly soluble in
water, and then those considered insoluble in water) since it has been
suggested that solubility may be an important factor in determining the
carcinogenic potency of Cr(VI) compounds (Ex 35-47). Solubility
characteristics described in this section are based on those cited in
the IARC Monograph (as cited in Ex. 35-43, pages 56-59).
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 VI-7.
Table VI-7.--Summary of Selected Carcinogenicity Studies in Experimental Animals Administered Hexavalent Chromium--Highly Water Soluble Chromates
--------------------------------------------------------------------------------------------------------------------------------------------------------
Sex/species/strain Dose administered \1\
Compound Route ( in exposed and observation Tumor incidence Reference/exhibit
groups) periods
--------------------------------------------------------------------------------------------------------------------------------------------------------
Chromic acid (Chromium trioxide)... Inhalation............ Female ICR mice (50 3.6 mg Cr(VI)/m3 for --Lung tumors: 7/48 Adachi et al. (1986,
per exposed group. 30 min per day, 2 d/ vs 2/20 for control. Ex. 35-26-1).
wk up to 12 mo. --5 benign adenomas
Histopatholoical and 2
evaluation at adenocarcinomas..
periods up to 18 mo.
Inhalation............ Female C57BL mice (23 1.8 mg Cr(VI)/m3 120 Nasal papilloma: 6/20 Adachi (1987, Ex. 35-
examined at 12 mo; 20 min 2 x week for 12 (< 0.05) at 18 mo; 219).
examined at 18 mo). months; Lung adenoma: 1/20
Histopatholoical (NS) at 18 mo.
evaluation at 12 and
18 mo.
Intrabronchial........ Male/female Porton- 1.0 mg Cr(VI) as Bronchial carcinoma Levy et al. (1986,
Wistar rats (50 per single dose mixed w (M/F combined): 2/ Ex. 11-2).
exposed group). cholesterol in steel 100 (N.S.).
pellet and evaluated
at 2 years.
Sodium dichromate.................. Inhalation............ Male Wistar rats (20 0.025, 0.050 and 0.10 Lung tumors: 0.025 mg/ Glaser et al. (1986,
per exposed group). mg Cr(VI)m3 22-23 hr/ m3--0/18; 0.05 mg/ Ex. 10-11).
day, 7 d/wk for 18 m3--0/018; 0.1 mg/
months; evaluated at m3--3/19(NS).
up to 30 months.
Intrabronchial........ Male/female Porton- 0.8 mg Cr(VI) as a Bronchial carcinoma Levy et al. (1986, 11-
Wistar rats (50 per single dose mixed w (M/F combined): 1/ 2).
exposed group). cholesterol in steel 100 (NS).
pellet and evaluated
at 2 years.
Intratracheal......... Male/female Sprague 5 x weekly: 0.0034, Lung tumors (M/F Steinhoff et al.
Dawley rats (40 per 0.017, 0.086 mg combined)-- 5 x (1986, Ex. 11-7).
exposed group). Cr(VI)/kg bw for 30 weekly: 0/80 in all
mo; 1 x weekly: groups; 1 x weekly:
0.017, 0.086, 0.43 0.017 mg/kg-0/80;
mg Cr(VI)/kg bw for 0.086 mg/kg-1/80;
30 mo. 0.043 mg/kg-14/80
(p< 0.01).
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Doses calculated and recorded as mg of Cr(VI), rather than specific chromate compound, where possible.
Not Statistically Significant--NS
Male/Female M/F.
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)/m3 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. As noted by IARC, a small number of animals (20 per group)
were used in this study. 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.
[[Page 59343]]
In an analysis prepared by Exponent and submitted by the Chrome
Coalition in response to OSHA's RFI, 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/m3) 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 0.05 mg/kg exposure group, 1/80 in 0.25 mg/kg exposure
group and 14/80 in 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. The
authors believe that the results of this study suggest that the dose-
rate for sodium dichromate is a significant factor in its carcinogenic
potency and that limiting occasional high dose exposures may be
critical to reducing the risk of carcinogenicity in humans
occupationally exposed to sodium dichromate.
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. The earlier Levy et al. study did not
report the incidence of squamous metaplasia. 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.
In the Hueper study, 26 rats (sex, age, and strain not specified)
were given intrapleural implantation for 27 months (Ex. 10-4). Dosage
was not specified. No significant increases in tumor incidence were
observed in rats exposed to sodium dichromate or in the control group
(0/26 vs. 0/34 in control).
Chromic acid (Chromium trioxide). In a study by Adachi et al, ICR/
JcI mice were exposed by inhalation to 3.63 mg/m3 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. Statistically significant increases in nasal papillomas
were observed in another study by Adachi et al., in which 43 C57B1 mice
were exposed by inhalation to 1.81 mg/m3 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 rates 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 a treatment with Cr(III)
containing materials. The incidence of squamous metaplasia was not
investigated in the 1986 Levy et al. study.
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).
Potassium chromate. No studies were found that administered this
compound by way of the respiratory tract. Borneff et al. exposed mice
to potassium chromate in drinking water for three generations at a dose
of 9 mg Cr(VI)/kg/day (as cited in ATSDR, Ex. 35-41, Pages 108 and
345). In treated mice, two of 66 females developed forestomach
carcinoma and 10/66 females and 1/35 males developed forestomach
papillomas. The controls also developed forestomach papillomas (2/79
females, 3/47 males), but no carcinomas were observed. The incidence of
forestomach tumors was not statistically significant.
b. Slightly Water Soluble Cr(VI) Compounds. Animal carcinogenicity
studies have been conducted on slightly water soluble calcium chromate
and strontium chromate. The key studies are summarized in Table VI-8.
[[Page 59344]]
Table VI-8: Summary of Selected Carcinogenicity Studies in Experimental Animals Administered Hexavalent Chromium--Slightly Water Soluble Chromates
--------------------------------------------------------------------------------------------------------------------------------------------------------
Sex/species/strain Dose administered \1\
Compound Route ( in exposed and observation Tumor incidence Reference/exhibit
groups) periods
--------------------------------------------------------------------------------------------------------------------------------------------------------
Calcium chromate................... Inhalation............ Male/female C57BL/6 4.3 mg Cr(VI)/m3, 5 Lung adenoma (M/F Nettesheim et al.
mice (136 per group). hr/d, 5d/wk over combined): 14/272 vs (1971, Ex. 10-8).
animal lifetime. 5/272 for controls.
Intrabronchial........ Male/female Porton- 0.67 mg Cr(VI) as a Bronchial carcinoma Levy et al. (1986,
Wistar rats (100 per single dose mixed w (M/F combined): 25/ Ex. 11-2).
group). cholesterol in steel 100 (p< 0.01).
pellet and evaluated
at 2 years.
Intratracheal......... Male/female Sprague 5 x weekly: 0.083 mg Lung tumors (M/F Steinhoff et al.
Dawley rats (40 per Cr(VI)/kg bw for 30 combined)--5 x (1986, Ex. 11-7).
group). mo; 1 x weekly: weekly: 0.083 mg/kg-
0.41.mg Cr(VI)/kg bw 6/80 (p< 0.01); 1 x
for 30 mo. weekly: 0.41 mg/kg-
13/80 (p< 0.01).
Intratracheal......... Male Sprague Dawley 0.67 mg Cr(VI)/kg bw Lung tumors: 1/44 Snyder et al. (1997,
rats (50 per exposed x 13 installations (NS). Ex. 31-18-12).
group). over 20 wks and
evaluated at 2 to
2.5 yr.
Strontium chromates (two different Intrabronchial........ Male/female Porton- 0.48 mg Cr(VI) as a Bronchial carcinoma Levy et al. (1986,
compounds). Wistar rats (50 per single dose mixed w (M/F combined): 43/ Ex. 11-2).
exposed group). cholesterol in steel 99 & 62/99 (p< 0.01).
pellet and evaluated
at 2 years.
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Doses calculated and recorded as mg of Cr(VI), rather than specific chromate compound, where possible.
Not Statistically significant--NS.
Male/Female--M/F.
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/m3 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
(7.975 mg Cr(VI)/kg), and calcium chromate alone group (8.700 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.
In the analysis submitted to OSHA by the Chrome Coalition, Exponent
stated that the ``intratrachael instillation data of Steinhoff et al.
1986 and Snyder et al. 1997 indicates there is a likely threshold for
lung cancer'' (Ex. 31-18-1, page 2). OSHA believes the results of the
Steinhoff et al. 1986 study show that the rate at which Cr(VI) is
administered may be an important determinant for carcinogenic potency
and thus useful for hazard identification purposes. However, in
accordance with the Agency's long standing cancer policy, OSHA believes
it is inappropriate to establish a threshold or ``no effect'' level of
exposure to a carcinogen (see 29 CFR 1990.143). Moreover, the Snyder
1997 study, in particular, used contaminated soil samples and an
irregular dosing protocol, creating additional complexities in relating
the results to workplace inhalation exposures.
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
[[Page 59345]]
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 IARC 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.
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.
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 VI-9.
Table VI-9.--Summary of Selected Carcinogenicity Studies in Experimental Animals Administered Hexavalent Chromium--Water Insoluble Chromates
--------------------------------------------------------------------------------------------------------------------------------------------------------
Sex/species/strain Dose administered \1\
Compound Route ( in exposed and observation Tumor incidence Reference/exhibit
groups) periods
--------------------------------------------------------------------------------------------------------------------------------------------------------
Zinc chromates (three different Intrabronchial........ Male/female Porton- 0.42 to 0.52 mg Bronchial carcinoma Levy et al. (1986,
compounds). Wistar rats (50 per Cr(VI) as a single (M/F combined): 3/61 Ex. 11-2); Levy and
exposed group). dose mixed w (p< 0.05), 5/100 Venitt (1986, Ex. 11-
cholesterol in steel (p< 0.05), 3/100 12).
pellet and evaluated (p=0.07).
at 2 years.
Zinc tetroxychromate............... Intrabronchial........ Male/female Porton- 0.18 mg Cr(VI) as a Bronchial carcinoma Levy et al. (1986,
Wistar rats (50 per single dose mixed w (M/F combined): 1/ Ex. 11-2).
exposed group). cholesterol in steel 100 (NS).
pellet and evaluated
at 2 years.
Lead chromates (seven different Intrabronchial........ Male/female Porton- 0.25 to 0.32 mg Bronchial carcinoma Levy et al. (1986,
compounds). Wistar rats (50 per Cr(VI) as single (M/F combined): 0-1/ Ex. 11-2).
exposed group). dose mixed w 100 (N.S.).
cholesterol in steel
pellet and evaluated
at 2 years.
Lead chromates (three different Subcutaneous.......... Male/female Sprague 1.5 to 4.8 mg Cr(VI) Sarcomas at injection Maltoni et al. (1974,
compounds). Dawley rats (20 per as a single dose in site (M/F combined): Ex. 8-25); Maltoni
exposed group). water and evaluated 26-36/40 vs 0/40 for (1976, Ex. 5-2).
after 2 years. controls.
Lead chromate...................... Intramuscular......... Male/female Fischer 1.29 mg Cr(VI) in Sarcomas at injection Furst et al. (1976,
344 rats (25 per trioctyanoin 1 x mo site (M/F combined): Ex. 10-2).
exposed group). for 9 mo and 31/47 vs 0/44 for
evaluated at up to 2 controls.
yr.
Female NIH-Swiss mice 0.72 mg Cr(VI) in Sarcomas at injection
(25 per exposed trioctyanoin 1 x mo site: 0/22 (NS).
group). for 4 mo and
evaluated at up to 2
yr.
Barium chromate.................... Intrabronchial........ Male/female Porton- 0.37 mg Cr(VI) as a Bronchial carcinoma Levy et al. (1986,
Wistar rats (50 per single dose mixed w (M/F combined): 0/ Ex. 11-2).
exposed group). cholesterol in steel 100 (NS).
pellet and evaluated
at 2 years.
--------------------------------------------------------------------------------------------------------------------------------------------------------
\1\ Doses calculated and recorded as mg of Cr(VI), rather than specific chromate compound, where possible.
Not Statistically significant--NS.
Male/Female--M/F.
Zinc chromate compounds. Animal studies have been conducted to
examine several zinc chromates that range from water insoluble to
slightly water soluble compounds depending on the form and composition.
In separate, but similarly conducted studies, Levy et al. and Levy and
Venitt studied two water-insoluble compounds (zinc chromate--lW and
zinc tetroxychromate) and two slightly water-soluble compounds (zinc
chromate--Norge composition and zinc potassium chromate) (Exs. 11-2;
11-12). Two milligrams of the compounds were administered by
intrabronchial implantation to 100 male and female Porton-Wistar rats.
The slightly water soluble 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 a statistically significant increase in bronchial tumors
in rats receiving water-insoluble zinc chromate--lW (5/100; p=0.04).
The bronchial tumor incidence with slightly water soluble zinc
chromate--Norge (3/100; p= 0.068) and water-insoluble zinc
tetroxychromate (1/100) were not statistically significant when
compared to a control group. Zinc potassium chromate (slightly water
soluble) was administered at doses of 0.42 mg Cr(VI), zinc chromate--
Norge (slightly water soluble) was administered at doses of 0.45 mg
Cr(VI), and zinc tetroxychromate (insoluble in water) was administered
at doses of 0.18 mg Cr(VI). These studies show that insoluble to
slightly water soluble zinc chromate compounds may produce
statistically significant elevated incidences of tumors in rats.
Basic potassium zinc chromate (slightly water soluble) 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
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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.
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 was 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 one alveologenic carcinoma and one
lymphoma observed in each control group.
In response to OSHA's RFI, the Color Pigments Manufacturers
Association (CPMA) stated that the lack of carcinogenic response in two
studies (Levy et al. 1986 and Furst et al. 1976) upon exposure to lead
chromate and lead chromate pigments in animals indicate these Cr(VI)
compounds are not carcinogenic to workers (Ex. 31-15). As described
above, the results of the Levy et al. 1986 study showed little tumor
development (0-1 tumor observed per 100 rats studied in each
experiment) after receiving a single dose of 2 mg of lead chromate or a
lead chromate compound by an intrabronchial implantation procedure in
which the compounds were imbedded in a metal mesh mixed with
cholesterol (Ex. 11-2). The total administered dose of the Levy et al.
study was relatively low at 0.67 mg Cr(VI)/kg when administered only
one time (body weight of the rat was around 0.5 kg). A small, single
total dose (e.g., 1.6 mg Cr(VI)/kg) of sodium dichromate implanted in
the lung also did not result in tumors. However, repeated weekly
intratracheal instillations of a lower dose level (0.43 mg Cr(VI)/kg)
of sodium dichromate over 30 months for a cumulative total dose of
about 56 mg Cr(VI)/kg produced a 17.5 percent lung cancer incidence.
Thus, a greater total dose of lead chromate instilled in the
respiratory tract may also produce a significant tumor incidence. The
lack of tumors in the Levy et al. study may also have resulted from the
inability of water insoluble lead chromate to leach out of the highly
non-polar cholesterol environment and gain entry into target lung
cells. OSHA, therefore, does not believe that the findings of this
study establish that lead chromate and lead chromate pigments are not
carcinogenic. OSHA does not believe the results of the Furst et al.
study show a lack of carcinogenic effect. The study found a 66 percent
tumor incidence at the site of injection after multiple intramuscular
administrations of lead chromate in rats (Ex. 10-2). Although the route
of exposure is not comparable to that found in occupational settings,
the carcinogenic potential of lead chromate is supported by the results
of several studies showing that pigment workers exposed to lead
chromate have significantly elevated lung cancer mortality (see section
V.B.2). Several short-term tests have also linked lead chromate with
genotoxicity and neoplastic transformation (see section VI.B.8).
Barium chromate. In the studies reviewed by IARC, 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
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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), Steinhoff et al. (Ex. 11-7), and Snyder
et al. (Ex. 31-18-12) 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 some zinc chromates showed the highest incidence of lung
tumors, as indicated in the results of the Steinhoff, Snyder, 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). More recent reviews have been done by Singh
et al. in 1998 (Ex. 35-149), ATSDR in 2000 (Ex. 35-41), and K.S. Crump
Group in 2000 (Ex. 35-47).
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. Aqueous 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).
Aqueous 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/cm2) 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).
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
reduction was pseudo-first order (i.e., rate of Cr(VI) reduction
appeared to be proportional to metal concentration rather than
concentration of reductant) with respect to Cr(VI), 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
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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.
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).
The evidence for cell membrane mediated uptake of Cr(VI) is consistent
with the intratracheal and intrabronchial instillation studies in
rodents that show greater carcingenicity with sparingly soluble (e.g.,
calcium chromate) than insoluble chromate (e.g., lead chromate)
particulates and soluble chromates (e.g., sodium chromate) (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.
[[Page 59349]]
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, 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. At this time, it is not clear which types of DNA damage
are the most critical to the carcinogenic process.
Cr(VI) compounds are mutagenic in most 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
insoluble Cr(VI) (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 zinc and 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 mutagenisis, clastogenesis, and neoplastic
transformation. On the other hand, Cr(III) compounds do not easily
cause mutations or chromosomal damage 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-dependant 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 scavangers, 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)
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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. Pritichard 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 aqueous
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insoluble and soluble Cr(VI) can be transported into the cell. In fact,
cell surface interactions with sparingly soluble and some insoluble
chromates likely create a concentrated microenvironment of chromate ion
resulting in higher intracellular levels of Cr(VI) than would occur
from 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. This
genotoxicity is functionally translated into impaired DNA replication,
mutagenesis, and altered gene expression that ultimately lead to
neoplastic transformation.
9. Preliminary Conclusions
OSHA preliminarily concludes that the study data summarized in the
previous sections support the determination that Cr(VI) compounds
should be regarded as carcinogenic to workers. The strongest evidence
comes from the many cohort studies reporting excess lung cancer
mortality in workers exposed to Cr(VI) during production of chromates
and chromate pigments. Additional evidence comes from the less
consistent elevations in lung cancer mortality found in workers exposed
to Cr(VI) in other occupations, increased tumor incidence in
experimental animals treated with Cr(VI), and cellular and molecular
data on mode of action.
Studies of chromate production workers in several countries have
consistently found significantly greater mortality from lung cancer
than expected. In the earliest studies of chromate workers in whom
Cr(VI) exposures were believed to be highest, the risk for respiratory
cancer was between 15 and 29 times expectation (Exs. 7-2; 7-13; 7-1).
Lung cancer risks of this magnitude cannot be explained by potential
confounders and other biases.
Later studies that were able to reconstruct exposure histories in
workers from production plants located in Baltimore, MD and
Painesville, OH found significant trends between lung cancer mortality
and both cumulative exposure to Cr(VI) and duration of employment (Exs.
31-22-11; 33-10). Workers were predominantly exposed to the highly
water soluble sodium chromate and sodium dichromate at these plants,
although probable exposure to other chromates also occurred. Gibb et
al. showed that a significant association between lung cancer and
Cr(VI) was evident, even in models that accounted for smoking (Ex. 31-
22-11). Other studies documented declines in lung cancer mortality
rates with reduced Cr(VI) exposures due to improvements in the
production process (Exs. 7-99; 7-91; 31-18-4). These trends serve to
strengthen the evidence for causal association between Cr(VI) and lung
cancer.
Studies of workers in the chromate pigment production industry also
consistently show significantly elevated lung cancer mortality. These
include cohorts from Norway, Great Britain, U.S., and France. The
workers were principally exposed to zinc and lead chromate pigments,
but the levels of Cr(VI) exposure were not well characterized. Some
studies presented data that suggested excess lung cancer was more
strongly associated with zinc chromate, although workers were exposed
to several chromium pigments (Exs. 7-41; 7-42).
Significantly elevated lung cancer mortality was found in two
British chromium electroplating cohorts (Exs. 35-62; 271). The workers
were exposed to Cr(VI) in the form of chromic acid mist as well as
nickel, another potential lung carcinogen. The association between lung
cancer and Cr(VI) in stainless steel welders and ferrochromium
production workers are confounded by substantial exposures to other
potential carcinogens and Cr(III). However, the generally elevated lung
cancer mortality in these workers supports the stronger evidence from
the soluble chromate and chromate pigment production cohorts.
A number of the epidemiological studies cited above were evaluated
by the IARC in 1990 (Ex. 35-43). IARC found ``sufficient evidence in
humans for the carcinogenicity of chromium [VI] compounds as
encountered in chromate production, chromate pigment production and
chromate plating industries'' (Ex. 35-43, p. 213). IARC gave Cr(VI)
compounds their highest Group 1 classification for agents considered
carcinogenic to humans. The EPA and ACGIH have designated Cr(VI)
compounds as known and confirmed human carcinogens, respectively (Exs.
35-52; 35-207). NIOSH considers Cr(VI) compounds to be potential
occupational carcinogens (Ex. 31-22-22, p. 8).
Experimental animals have generally been administered Cr(VI)
compounds by routes other than inhalation. A number of studies in which
Cr(VI) compounds were directly instilled in the respiratory tract of
rodents produced a significant incidence of lung tumors (Exs. 11-2; 11-
12; 11-7). The findings indicate different tumorigenic potencies among
Cr(VI) compounds. The less water soluble calcium chromate, strontium
chromates, and zinc chromates cause higher numbers of lung tumors at
similar doses than the more water soluble sodium dichromate and chromic
acid. Experimental research suggests that cellular uptake of the water-
insoluble lead chromate is enhanced by the ability to achieve a high
local concentration at the lung cell surface that does not occur during
uptake of soluble chromates (Ex. 35-149). Because of the greater cancer
potency in animal studies, ACGIH has recommended a lower occupational
TLV for insoluble Cr(VI) compounds (10 [mu]g/m\3\) than for water-
soluble Cr(VI) compounds (50 [mu]g/m\3\).
The few available inhalation studies are limited by abbreviated
exposure durations, low exposure levels, or small number of animals per
dose group. These studies report slightly elevated lung tumor incidence
that are not statistically significant (Exs. 10-11; 35-26-1) or
marginally significant (Exs. 10-8; 35-26). Cr(VI) administered to
animals by intramuscular, subcutaneous, and other routes of
administration have consistently produced a high incidence of tumors,
usually near the site of administration.
Evidence from in vitro research shows that Cr(VI) enters the cell
and is rapidly converted to several lower oxidation forms able to bind
to and crosslink DNA. ROS (reactive oxygen species) are produced during
intracellular reduction/oxidation of Cr(VI) that can further damage
DNA. 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.
Therefore, OSHA regards all Cr(VI) compounds as agents able to induce
carcinogenesis through a genotoxic mode of action.
The rate, as well as the magnitude of the Cr(VI) dose, that reaches
the lung has been shown to influence carcinogenic outcome in
experimental animals (Ex. 11-7). Less frequent, but higher dose levels
of Cr(VI) instilled in the tracheas of rats caused greater tumor
incidence than the same total amount of Cr(VI) instilled more
frequently but at lower dose levels. This may result from a
proliferation of neoplastic cells triggered by lung inflammation at the
high Cr(VI) dose levels or from overwhelming any of a number of
molecular pathways that serve to protect against Cr(VI)-induced
respiratory
[[Page 59352]]
carcinogenesis, including extracellular reduction to poorly absorbed
Cr(III), intracellular binding of reactive forms to non-critical
macromolecules, or repair of DNA damage. The existence of dose rate
effects could potentially introduce non-linearities in the Cr(VI)
exposure-cancer response. As discussed in the quantitative risk
assessment section (section VII), OSHA is not aware of reliable data on
which to confidently predict the range of Cr(VI) air levels at which
presumed non-linearities might occur or empirical data that
convincingly establishes the existence of a threshold exposure for
carcinogenicity.
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 work place exposure by
inhalation exposure to Cr(VI) compounds below the current PEL.
It is very clear from the evidence that workers may develop nasal
irritation, nasal septum ulcerations, and nasal septum perforations at
occupational exposures level at or below the current PEL of 52 [mu]g/
m3. However, it is not clear what occupational exposure
levels lead to the development of occupational asthma or bronchitis.
1. Nasal Irritation, Nasal Septum Ulcerations and Nasal Septum
Perforations
Occupational exposure to Cr(VI) can lead to nasal septum
ulcerations and nasal septum perforations. The nasal septum separates
the nostrils and is composed of a thin strip of cartilage with 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 (Ex. 35-1; Ex. 7-3).
If exposure is discontinued, the ulcer progression will stop and a scar
may form. However, if exposure continues, the ulcer may break through
the septum, resulting in a nasal septum perforation 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. It is currently not known precisely what level would trigger
such nasal problems, but, as stated earlier, it is evident that workers
are developing nasal problems at levels at or below the current PEL.
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 and conducted
its own literature search to update and supplement the review. 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, 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, changes in the nasal septum,
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 and at stations close to the
chrome baths to evaluate peak exposures and variations in exposure on
different days over the week. Nineteen office employees were not
exposed to Cr(VI) 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 ulcerations and perforations in a
group of workers exposed at the highest peak exposure levels (ranging
from 20 [mu]g/m\3\/day to peak levels of 46 [mu]g/m\3\/day) to chromic
acid as Cr(VI); 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, seven developed nasal ulcerations. In
addition to nasal ulcerations, 2 of the 7 also had progressed to nasal
perforations. Furthermore, three individuals developed nasal
perforations only, at the same exposure levels. 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). Atrophy, which is a precursor to ulcerations and
perforations, was only observed in occupationally exposed workers 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) daily TWA average levels of 2
[mu]g/m\3\ or higher. The effects were small, not outside the normal
range and transient (recovery after 2 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
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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 the ``administrative area'' (TWA 0.16 < plus-
minus> 0.10 [mu]g/m\3\) of the Cr(VI) electroplating plant. The
duration of sampling was not indicated. The results of the lung
function tests showed significantly lower values among Cr(VI)
electroplaters compared to the other two exposure groups in regards to
vital capacity, forced vital capacity, and forced expiratory volume in
one second.
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,
including providing details on 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
abnormal finding was discovered to have 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 seven cases out of nine of chrome
electroplaters having nasal septum ulcerations (Ex. 9-41). 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 as early as one
month of employment in some workers.
Royle, using questionnaire responses, reported a significant
increase in the prevalence of nasal ulcerations among 997 British
electroplaters exposed to chromic acid with an increasing prevalence
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 was at 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 the
median 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 had
reported nasal perforations. Based on historical data, the authors
believe that the nasal findings are attributed to Cr(VI) exposure.
[[Page 59354]]
Gibb et al. also used a Proportional Hazard Model to evaluate the
relationship between Cr(VI) exposure and 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 model indicated that airborne Cr(VI)
exposure was associated with the occurrence of nasal septum ulceration
(p = 0.0001). The lack of an association of airborne Cr(VI) exposure to
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 believes poor housekeeping and hygiene practices may
have contributed to these health effects as well as Cr(VI) airborne
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 saw a reduction in
the incidence of nasal findings in the later years. They found that
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 observed even in workers
during their first year on the job.
Case reports provide further evidence that airborne exposure to
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 minutes 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, 2 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 hyper responsiveness 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. Many workers develop an asthmatic attack. An attack may be
triggered by particles in the air (Ex. 35-3; Ex. 35-6). It is not clear
what occupational exposure levels of Cr(VI) compounds would lead to 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), even though the studies generally show an increased
prevalence of workers having difficulty breathing and other asthmatic-
related symptoms following inhalation of multiple chemicals. 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 were
among 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 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
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]
[[pp. 59355-59404]] Occupational Exposure to Hexavalent Chromium
[[Continued from page 59354]]
[[Page 59355]]
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 inhaling 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. Inhalation challenge tests given by
physicians using chromium sulfate and nickel salts, in separate
challenges, both resulted in positive reactions. The worker immediately
had difficulty breathing and started wheezing in both challenges. The
forced expiratory volume in 1 second decreased by 22% and the forced
expiratory volume in 1 second/forced vital capacity ratio also
decreased from 74.5% to 60.4%. The author believes the worker's
bronchial asthma was induced from inhaling chromium sulfate and nickel
salts, individually. 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 1 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, the following 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). He 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 bronchial provocation test (with chromium sulfate as the
test agent). This individual developed an immediate reaction upon given
chromium sulfate as the test agent. He experienced wheezing, coughing
and dyspnea. Peak expiratory flow rate decreased by about 20%. His
physician determined that exposure to chromium sulfate was contributing
to his asthma condition. Two 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/m3. 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).
The specific Cr(VI) compound, extent, and frequency that the workers
were exposed to were not 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 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 on
the extent, duration, and amount of specific Cr(VI) compound the
workers were exposed to during the study.
While the evidence for bronchitis is limited, evidence from
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
[[Page 59356]]
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, possibly in response to Cr(VI)--induced damage
to 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 these Cr(VI) dose
levels. At levels of 50 and 100 [mu]g Cr(VI)/m3, the
responses are indicative of inflammatory changes 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, and that inflammation is essential for the induction of
most effects observed following inhalation exposure.
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 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 numerous well documented case reports in the literature
describing occupational asthma specifically triggered by Cr(VI) in
sensitized workers. However, OSHA is not aware of any data from the
literature to determine a Cr(VI) dose in the work place that leads to
the asthmatic condition or to determine how many people may be affected
by such Cr(VI) exposure.
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 current PEL.
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-
[[Page 59357]]
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).
Cement dermatitis can be caused by direct irritation of the skin,
by sensitization to Cr(VI), or both (Ex. 35-317, p. 147). However,
sensitization is considered to be of greater importance than irritation
in causing cement dermatitis (Ex. 35-317, p. 147). Burrows (1983)
combined the results of 16 separate studies to report that, on average,
over 80% of cement dermatitis cases were found to be sensitized to
Cr(VI) (Ex. 35-317, p. 148). 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).
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%.
Both of these results were statistically significant. There was no
significant change in the frequency of skin irritation.
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\ CrO\3\). 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
[[Page 59358]]
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 up 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). Job changes reportedly 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
[[Page 59359]]
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
mimic the occupational experience. 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. Preliminary 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 also considers it likely that
conjunctivitis can result from 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
preliminary 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 current OSHA PEL.
There is some positive evidence that workplace inhalation to Cr(VI)
results in gastritis and gastrointestinal ulcers, especially at high
exposures (generally over OSHA's current 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 current 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 elevations 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). 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
studies reported no changes in renal markers (Exs. 7-27; 35-104) and
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, and 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
[[Page 59360]]
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 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.
VII. Preliminary 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.''
Although the Court in the Cotton Dust case, (American Textile
Manufacturers Institute v. Donovan, 452 U.S. 490 (1981)) rejected the
use of cost-benefit analysis in setting OSHA standards, it reaffirmed
its previous position in the ``benzene'' case 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 VI.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 two recently studied occupational cohorts have the strongest
data sets on which to quantify lung cancer risk from cumulative Cr(VI)
exposure (i.e., air concentration x exposure duration). Using a linear
relative risk model on these data to predict excess lifetime risk, OSHA
preliminarily estimates that the lung cancer risk from a 45 year
occupational exposure to Cr(VI) at an 8-hour TWA at the current PEL of
52 [mu]g/m3 is 106 to 334 excess deaths per 1000.
Quantitative lifetime risk estimates from a working lifetime exposure
at several lower alternative PELs under consideration by the Agency are
also estimated. For example, the projected risk at 0.5 [mu]g/
m3 Cr(VI) is 1.1 to 4.3 per 1000. 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, the key issues that
arise as result of the quantitative risk assessment as well as a
summary describing comments from an expert peer review and the OSHA
response.
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 than
human studies. 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 section VI.B.7.
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 as well characterized. While difficult to quantitate, the data
indicate that the risk of damage to the nasal mucosa would be
significantly reduced by lowering the current PEL, discussed further in
section VIII 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 current PEL (52 [mu]g/
m3). Since
[[Page 59361]]
the non-cancer effects occur at relatively high Cr(VI) air
concentrations, OSHA believes that lowering the PEL to reduce the risk
of developing lung cancer over a working lifetime would also eliminate
or reduce the risk of developing these other health impairments. As
discussed in section VI.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/m3-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.
Evidence of exposure-response relationship was also important.
Two recently studied cohorts of chromate production workers 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.
Four other cohorts had less satisfactory data for quantitative
assessments of lung cancer risk (Exs. 7-11; 23; 7-14; 7-120; 31-16-3).
While the lung cancer response in these cohorts was stratified across
multiple exposure groups, there were limitations to these data that
affected the certainty of the risk projections. The cohorts include
chromate production workers, stainless steel welders, and aerospace
manufacturing workers. Risk estimates from these lesser cohorts were
used to examine the robustness of the more precise estimates from the
Gibb and Luippold cohorts. The strengths and weaknesses of all six
cohorts in terms of their use in exposure-response analysis are
discussed in more detail below. Emphasis has been placed on the
quantitative information available for each cohort.
Three other cohort studies that were used in the past to develop
crude risk estimates from worker exposure to Cr(VI) are not being
relied upon in the present assessment and therefore are not reviewed
below (Exs. 7-37; 7-62; 7-95). In these cohorts, risk estimates were
determined from background lung cancer rates and excess lung cancer
mortality associated with a single, rather than multiple Cr(VI)
exposure levels. There were also a number of other limitations to the
study data that required the use of unsupported assumptions and raised
uncertainties in the risks. The exposure-response data from the three
studies and the resulting assessments are discussed in the 1995 report
from the K.S. Crump Division (Ex. 13-5). OSHA believes the recent
availability of several higher quality cohort studies cited above
eliminates the need to rely on these more problematic cohorts to assess
lung cancer risk from occupational Cr(VI) exposure.
1. Gibb Cohort
The Gibb et al. study was one of the stronger studies for
quantitative risk assessment, especially in terms of cohort size,
historical exposure data, and evidence of exposure-response (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 VII.B.4). The cohort consisted of 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 member. Smoking status at the start of
employment was available for 91% of the cohort members.
A significant advantage of the Gibb data was the sizable amount of
personal and area sampling measurements from a variety of locations and
job titles collected concurrently over the years during which the
cohort members were exposed (from 1950 to 1985, when the plant closed).
Using these concentration estimates as the basis, 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, even with models that accounted for
the smoking data at hire. This included a greater than expected number
of premature lung cancer deaths in some 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 detailed reporting of the cumulative exposure, including mean
values for four categories defined by the quartiles of cumulative
exposure versus age, was another significant advantage. This level of
documentation reduced some of the uncertainty associated with the
estimation of cumulative exposure. Moreover, the cross-classification
of cumulative exposure with age allowed the application of more
elaborate models that consider the effect of age on lung cancer risk.
Since the publication of Gibb et al., the data file containing the
demographic, exposure, and response data for the individual cohort
members was made available (Ex. 295). These data have been used in a
recent reanalysis (see subsection VII.C.1). The advantages of the study
mentioned above are even greater now that the detailed cohort data can
be accessed. Among other things, the exposure groups can be defined in
alternative ways, the effect of considering different reference
populations can be examined, and additional models can be applied in
the dose-response analysis.
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
[[Page 59362]]
who started work between 1940 and 1972 at the same Painesville, Ohio
plant studied earlier by Mancuso (Ex. 33-10) (see subsection VII.B.3).
Mortality status was followed through 1997 for a total of 14,048
person-years and an average length of 30 years. 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 more limited
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).
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 starting in
1940 and, coupled with detailed work histories available for the cohort
members, cumulative exposures were calculated for each person-year of
observation. The cumulative Cr(VI) exposures, which ranged from 0.003
to 23 (meanSD = 1.582.50) mg Cr(VI)/m\3\ - yr,
were generally higher but overlapped those of the Gibb cohort.
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. The data on exposure-response for this
cohort are relatively strong. 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. 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 analyses of this cohort (Exs.
31-18-1; 35-205; 35-58).
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 cohorts consisted of a completely different set 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 presented observed lung cancer deaths and age-adjusted
death rates stratified by age group and cumulative total, soluble and
insoluble chromium exposure groups (Ex. 23). However, the study did not
provide the expected numbers of lung cancers for the exposure
groupings, making it more difficult to apply appropriate risk models to
the data. Approaches that attempt to circumvent this limitation are
discussed in subsection VII.E.1. Mancuso (Ex. 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.
Although a 1995 risk assessment based on data from the 1975 Mancuso
study was prepared for OSHA under contract (Ex. 13-5), it has been
superseded by an updated assessment from the more complete 1997 Mancuso
data (Ex. 33-15). Specific limitations with respect to quantitative
risk estimation from the Mancuso cohort are discussed in section
VII.E.1 on supporting 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 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
considered to have a 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.
Later on, Braver et al. (Ex. 7-17) estimated average cumulative
soluble chromium, (presumed by the authors to be Cr(VI)) exposures for
four subgroups of the Hayes cohort. 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
[[Page 59363]]
cumulative exposure for the subgroups were estimated from the yearly
average Cr(VI) exposure for the entire plant and their 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.
Another weakness is that exposures attributed to many workers (e.g.,
those hired after 1950) were based on chromium measurements during an
earlier period (i.e., 1949-1950).
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, the inability
to measure insoluble forms of Cr(VI) even though soluble Cr(VI)
compounds were primarily produced at the plant, and the likelihood that
samples may have been collected mainly in potential problem areas.
However, the biggest source of uncertainty was the assumption of rather
high Cr(VI) air levels in the newly renovated facility at the Baltimore
site throughout the 1950s based on measurements made 1945 to 1950 in an
older facility, as explained in section VII.E.2.
5. Gerin Cohort
Gerin et al. (Ex. 7-120) developed a job exposure matrix that was
used to quantify 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 for a total of 164,077 person-
years. This resulted in an average of 14.8 person-years of risk for
each member of the cohort. The number 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 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,
considering time and length of employment, type of welding, base metal,
and ventilation status (e.g., confined area, use of local exhaust
ventilation, etc.) to estimate the cumulative Cr(VI) exposure.
Unfortunately, the industrial hygiene data used to develop the
Gerin exposure matrix included measurements in the 1970s from only 8 of
the 135 companies that employed welders in the cohort. Individual work
histories were also 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 specific Cr(VI) air measurements and work practice information for
this cohort raises questions concerning the accuracy of the exposure
estimates.
Gerin et al. reported lung cancer mortality across four cumulative
Cr(VI) exposure categories for two subcohorts of 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. There was no upward trend in lung
cancer with respect to cumulative Cr(VI) exposure for either subcohort.
Because of uncertainties in the exposure estimates, the lack of
exposure-response, and possible confounding co-exposure to nickel, the
Gerin cohort was not considered a featured data set for exposure-
response assessment.
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 averaged a relatively short 8.9 years per
cohort member.
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 each person-year of observation. As further discussed in
section VII.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. The importance of the exposure assignments
to the quantitative assessment of risk is further discussed in section
VII.E.4.
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 above. 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. There was no positive trend in lung cancer
incidence with increasing Cr(VI) exposure. This cohort study was
limited by the relatively young age of the cohort members, the short
follow-up time, and lack of information on smoking. 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, the Alexander cohort was
not considered as strong a data set for quantitative exposure-response
analysis as the Gibb and Luippold cohorts.
7. Studies Selected for the Quantitative Risk Assessment
The epidemiologic database is quite extensive and contains several
studies that have adequate data suitable for quantitative risk
assessment. OSHA considers certain studies to be better suited for
quantitative assessment than others. The Gibb and Luippold cohorts are
considered the preferred sources for quantitative estimation because
they have larger cohort sizes, extensive follow-up periods, fairly well
documented historical Cr(VI) exposure levels, and because analysts have
had access to the individual job histories and associated exposure
matrices.
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 a risk
assessment. Similarly, the Gerin and Alexander cohorts are less
suitable either because of the small size of the cohort, the shorter
follow-up, or limitations with respect to exposure estimation. For
example, the lung cancer status of the Alexander cohort had only been
tracked for an average of nine years. This is in contrast to the Gibb,
Luippold, and Mancuso cohorts that accumulated an average 30 or more
years of observation. 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 twenty years. The
Alexander cohort would need additional 20 years of
[[Page 59364]]
follow-up to achieve the person-years of observation accumulated by the
Gibb cohort of about the same number of workers. The Guerin cohort is
also limited by lack of follow-up, since the lung cancer status of the
stainless steel welders are believed to have only been observed for an
average of about 15 years.
Despite the limitations, the lesser studies each provide
independent estimates of risk, albeit with more uncertainty, that can
be compared to the estimates derived from the preferred data sets. OSHA
believes evaluating consistency in risk among several different worker
cohorts adds to the overall quality of the assessment. 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.
The following sections, describing the quantitative estimates of
risk, start with the preferred Gibb and Luippold cohorts. The risk
estimates from the supporting studies and previous risk assessments are
then discussed. A discussion of remaining issues and uncertainties
follows the quantitative presentation.
C. Quantitative Risk Assessments Based on the Gibb Cohort
Quantitative risk assessments have recently been 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). The Environ analysis relied on a summary of the person-
years of observation and observed and expected lung cancer deaths
broken down by age and cumulative exposure (Ex. 31-22-11, Table V).
These data are presented in Table VII-1. The job exposure matrix was
the basis for the calculation of individual cumulative exposure
estimates for all 2357 members of the cohort. The cumulative exposure
estimates were lagged 5 years (i.e., 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 the dose-response analysis of 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). The cross-classification
of cumulative exposure with age allowed Environ to evaluate models that
considered the effect of age on lung cancer risk. A total of 71,994
person-years summed up from Table V of the Gibb et al. study was
slightly greater than the reported 70,736 cited in their publication
(Ex. 31-22-11, p. 119).
Table VII-1.--Dose-Response Data From Gibb et al. (Ex. 31-22-11): Observed and Expected Number of Lung Cancer
Deaths Grouped by Age and Four Cumulative Cr(VI) Exposure Categories
----------------------------------------------------------------------------------------------------------------
Age
Cumulative Cr(VI) exposure --------------------------------------------------------------
([mu]g/m\3\-years) 20-29 30-39 40-49 50-59 60-69 70-79 80+
----------------------------------------------------------------------------------------------------------------
0-0.77........................ Observed......... 0 1 0 14 8 2 1
Expected......... 0.018 0.39 2.5 7.56 10.79 5 0.88
Person-Years..... 5003 7684 6509 5184 3104 865 163
Mean Exposure.... 0.21 0.21 0.27 0.28 0.26 0.24 0.21
0.78-4.6...................... Observed......... 0 0 2 10 10 4 2
Expected......... 0.001 0.18 1.97 6.09 7.85 3.25 0.44
Person-Years..... 349 3139 4643 3928 2183 558 79
Mean Exposure.... 2.2 2.2 2.2 2.2 2.2 2.0 1.9
4.7-40........................ Observed......... 0 0 3 10 11 4 2
Expected......... 0.002 0.19 1.93 5.7 7.66 3.26 0.38
Person-Years..... 457 3520 4732 3720 2128 559 78
Mean Exposure.... 16 16 16 16 15 15 14
40-2730....................... Observed......... 0 0 8 8 18 3 1
Expected......... 0.001 0.17 1.82 5.63 6.71 2.48 0.18
Person-Years..... 200 2874 4294 3663 1926 423 29
Mean Exposure.... 110 170 210 270 330 410 450
----------------------------------------------------------------------------------------------------------------
A 5-year lag was used in the calculation of the cumulative exposures. The exposure estimates themselves have
been converted from those shown in Gibb et al., Table V, by multiplying by 0.52, to convert from chromate
concentration to hexavalent chromium concentration and by 1000 to convert from mg/m\3\ - years to [mu]g/m\3\-
years
A set of ``externally standardized'' models was applied to the data
in Table VII-1. These are externally standardized because they required
estimates of expected lung cancer deaths from a standard reference
population. The 2002 Environ analysis relied on expected lung cancer
deaths from age-specific Maryland rates, as provided in Gibb et al. The
observed numbers of cancer cases were assumed to have a Poisson
distribution, with expected values corresponding to three different
dose-related models. A Poisson distribution is assumed because it has
been commonly used in statistics to describe the allocation of rare
events that occur during a given time period. Regression techniques are
then used to link explanatory variables (e.g., cumulative exposure) to
responses of interest (e.g., lung cancer deaths).
The set of models used was mathematically described as follows:
E1. Ni = C0 * Ei *
exp{kti{time} * (1 + C1Di +
C2Di\2\)
E2. Ni = C0 * Ei * (1 +
C1Di * exp{kti{time} )
E3. Ni = C0 * Ei + (PYi
* C1Di)
where Ni is the predicted number of lung cancers in i\th\
group PYi is the
[[Page 59365]]
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, C2, and k are parameters
to be estimated. In equations E1 and E2, ti the mean age for
group i.
Models E1 and E2 are relative risk models that differ with respect
to the effect of age. In model E1, the background rates are adjusted
for age whereas in E2 the dose coefficient is modified by the age. On
the other hand, Model E3 is an additive risk model. In the case of
additive risk models, the exposure-related estimate of 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 is always relative to
background.
Estimation of parameters (i.e., C0, C1,
C2, and k) was accomplished by maximum likelihood
techniques. For the externally standardized models, 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 were excluded from consideration.
Goodness-of-fit for each model was evaluated by considering the
deviance, a likelihood-based statistic for which larger p-values
indicate better model fit. In addition, the fits of different models
were compared using the Akaike Information Criterion (AIC) value, a
statistic based on the model's maximized likelihood and the number of
parameters used. For the quadratic model E1, addition of a dose-squared
term did not significantly improve the fit of model to the data (i.e.,
C2 estimated to be zero) relative to a linear model. For
models E1 and E2, the parameter k was not determined to be different
from 0, and thus models E1 and E2 defaulted to the same linear relative
risk model. The deviance-based test of fit suggested an adequate
correspondence between model predictions and the observations (p >=
0.13).
A second set of ``internally standardized'' models, which did not
require estimation of the expected number of lung cancers, was also fit
to the data in Table VII-1 (Ex. 33-15). Model parameters were estimated
by the maximum likelihood procedures described above. The test for
goodness-of-fit indicated that these models did not fit the data well
(p < = 0.01). The formulation and a more detailed description of these
models can be found in the 2002 Environ report (Ex. 33-15).
Lifetable calculations were made of the number of extra lung
cancers per 1000 workers exposed to Cr(VI), assuming a constant
exposure from age 20 through a maximum of age 65. The lifetime
probability of a lung cancer death was cumulated to age 100, resulting
in a negligible loss of accuracy since the probability that a person
will live longer than that is extremely small. Rates of lung cancer and
other mortality for the lifetable calculations were based,
respectively, on 1998 U.S. lung cancer and all-cause mortality rates
for both sexes and all races.
The lifetable calculation of additional lifetime risk was completed
for the maximum likelihood parameter estimates for each model. In
addition, 95% confidence intervals for the additional lifetime risk
were derived by a likelihood profile method. Details about the
procedures used to estimate parameters, model fit, lifetable
calculations, and confidence intervals are described in the 2002
Environ report (Ex. 33-15, p. 24-26).
Based on comparison of the models' AIC values, Environ indicated
that the linear relative risk model (simplified E1/E2) was preferred
over the E3 additive risk model. The relative risk model is also
preferred over an additive risk model (fits being adequate in both
cases) in the case of lung cancer because of its variable background
rate 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 50, where background rates are much higher.
The linear relative risk model predicted an excess lifetime risk of
lung cancer associated with an occupational exposure of 45 years to 1
[mu]g/m3 Cr(VI) to be 6 per 1000 (95% CI: 0.8 to 14). The
additive model predicted a slightly lower lifetime risk of 4.4 per 1000
(95% CI: 0.0 to 11). At the OSHA PEL (52 [mu]g/m3), the
maximum likelihood estimate (MLE) using the linear relative risk model
is 253 per 1000 (95% CI: 39 to 456).
Since the completion of the 2002 Environ analysis, individual data
for the 2,357 men in the Gibb et al. cohort have become 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 several
additional analyses that could not be done previously, including
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.
In the 2002 analysis, Environ used the same four-group
categorization of cumulative exposure reported by Gibb et al. and
presented in Table VII-1. The individual data allowed Environ to
investigate alternate groupings of cumulative exposure categories.
Environ 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 and, therefore, the expected numbers of lung
cancers 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 VII-2.
[[Page 59366]]
Table VII-2.--Dose-Response Data From Environ (2003, Ex. 33-12): Observed and Expected Lung Cancer Deaths for
Gibb Cohort Grouped by Ten Cumulative Cr(VI) Exposure Categories
----------------------------------------------------------------------------------------------------------------
Cumulative Mean Cr(VI) Expected lung cancers
Cr(VI) exposure Person- Observed -------------------------
exposure [mu]g/ ([mu]g/m\3\- years lung Maryland Baltimore
m\3\-years) yr) cancers rates rates
----------------------------------------------------------------------------------------------------------------
Alternative 1: Roughly Equal 0-0.151 0.0246 17982 12 10.3 13.37
Observed Cases per Group...... 0.151-0.686 0.395 9314 12 13.0 16.80
0.686-2.08 1.25 8694 12 10.3 13.55
2.08-4.00 2.96 5963 12 7.38 9.42
4.00-8.32 5.89 5102 12 5.63 7.32
8.32-18.2 12.4 5829 13 7.09 9.21
18.2-52 31.1 6679 13 6.83 9.05
52-182 105 6194 12 5.77 7.73
182-572 314 4118 12 5.79 7.66
>572 979 945 12 2.07 2.62
Alternative 2: Roughly Equal 0-0.052 0.00052 14282 4 5.08 6.63
Number of Person-Years per 0.052-0.273 0.147 6361 11 9.05 11.58
Group......................... 0.273-0.65 0.455 6278 7 8.71 11.33
0.65-1.43 0.996 6194 11 7.30 9.58
1.43-3.12 2.19 6395 12 8.17 10.52
3.12-6.89 4.59 6207 11 6.90 8.95
6.89-16.1 10.7 6296 17 7.77 10.05
16.1-41.6 25.9 6230 12 6.50 8.57
41.6-1.43 81.5 6287 10 5.56 7.52
>143 384 6289 27 9.17 11.99
--------------
Total...................... .............. ........... 70819.38 122 74.2 96.7
----------------------------------------------------------------------------------------------------------------
The lower bounds of the ranges are inclusive; the upper bounds are exclusive.
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 appropriate
reference population if the elevated lung cancer rates primarily
reflect extensive exposure to industrial carcinogens. This could lead
to an under representation of relative risk attributable to Cr(VI)
exposure.
The 2003 analysis used two externally standardized models, a
quadratic relative risk model (model E1 from above, without the age
factor) and a quadratic additive risk model (model E3 from above with
the additional term C2Di2) defined as
follows:
E4. Ni = C0 * Ei + PYi *
(C1Di + C2Di2).
The age factor was dropped from model E1 because the individual data
obviated the need to rely on the cross-classifications of cumulative
exposure. The availability of individual data also allowed a more
refined approach to internally standardized modeling than employed in
the 2002 assessment. Two Cox proportional hazards models were fit to
the individual exposure-response data that incorporated the individual
ages at death of all the lung cancer cases. The model forms were:
C1. h(t;z;D) = h0(t)*exp([bgr]1z +
[bgr]2D)
C2. h(t;z;D) = h0(t)*[exp([bgr]1z)][1 +
[bgr]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), [bgr]2 is the
cumulative dose coefficient, and [bgr]1 is a vector of
coefficients for other possible explanatory variables (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. 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. The two
forms of the Cox models are consistent with those originally discussed
by Cox. 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.
All externally standardized models 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 E4. However, the choice of
reference rates had some effect, notably on the ``background''
parameter, C0, which was included in the models to adjust
for differences in background lung cancer rates between cohort members
and the reference population. Such an adjustment was necessary for the
Maryland reference population (C0 was significantly
different from its default value, 1), but not for the Baltimore city
reference population (C0 was not significantly different
from 1). The inclusion of the C0 parameter allowed the model
to fit the data and yielded a cumulative dose coefficient that
reflected the effect of exposure and not the effect of differences in
background rates. The model results indicated a relatively consistent
cumulative dose coefficient, regardless of reference population.
Details about the procedures used to estimate parameters, model fit,
lifetable calculations, and confidence intervals
[[Page 59367]]
are described in the Environ report (Ex. 33-12, p. 8-9).
The coefficient for cumulative dose in the model ranged from 2.87
to 3.48 per mg/m3-yr for the relative risk model, E1, and
from 0.0061 to 0.0071 per mg/m3-person-yr for the additive
risk model, E4. These coefficients determine the slope of the linear
cumulative Cr(VI) exposure-lung cancer response relationship. The
cumulative dose coefficients for the relative risk model (E1) were only
slightly greater than that obtained from model E1 in the 2002 Environ
analysis. For the additive risk model (E4), the dose coefficients were
approximately twice the value obtained from model E3 in the 2002
analysis (i.e., 0.0033). In no case did the new analysis suggest that a
quadratic model fit the data better than a linear model.
For the internally standardized 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
non-linear 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, [bgr]2, was 1.00 for model
C1 and 2.68 for model C2. Model C2 provided a slightly better fit to
the data than did model C1. A more complete description of the models
and variables can be found in the 2003 Environ analysis (Ex. 33-12, p.
10).
BILLING CODE 4510-26-P
[[Page 59368]]
[GRAPHIC] [TIFF OMITTED] TP04OC04.000
Table VII-3 shows each model's predictions of excess lifetime lung
cancer risk from various occupational exposures. 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 (the
only nonlinear model among the set being considered). Confidence limits
for all models, including C1, tend to overlap, suggesting a fair degree
of consistency.
The estimates based on the individual data files were slightly
greater than
[[Page 59369]]
those reported in the previous Environ analysis (Ex. 33-15). For
example, the 2003 Environ analysis estimated additional lifetime risk
from 45 years of exposure at the OSHA PEL to be between 290 and 380 per
1000, whereas the previous analysis estimated 253 per 1000 (Ex. 33-12,
Table 9). This difference may be partly attributed to the availability
of individual data, as opposed to data from summary tables, allowing a
better definition of exposure categories. Some of the difference may be
attributable to slightly different total person-years of follow-up
reported by Gibb et al. in their summary table (71,994 from Table V,
Ex. 31-22-11) and the total person-years accounted for in the
individual data files (70,819 from Ex. 295). The reason for this
variation in total person-years is unknown.
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
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 specified) 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 mg CrO3/
m3-yr. (Ex. 33-13, Table 4). If the exposures were converted
to units of mg Cr(VI)/m3-yr, the estimated cumulative dose
coefficient would be 2.78 (95% CI: 1.04 to 5.44) per mg/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 VII-4. The
values are very similar to the estimates predicted by the Environ 2003
analysis (Table VII-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 VII.C.4.
[GRAPHIC] [TIFF OMITTED] TP04OC04.001
[[Page 59370]]
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 (Ex. 31-18-
15-1) prepared an analysis of lung cancer mortality from the Gibb
cohort. Like 2003 Environ and NIOSH, 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, C0, (as was 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/
m3 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 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 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 risk of 9 per
1000 for workers exposed to 1 [mu]g/m3 Cr(VI) for 45 years.
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 VII-3). 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 more accurately
represent the background lung cancer rate for this cohort.
The lowest excess lifetime risk for workers exposed to 1 [mu]g/
m3 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
current OSHA PEL (52 [mu]g/m3) from the risk analysis.
Moreover, no matter what current exposures might be, data on higher
cumulative exposures are still 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.
Exponent conducted analyses to further explore the dose-response
relationship in addition to the assessments described above (Ex. 31-18-
1). Of particular interest was an examination of short-term workers'
likely impact on the dose-response assessment and an SMR analysis based
on peak exposure estimates. A substantial proportion of the Gibb cohort
worked less than one year at the Baltimore plant. Inclusion of these
workers in the exposure-response assessment could potentially bias the
results, if, for example, these workers incurred unrecorded Cr(VI)
exposures at other jobs. In brief, Exponent found that excluding these
short-term workers would not likely impact the dose-response analysis.
Exponent reported that SMRs for workers with ``peak'' exposures
less than 0.18 mg CrO3/m3 (0.094 mg Cr(VI)/
m3) were not significantly elevated and that this exposure
level may represent a ``threshold'' (i.e., exposure below which the
probability of cancer is zero), such that workers exposed to
concentrations below the threshold may not have excess cancer risk (Ex.
31-18-1). However, the analysis used peak exposure estimates based on
recorded average annual exposures. True peak exposures were unavailable
for the Gibb cohort members. The use of the highest recorded average
annual Cr(VI) air level as an exposure metric ignores any risk
contribution from the duration of exposure. It assumes the same lung
cancer risk regardless of whether the worker is exposed at a particular
Cr(VI) concentration for one month or ten years. This is clearly
inconsistent with the study results.
The validity of the ``peak exposure'' analysis also suffers from
Exponent's problematic definition of exposure categories, which is
similar to the six-part grouping used in the dose-response assessments.
As with Exponent's cumulative exposure groups, the peak exposure
grouping allocates most of the observed cancers and person-years to the
lowest exposure groups, reducing the power to detect significant
differences from background at more moderate exposure concentrations
below 0.094 mg Cr(VI)/m3. The implication that the data
indicate a ``threshold'' at 0.094 mg Cr(VI)/m3 is,
therefore, misleading, and not considered a valid analysis for
estimating risk of lung cancer to workers exposed to Cr(VI).
4. Summary of Risk Assessments Based on the Gibb Cohort
OSHA finds remarkable consistency among the risk estimates from the
[[Page 59371]]
various quantitative analyses of the Gibb cohort. The excess lifetime
risks from cumulative Cr(VI) exposure were similar whether the analyses
were based on the summary information reported by Gibb et al. or on the
information provided in the individual data file.
Both Environ and NIOSH determined that linear relative risk models
with respect to cumulative exposure generally provided a superior fit
to the data when compared to other relative risk 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-3 and VI-4).
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 lung cancer
rates, and included a generic background adjustment term. The
adjustment 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 contribute to
accurate risk estimation by helping to correct for confounding risk
factors. The internally standardized Cox models, especially the linear
Cox model, which also adjusted for smoking 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 to the validity of 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 current PEL (52 [mu]g Cr(VI)/m\3\) 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 TWA
exposure concentrations of 1 [mu]g Cr(VI)/m3 for a working
lifetime range from 7.1 to 9.4 per 1000 with the lowest 95% confidence
bound being 2.7, and the highest 95% confidence bound being 16 (Table
VII-3). 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.
It is instructive to examine whether the excess lung cancer risk
estimated from the mathematical modeling reasonably predicts the risk
based on the mortality observed in the Gibb et al. study. There were
855 deaths in the Gibb cohort of which 122 were from cancer of the lung
(Ex. 31-22-11, Table I). The expected number of lung cancer deaths from
the age-, gender-, race-, and calendar year-adjusted reference
population in Baltimore was 96.7 (Table VII-2). Therefore, there were
about 25 lung cancer deaths (i.e., 122--96.7) presumably attributable
to Cr(VI) exposure out of the 855 total deaths, or 29 per 1000 workers
(i.e., 25/855 x 1000). If lung cancer were to continue to occur with
the same proportionate mortality in this cohort (64 percent of the
cohort were still living), their excess lifetime lung cancer risk would
be close to three percent.
The mean cumulative exposure for the Gibb cohort was 0.134 mg
CrO3/m\3\ - yr with a mean 3.1 years of work (Ex. 31-22-11,
Table II). An approximate average Cr(VI) air level of 22.5 [mu]g
Cr(VI)/m\3\ can be calculated after converting from CrO3 to
Cr(VI). Using the average Cr(VI) air concentration (22.5 [mu]g/m\3\),
mean exposure duration (3.1 yr), and mean age of hire of 30 years of
age (Ex. 31-22-11, Table III), the linear relative risk model E1 (equal
PYRs per group, Table VII-3) predicts an excess lifetime lung cancer
risk of 14.8 per 1000 (95% CI: 6.97 to 25.1 per 1000) for workers with
the mean cumulative exposure of the Gibb cohort. These Cr(VI) levels
are below the current PEL for considerably shorter than a full working
lifetime.
The model-predicted lung cancer risk is about half the risk
calculated from the observed mortality in the Gibb et al. study. This
is probably due, in part, to the higher cumulative Cr(VI) exposure for
the subset of workers who had already died. The mean Cr(VI) exposure of
the lung cancer cases was slightly over two-fold higher (i.e., 0.294 mg
CrO3/m\3\ - yr) than the cohort as a whole (Ex. 31-22-11,
Table II). It also seems likely that the workers who already died of
causes other than lung cancer would be older cohort members that may
have experienced higher Cr(VI) exposure than the presumably younger
cohort members hired more recently and still living. If their mean
cumulative Cr(VI) exposure were more like that of the lung cancer cases
than the total cohort group, the relative risk model would predict
risks close to the three percent excess lung cancer risk derived from
the observed mortality data.
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 dose-related trends for lung
cancer SMR as a function of year of hire, duration of employment, and
cumulative Cr(VI) exposure. Overall, there was significantly increased
SMR for lung cancer deaths of 241 (95% CI: 180 to 317).
[[Page 59372]]
Table VII.-5--Dose-Response Data From Luippold Cohort as cited by Environ (2002, Ex. 33-15): Observed and
Expected Numbers of Lung Cancer Deaths Grouped by Five Cumulative Cr(VI) Exposure Categories
----------------------------------------------------------------------------------------------------------------
Mean Cr(VI)
exposure Observed Expected Person-
Cumulative Cr(VI) exposure (mg/m\3\ - yrs)\a\ (mg/m\3\ - lung lung years
yrs)\a\ cancers cancers\b\
----------------------------------------------------------------------------------------------------------------
< 0.20...................................................... 0.10 3 4.5 2952
0.20-0.49................................................... 0.36 8 4.4 2369
0.49-1.05................................................... 0.74 4 4.4 3077
1.05-2.70................................................... 1.79 16 4.4 3220
2.70-27.8................................................... 4.81 20 4.3 2482
----------------------------------------------------------------------------------------------------------------
\a\ Note that units mg/m\3\ - yrs is 1000 times greater than [mu]g/m\3\ - yrs in data tables for Gibb cohort.
\b\ Expected lung cancer deaths derived using Ohio state mortality rates.
Environ conducted a risk assessment based on the cumulative Cr(VI)
exposure-lung cancer mortality data from Luippold et al. and presented
in Table VII-5 (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 E3, to the data
in Table VII-5. Model E1 was applied without the
exp{kti{time} term, because no categorization by age was
available. Addition of a quadratic term did not improve the fit over
that of a linear relative risk model. Model E2 was not applied, because
without the exp{kti{time} term model E2 is the same as E1.
The background rate parameter, C0, was assumed to be 1.0 in
both models since other values did not significantly improve model fit.
Linear relative and additive risk models fit the Luippold cohort
data adequately (p>=0.25). 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/m\3\ - yr and 0.0014
per mg/m\3\ - 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)/m\3\ 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 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 VII-6. Ohio reference rates were again used
in calculating the expected lung cancer deaths and cumulative exposures
were lagged 5 years.
Table VII-6.--Dose-Response Data From Crump et al. (Ex. 35-58): Observed
and Expected Numbers of Lung Cancer Deaths for Luippold Cohort Grouped
by Ten Cumulative Cr(VI) Exposure Categories
------------------------------------------------------------------------
Mean
Cr(VI) Observed Expected
Cumulative Cr(VI) exposure exposure lung lung Person-
(mg/m3-yrs) a (mg/m3- cancers cancer b years
yrs) a
------------------------------------------------------------------------
0-0.06...................... 0.0098 0 2.09 3112
0.06-0.18................... 0.11 3 2.19 1546
0.18-0.30................... 0.23 3 2.21 1031
0.30-0.46................... 0.38 5 2.13 1130
0.46-0.67................... 0.56 0 2.22 1257
0.67-1.00................... 0.80 4 2.23 1431
1.00-1.63................... 1.25 12 2.23 1493
1.63-2.60................... 2.10 3 2.18 1291
2.60-4.45................... 3.27 10 2.18 1248
4.45-29.0................... 7.55 11 2.12 904
------------------------------------------------------------------------
The lower bounds of the ranges are inclusive; the upper bounds are
exclusive.
a Note that units mg/m3-yrs is 1000 times greater than [mu]g/m3-yrs in
data tables for Gibb cohort.
b Expected lung cancer deaths derived using Ohio state mortality rates.
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 relative and 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 data was not presented.
The dose coefficients reported by Crump et al. were very
[[Page 59373]]
similar to those obtained by Environ above, even though different
exposure groups were used and the lag for the cumulative exposure
calculation was slightly different. 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) after eliminating the nonmonotonic (i.e., not
progressively increasing with exposure) scatter contributed by the many
lower exposure categories where there are few observed and expected
cancers. This nonmonotonic pattern is avoided by using more stable
exposure groupings with greater number of cancers. The reduction in
number of exposure groups did not significantly change the dose
coefficient estimates.
The maximum likelihood estimate for the cumulative dose coefficient
using the linear Cox regression model (i.e., 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).
Crump et al. also presented benchmark dose estimates
(EC10s) of 52 [mu]g/m3 (95 percent lower
confidence bound, LEC10, of 37 [mu]g/m3) and 49
[mu]g/m3 (LEC10 of 35 [mu]g/m3) for
the relative risk and additive risk models, respectively. The
EC10 is an estimate of the dose associated with a ten
percent, or 100 in 1000, risk. The EC10 and its
LEC10 are being considered by the U.S. EPA, under certain
circumstances, as a reasonable point of departure for extrapolation
modeling below the biologically observable range (Ex. 35-53, p. 3-12 to
3-15). These results are very consistent with those predicted by
Environ (Ex. 33-15) for the Luippold et al. cohort (e.g., approximately
100 lung cancer cases per 1000 workers from estimated working lifetime
at the OSHA PEL of 52 [mu]g/m3). There were only minor non-
significant changes in benchmark dose estimates when exposure lags were
varied from 5 to 20 years using Poisson or Cox linear regression
models.
Given the similarity in results, OSHA believes it is reasonable to
use the dose coefficients reported by Exponent based on their groupings
of the individual cumulative exposure data to estimate excess lifetime
risk from the Luippold cohort. Table VII-7 presents the excess risk for
a working lifetime exposure to various TWA Cr(VI) levels as predicted
by the relative and additive risk models using a lifetable analysis
with 2000 U.S. rates for all causes and lung cancer mortality. The
maximum likelihood estimates and 95 percent confidence limits from the
Luippold cohort indicate that working lifetime exposures to the current
Cr(VI) PEL would entail excess lifetime lung cancer risks around 100
per 1000 and that risks of 1.2 to 3.3 per 1000 would be expected from
TWA exposures of 1 [mu]g Cr(VI)/m3 for a working lifetime.
[GRAPHIC] [TIFF OMITTED] TP04OC04.002
The excess lung cancer risk predicted from the mathematical
modeling can be compared with the risk expected based on the actual
mortality experience of the Luippold cohort. There were 303 observed
deaths in the cohort of which 51 were from cancer of the lung (Ex. 33-
10, Table 2). The expected number of lung cancer deaths from the age-,
gender-, race-, and calendar year-adjusted reference population from
Ohio was 21.2. Therefore, there were about 30 lung cancer deaths (51-
21.2) presumably attributable to Cr(VI) exposure out of 303 total
deaths, or 98 per 1000 workers (29.8/303 x 1000). If lung cancer were
to continue to occur with the same proportionate mortality in this
cohort (37 percent of the cohort was still living), their excess
lifetime lung cancer risk would be about ten percent.
The mean cumulative exposure for the Luippold cohort was 1.58 mg
Cr(VI)/
[[Page 59374]]
m3-yr (Ex. 33-10, Table 1), which is about twenty-three
times the mean exposure for the Gibb cohort (i.e., 0.0697 mg Cr(VI)/
m3-yr). Although the mean length of employment of the
Luippold cohort was not reported, a crude distribution of the years
employed is consistent with an average of about ten years (Ex. 33-10,
Table 1). If the cohort were exposed an average ten years then their
average Cr(VI) air level would be roughly 158 [mu]g Cr(VI)/
m3 (1.58 x 10 yr / 1000 [mu]g/mg). Using this Cr(VI) air
concentration (158 [mu]g/m3), the estimated mean exposure
duration (10 yr), and the mean age of hire of 34 years of age (Ex. 33-
10, Table 1), the linear relative risk model E1 predicts an excess
lifetime lung cancer risk of 74 per 1000 (95% CI: 46 to 110 per 1000).
This is slightly lower than the 98 per 1000 excess lung cancer deaths
attributable to Cr(VI) determined from the observed study data. The
Luippold cohort workers were exposed to mean Cr(VI) levels about three-
fold higher than the current PEL for an average duration that was
slightly less than a quarter of a full 45 year working lifetime.
As previously explained, it is not surprising that the relative
risk model may underpredict the excess risks calculated from study
mortality data. The risk model predicts the probability of lung cancer
risk in an individual or set of workers, all with the same cumulative
Cr(VI) exposure. The excess lung cancer risk calculated from the
observed mortality data were for a group of workers with a wide range
of Cr(VI) exposures. Like the Gibb study, the lung cancer cases had a
mean cumulative Cr(VI) that was twice that of the entire cohort.
Therefore, their risk may be somewhat higher than predicted for the
cohort as a whole. Since most of the Luippold cohort had died (i.e., 63
percent), the model-derived lung cancer risk based on the mean exposure
of the entire Luippold cohort may better predict the mortality-derived
excess risk estimate than was the case for the Gibb cohort, which had a
lower percentage of deaths (i.e., 36 percent).
Crump et al. reported on tests of trend and of excess lung cancer
mortality by highest reported monthly TWA Cr(VI) concentration and
cumulative Cr(VI) exposure for the workers in the Luippold cohort. The
former analysis examined air concentration irrespective of exposure
duration, even though there was a significant positive trend for excess
lung cancer mortality with duration of employment (Ex. 33-10, Table 3).
They found that a statistically significant excess mortality was not
observed in workers exposed to less than the current OSHA PEL (i.e., 52
[mu]g/m3). An analysis of cumulative Cr(VI) exposure found
that a statistically significant exposure-related trend in lung cancer
mortality only occurred if cumulative Cr(VI) exposure estimates above
1.0 mg/m3-yr were included. Crump et al. acknowledged that
their analysis had limited statistical power (i.e., the magnitude of
excess mortality needed to achieve statistical significance) to detect
increases in excess mortality at the lower cumulative Cr(VI) exposures
(Ex. 35-58, p. 1147).
The lack of statistical significance for the subset of 103 workers
in the Luippold cohort whose highest monthly TWA exposure was less than
the OSHA PEL is readily explained by a further examination of the data.
The highest monthly TWA exposures of those workers averaged 27 [mu]g/
m3 for an average duration of 34 months (Ex. 31-18-3, Table
8). Using the dose coefficient from the linear relative risk model
based on cumulative exposure fit to the full Luippold data set in a
lifetable analysis, where workers were exposed to this Cr(VI) air
concentration and duration starting at age 34 (the average starting age
for the Luippold cohort), the additional lifetime risk is predicted to
be 4.5 per 1000. This means that less than one additional lung cancer
case would be projected for the Luippold subcohort of approximately 100
workers whose highest reported eight-hour TWA (i.e., average 27 [mu]g/
m3) was below the PEL using a linear model without a
threshold.
Exponent suggested that the lack of a statistically significant
increase in lung cancer mortality observed among workers whose reported
average monthly TWA Cr(VI) was not above the PEL was evidence of an
absence of increased risk at this level (Ex. 31-18-1). This assertion
is not supported by the data. As explained above, the Crump et al.
analysis lacks the statistical power to support this conclusion. Since
exposure at the highest reported TWA accounts for almost all of the
cumulative exposure experienced by those workers (Ex. 31-18-3, Table
8), the lack of an observed increase in the lung cancer SMR is entirely
consistent with a small, but significant, lung cancer risk as predicted
by a linear, non-threshold relative risk model.
E. Supporting Quantitative Risk Assessments
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
(Ex. 33-15) recently did quantitative risk assessments on study data
for all but the Hayes cohort. Several years earlier, the K.S. Crump
Division (Ex. 13-5) did quantitative assessments on data from the
Mancuso and Hayes cohort, under contract with OSHA. The U.S. EPA (Exs.
19-1; 35-52) developed quantitative risk assessments from the Mancuso
cohort data for its Integrated Risk Information System (IRIS). 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 supporting 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). While the risk estimates from these data sets are associated
with a greater degree of uncertainty, it is nevertheless valuable to
compare them to the risk estimates from the preferred Gibb and Luippold
cohorts. The cohort data sets and the analyses conducted on them are
discussed below.
The Mancuso and Hayes cohorts worked at the Painesville and
Baltimore chromate production plants, respectively. Even though the
entry date requirements, other cohort selection criteria, and the
studied site facilities were different, the lung cancer risk estimated
from the Hayes data set may not be completely independent from that
estimated from the Gibb data set. A similar situation exists between
the Mancuso and Luippold data sets. Unlike the Mancuso and Hayes
cohorts, the Gerin and Alexander cohorts were not chromate production
workers and lung cancer mortality did not show a statistically
significant positive trend with cumulative Cr(VI) exposure. Environ
performed quantitative assessments on these data sets to determine if
the predicted lung cancer risks had statistical precision that was
compatible with those estimated from the preferred Gibb and Luippold
cohorts.
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,
[[Page 59375]]
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. However, no
expected numbers of lung cancers were computed, either for the cohort
as a whole or for specific groups of person-years. Environ used two
methods for dealing with the lack of expected numbers in order to
complete the risk assessment based on this cohort.
In the first method, Environ used the recorded median age and year
of entry into the cohort to estimate the calendar years that
corresponded to the middle of the age categories for which expected
numbers of lung cancers were needed. Data in the Mancuso study
indicated that the median age at entry into the cohort was somewhere
between 25 and 29 years and that the median year of entry into the
cohort was in 1933 or 1934 (Ex. 23). Person-years of observation for
the 40-44 age category would have been centered around 1948-49 (i.e.,
15 years after 1933-34, where 15 is the difference between the age
group under consideration and the median age at entry into the cohort,
equal to 40-25 or 44-29). Similar calculations were made for the other
age categories. Expected numbers were then derived from the U.S. lung
cancer mortality rates for years as close to the target years as could
be obtained.
The exposure-response data with the resulting expected number of
lung cancer deaths are reported 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 assumed for calculating the cumulative exposures. Environ
applied three externally standardized models (see models E1-E3 in
subsection VII.C.1) to these data. Unlike other data sets modeled by
Environ, the age-related parameter k for the Mancuso data set was
estimated to be different from 0, so that models E1 and E2 had
different dose coefficients (Ex. 33-15, Table 6, p. 42). The quadratic
term (i.e., C2 in model E1) did not significantly improve
model fit, so E1 was linear with respect to cumulative exposure.
Since the expected numbers of lung cancers for the Mancuso cohort
could only be approximated, Environ also applied a set of internally-
standardized models that did not require estimation of expected number
of lung cancers to the exposure-response data (Ex. 33-15, p. 24-25).
While both externally- and internally-standardized models provided
adequate fit to the data (p>=0.13), the AIC procedure indicated that
model E2, the linear relative risk model with an age-dependent exposure
term, provided a superior fit over the other models. The next best
fitting models, E1 and I2, presented other problems. Model E1 estimated
risk predictions that were apparent outliers and the confidence
intervals around risk predictions from model I2 were unusually wide
(Ex. 33-15, Table 8, p. 43). Further explanation for the inherent
instability of these models can be found in the 2002 Environ report
(Ex. 33-15, p. 28-29).
The excess risk of lung cancer from a working lifetime exposure to
Cr(VI) at the current OSHA PEL using the preferred model E2 is 293 per
1000 workers (95% CI: 188 to 403). The maximum likelihood estimate from
working lifetime exposure to 1.0 [mu]g/m3 Cr(VI) is 7.0 per
1000 workers (95% CI: 4.1 to 11 per 1000). These estimates are close to
those predicted from the Gibb cohort but are higher than predicted from
the Luippold cohort. This result indicates that the non-overlapping
Painesville worker cohorts (i.e., Mancuso and Luippold cohorts)
probably generate independent estimates of risk, even though they were
drawn from the same plant.
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 was 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 may not have underestimated 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 may have died before 1940 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.
Several earlier quantitative risk assessments 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
[[Page 59376]]
included not only carcinogenic Cr(VI) but substantial amounts of non-
carcinogenic Cr(III).
The 1995 risk analysis by K.S. Crump Division, under contract with
OSHA, estimated cumulative Cr(VI) exposures by multiplying cumulative
total chromium exposure by an adjustment factor of 0.4 (Ex. 13-5). This
factor is roughly the average contribution of soluble chromium to the
total chromium exposure levels measured across departments in the
Painesville plant by Bourne and Yee in 1949 (Ex. 7-98). The K.S. Crump
Division used the lung cancer mortality data cross-classified by the
eight exposure categories and three age groups reported in Table IX of
the 1975 Mancuso report (Ex. 7-11). They estimated the expected number
of lung cancer deaths in a manner similar to the Environ assessments in
2002. The median age at entry for the cohort was estimated to be 28.5
years from the 1975 Mancuso study with an estimated median start date
of 1934. Average values for cumulative exposure in each group were
estimated by the arithmetic mean of the endpoints defining the group.
An externally standardized linear relative risk model was used to
fit the exposure-response data. A sensitivity analysis was used to
examine the impact of different average cumulative exposure estimates
to represent the highest exposure group (>3.0 mg-yr/m3)
since an arithmetic average could not be calculated for this category.
The maximum likelihood estimates for the dose coefficient were
relatively constant over a wide range of assumed average exposures.
However, the best fit occurred when the high-exposure group was
excluded from the analysis (p=0.49). This was because the lung cancer
mortality ratios observed for workers with the highest cumulative
chromium exposure in the Mancuso data set tended to be lower than
predicted by linear projections based on the lung cancer mortality data
from workers exposed to lower cumulative exposures. The excess lung
cancer risks for a working lifetime at the current OSHA PEL (52 [mu]g/
m3) for Cr(VI) range from 246 to 342 per 1000 workers using
the different assumptions about the highest exposure group (Ex. 13-5,
Table 8). The excess risk estimates from a working lifetime exposures
to 0.5 [mu]g/m3 Cr(VI) ranged from 2.9 to 4.4 per 1000
workers. This was similar to the risk estimated by Environ using the
more updated Mancuso data set.
Like Environ, the K.S. Crump Division explored another method of
Poisson regression that internally controlled for age, and which
consequently alleviated the need to estimate background rates from an
external control population. The dose coefficients estimated for the
internally standardized linear relative risk model were similar to
those from the externally controlled model. However, sensitivity
analysis indicated that the internally standardized model may lead to
less stable risk estimates, in that relatively minor changes in average
exposure assumptions led to bigger changes in the risk estimates.
The U.S. EPA also used exposure-response data presented in Table IX
of the 1975 Mancuso report (Ex. 7-11) as the primary data source for
calculating its unit risk estimate . The unit risk refers to an
incremental lifetime cancer risk over background occurring in a
hypothetical population in which all individuals are exposed
continuously throughout life to a concentration of 1 [mu]g Cr(VI)/
m3 in the air that they breathe. Like the K.S. Crump
Division, the EPA relied on the observed lung cancer deaths cross-
classified by age group and cumulative exposure to total chromium.
However, rather than estimate the year of cohort death based on age at
entry into the study, the EPA chose to determine expected number of
lung cancers for the entire cohort, regardless of age at death, using
lung cancer mortality statistics for 1964. They estimated that a large
proportion of lung cancer deaths in the cohort probably occurred around
that year.
The U.S. EPA assessment did not adjust the total cumulative
chromium exposure estimates of Mancuso for the contribution of Cr(VI).
While the EPA acknowledged that the resulting overestimation of dose
would likely lead to an underestimation of risk, they judged that this
would be potentially balanced by two factors that tend to overestimate
the risk of lung cancer. One factor was the likelihood that the
airborne Cr(VI) levels in the 1930s and 1940s were higher than measured
by Bourne and Yee in 1949, as mentioned previously. EPA also suggested
the possibility that the Mancuso cohort may have smoked more than the
general population so that the expected numbers of lung cancer deaths
associated with Cr(VI) exposure would be low and the relative risk
overestimated for the cohort.
The 1984 U.S. EPA assessment employed an exposure-dependent
multistage model of additive risk to fit the 1975 Mancuso cohort data
that relied on average chromium exposure, rather than the cumulative
workplace exposure (Ex. 19-1). In their review of the U.S. EPA
assessment, the K.S. Crump Division pointed out potential flaws in the
EPA conversion of cumulative workplace exposure to their ``continuous
exposure equivalent'' that resulted in high average chromium exposure
estimates and a correspondingly low unit risk (Ex. 13-5, p. 19-21). The
U.S. EPA determined that the maximum likelihood estimate of additional
lung cancer risk associated with continuous lifetime exposure to 1
[mu]g/m3 of Cr(VI) was 0.012 (i.e., 12 per 1000). More
recently, the EPA corrected its dose conversion for the Mancuso cohort
which yielded a higher unit risk estimate of 0.016 per [mu]g Cr(VI)/
m3 (Ex. 35-52).
In 1985, the California Department of Health Services (CDHS)
estimated a cancer potency factor for Cr(VI) in support of its Toxic
Air Contaminants Program (Ex. 35-54, p. 210-215). They estimated the
relative lung cancer risks and continuous total chromium exposure
equivalents for the 1975 Mancuso data set using the same assumptions
and procedures as the 1984 EPA assessment. An average relative risk and
average total chromium exposure level, weighted by the person-years per
age and exposure category, were calculated for all groups combined. The
average total chromium exposure level was multiplied by one-seventh
(0.142) as an assumed adjustment for the fraction of total chromium
present as Cr(VI). A linear relative risk model was then used to
calculate a ``crude'' approximation of the excess risk from continuous
exposure to 1 [mu]g/m3 of Cr(VI) for a lifetime. The CDHS
chose the 95 percent upper confidence limit of 0.15 per [mu]g Cr(VI)/
m3 as their cancer potency factor which is about an order of
magnitude greater than the EPA unit risk estimate.
The Public Citizen Health Research Group (PCHRG) attempted to
estimate the magnitude of lung cancer risks associated with
occupational exposure to Cr(VI) from the 1984 U.S. EPA unit risk for
continuous lifetime exposure (Ex. 1). They reported that the excess
lung cancer risk from a working lifetime exposure to Cr(VI) at the OSHA
PEL (52 [mu]g/m3) was 220 per 1000 workers. As described in
the 1995 report by K.S. Crump Division (Ex. 13-5, p. 27-29), there were
several errors in the PCHRG analysis and the correctly calculated
excess occupational risk at the OSHA PEL using the EPA unit risk method
is 80 cases per 1000 workers. This risk is lower than the estimate from
Environ and the K.S. Crump Division, probably as a result of the EPA
conversion of occupational cumulative chromium exposure to a continuous
average Cr(VI) exposure for an individual lifetime.
[[Page 59377]]
The U.S. Air Force Armstrong Laboratory (AFAL) estimated lung
cancer risks to U.S. Navy workers from Cr(VI) exposures as a result of
welding, abrasive blasting, spray painting, and other operations (Ex.
35-51). They used a cancer potency factor of 41 per mg Cr(VI)/kg-day
derived from the 1984 EPA unit risk adjusted for an average breathing
rate of 20 m3/day and body weight of 70 kg. They also
reduced their measured airborne Cr(VI) dust concentrations by an
assumed respirable fraction of 0.23. The estimated excess lifetime risk
from a 45-year occupational exposure to an eight hour TWA 0.5 [mu]g/
m3 using the AFAL methodology and assumptions is about 0.2
per 1000 workers. This is lower than the Environ and K.S Crump Group
estimates due to the lower EPA potency factor and the added adjustment
for the respirable fraction.
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. The other
assessments used older cohort mortality data with fewer years of
follow-up and more problematic exposure estimates and calculations.
2. Hayes Cohort
The K.S. Crump Division (Ex. 13-5) and Gibb et al. (Ex. 7-102)
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 VII.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)/m3-yr with a 90% confidence bound of between
0.45 and 1.1 per mg Cr(VI)/m3-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
later result indicates that the two Baltimore chromate production
cohorts (i.e., Hayes and Gibb cohorts) probably generate independent
estimates of risk, even though they were drawn from facilities at the
same site for overlapping periods of time. 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 OSHA PEL (52 [mu]g/m3) to be 88
lung cancer cases per 1000 workers (95% CI: 61 to 141). For 1 [mu]g/
m3, about 2 excess lung cancer deaths per 1000 (95% CI: 1.2
to 3.0) were predicted 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/m3) 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.
Gibb et al. provided a risk assessment for the U.S. EPA of the same
Braver exposure-response data used by the K.S. Crump Division (Ex. 7-
102). In order to determine the EPA unit risk, the cumulative
occupational exposures were converted to average lifetime concentration
(as discussed in section VII.E.2) and an average age of 55 was assumed
at the end of follow-up for members of the Hayes cohort. Gibb et al.
used the additive risk model E3 with the default value of 1 for
C0, to fit the data. They reported that the maximum
likelihood estimate for the dose coefficient was 0.13 per mg/
m3-yr and it yields a unit risk similar to that derived by
the EPA from the 1975 Mancuso cohort (Ex. 19-1). Since the excess lung
cancer risk from lifetime occupational exposure to Cr(VI) at the OSHA
PEL was 80 cases per 1000 workers based on the EPA unit risk from the
Mancuso cohort, a similar occupational risk estimate is likely from the
Gibb et al. unit risk based on the Hayes cohort. This would be
consistent with the occupational risk (e.g., 88 cases per 1000 workers)
at the OSHA PEL projected from the assessments of the K.S. Crump
Division.
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 come 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 mentioned in section VII.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 subcohort examined, there was no obvious indication of a Cr(VI)
exposure-related effect on lung cancer mortality. This may be explained
by the
[[Page 59378]]
uncertainties in the exposure estimates and presence of co-exposures
discussed in section VII.B.5.
Environ used their externally standardized models, E1 to E3, 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 dose
coefficients considerably lower than for the Gibb or Luippold cohorts
(Ex. 33-15, Table 6). In fact, the maximum likelihood estimates for the
dose coefficients were not statistically different from 0 at the p=0.05
significance level, which would be expected when there is no exposure-
related trend.
Environ chose the linear relative risk model, E2, as the best
fitting model based on the AIC value. The projected excess risk of lung
cancer from a working lifetime exposure to Cr(VI) at the current OSHA
PEL using the preferred model E2 was 46 (95% CI: 0 to 130) cases per
1000 workers. The maximum likelihood estimates of excess risk from
working lifetime exposure to 1.0 [mu]g Cr(VI)/m\3\ was 0.9 (95% CI: 0
to 2.8) cases per 1000 workers, respectively. The rather large 95
percent confidence interval around the maximum likelihood estimate
reflects the greater statistical uncertainty associated with risk
estimates from the Gerin cohort. The confidence interval overlaps that
for equivalent risk estimates from the Luippold cohort but not the Gibb
cohort.
4. Alexander Cohort
Environ (Ex. 33-15) did a quantitative assessment of the observed
and expected lung cancer incidence in 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 lung cancer
data come from a retrospective study with a small number (15) of
observed lung cancers in a young cohort (median age of 42 years at end
of follow-up) with a relatively short follow-up period (median nine
years per member). 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). 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).
Alexander et al. grouped the lung cancer data by cumulative
exposure with and without a ten year lag period (Ex. 31-16-3). They
found no statistically significant elevation in lung cancer incidence
among the chromate-exposed workers or clear trend with cumulative
chromate exposure. Environ used the externally standardized linear
relative risk model to fit the unlagged data (Ex. 33-15). The
additional risk model, E3, could not be applied because no person-years
of observation were presented by Alexander et al. Environ assumed
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 did not fit the data particularly well
(p=0.04) and the dose coefficient was considered to be 0 since positive
values did not significantly improve the fit. This is not surprising
considering the lack of a positive trend between lung cancer incidence
and cumulative Cr(VI) exposure for this cohort. Possible reasons for
the lack of a positive association between Cr(VI) exposure and lung
cancer incidence in this cohort were previously discussed in section
VII.B.6.
The best estimate of excess risk of lung cancer from the Alexander
cohort was 0 for all exposures to Cr(VI) based on the default dose
coefficient. The upper 95 percent confidence bound on the risk was
estimated to be 212 cases per 1000 workers from a working lifetime
exposure to Cr(VI) at the current OSHA PEL. The upper 95 percent
confidence bound on risk from working lifetime exposure to 1.0 mg
Cr(VI)/m\3\ is 4.8 cases per 1000 workers. The confidence intervals
around the risk estimates from the Alexander cohort are greater than
those from the Gerin cohort reflecting greater statistical uncertainty.
However, the 95 percent confidence intervals for the risk estimates
from the Alexander cohort overlap those for equivalent risk estimates
from both the Luippold and Gibb cohorts.
If the cumulative exposures from Alexander et al. are assumed to be
cumulative chromate (CrO4-2) estimates, then
exposures in terms of Cr(VI) would be calculated by dividing by 0.45.
As a result, the upper confidence bound on risk would be higher by
1/.45 = 2.2-fold, which would also be statistically consistent with the
risk estimates based on the Gibb and Luippold data sets.
F. Summary of Risk Estimates Based on Gibb, Luippold, and Supporting
Cohorts
OSHA believes that the best estimates of excess lifetime lung
cancer risks are derived from the Gibb and Luippold cohorts. These two
cohorts have accumulated a substantial number of lung cancer deaths
that were extensively examined in terms of cumulative Cr(VI) exposure.
Cohort exposures were reconstructed from air measurements and job
histories over three or four decades. The linear relative risk model
adequately fitted the Gibb and Luippold data sets, as well as several
other supporting data sets. 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
fitted 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 that the cohorts worked
in different chromate production facilities and the potential
uncertainties involved in estimating cancer risk from the data (see
section VII.G). Since the analyses based on these two cohorts are each
of high quality and their projected risks are reasonably close (e.g.,
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.
[[Page 59379]]
Table VII-8.--OSHA Estimates of Excess Lung Cancer Cases per 1000 Workers\a\ Exposed to Various Eight Hour TWA Cr(VI) With 95 Percent Confidence
Interval Comparisons by Cohort
--------------------------------------------------------------------------------------------------------------------------------------------------------
95% confidence interval on risk estimates by cohort\c\
Best -----------------------------------------------------------------------------
Cr(VI) ([mu]g/m\3\) estimates Featured cohorts Supporting cohorts
of risk\b\ -----------------------------------------------------------------------------
Gibb Luippold Mancuso Hayes Guerin Alexander
--------------------------------------------------------------------------------------------------------------------------------------------------------
0.25......................................................... 0.52-2.3 1.0-3.9 0.31-0.79 1.0-2.7 0.31-0.75 0.0-0.7 0.0-1.2
0.5.......................................................... 1.0-4.6 2.0-7.8 0.62-1.6 2.0-5.4 0.62-1.5 0.0-1.4 0.0-2.4
1.0.......................................................... 2.1-9.1 4.0-16 1.2-3.1 4.1-11 1.2-3.0 0.0-2.8 0.0-4.8
2.5.......................................................... 5.2-23 10-37 3.1-7.8 10-27 3.1-7.5 0.0-6.9 0.0-12
5.0.......................................................... 10-45 20-75 6.2-15 20-52 6.1-15 0.0-14 0.0-24
10........................................................... 21-86 39-142 12-31 n/a 12-30 0.0-29 0.0-50
20........................................................... 41-163 76-256 21-60 n/a 24-51 0.0-54 0.0-91
52........................................................... 101-351 181-493 62-147 188-403 61-141 0.0-130 0.0-212
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\a\ The workers are assumed to start work at age 20 and continue to work for 45 years, at a constant exposure level. All estimates were recalculated
using year 2000 U.S. reference rates, all races, both sexes, for lung cancer and all causes, except for those from Mancuso, for which 1998 rates were
used.
\b\ OSHA preliminarily finds that the estimates of risk best supported by the scientific evidence are the ranges bounded by the maximum likelihood
estimates from the linear relative risk models presented in Table VII-3 (Baltimore reference population/exposure grouping with equal person-years) for
the Gibb cohort and Table VII-7 for the Luippold cohort.
\c\ The confidence intervals for the Gibb and Luippold cohorts are from Tables VII-3 and VII-7. The confidence intervals for the Mancuso, Guerin and
Alexander cohorts are derived from parameters reported by Environ (2002, Ex. 33-15). All are from the best fitting linear relative risk models and are
95% confidence intervals. The confidence interval for the Hayes cohort was calculated from the 90 percent confidence interval on the dose coefficient
for the linear relative risk model reported by the K.S. Crump Division (1995, Ex. 13-5).
OSHA's best estimates of excess lung cancer cases from a 45-year
working lifetime exposure to Cr(VI) are presented in Table VII-8. This
range of projected risks lie between the maximum likelihood estimates
derived from the Gibb and Luippold data sets. 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 VII-7). To characterize the statistical uncertainty of
OSHA's risk estimates, Table VII-8 also presents the 95% confidence
limits associated with the maximum likelihood risk estimates from the
Gibb cohort and the Luippold cohort. The confidence interval on the
risk estimates from the Luippold data set is smaller (i.e., just over a
two-fold range) than those for the Gibb data set (i.e., about a 3.5-
fold range) but the Gibb cohort is larger. Therefore, it appears
reasonable to consider both analyses jointly in providing estimates of
lung cancer risk.
OSHA finds that the most likely lifetime excess risk at the current
PEL of 52 [mu]g/m\3\ Cr(VI) lies between 101 per 1000 and 351 per 1000,
as shown in Table VII-8. That is, OSHA predicts that between 101 and
351 of 1000 workers occupationally exposed for 45 years at the current
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 roughly falls
proportionally with exposure so that estimates at 5 [mu]g/m\3\ are
about 10 to 45 cases per 1000 workers and estimates at 0.5 [mu]g/m\3\
are about 1 to 4.5 cases per 1000 workers.
The 95 percent confidence limits on estimates of risk for the four
supporting cohort data sets are also presented in Table VII-8. As
discussed previously, the exposure-response data from supporting
cohorts are not as strong as those from the two featured cohorts. The
cumulative Cr(VI) exposure reconstructions in these data sets were
based on more limited air measurements and were frequently not linked
to cohort workers on an individual basis. Some of the cohort data sets
were weaker in terms of either number of workers, length of follow-up,
documented mortality data, and possibility of co-exposures or a healthy
worker survivor effect. These features may have introduced bias into
the estimates of risk determined from the studies. However, observed
lung cancers were grouped across multiple exposure groups in these more
problematic cohorts that allowed quantitative assessments to be done
and compared against the stronger Gibb and Luippold cohorts.
OSHA believes the supplemental assessments support the range of
projected excess lung cancer risks from the Gibb and Luippold cohorts.
This is illustrated by the 95 percent confidence intervals shown in
Table VII-8. The confidence interval encompasses those risk estimates
that are consistent with the cohort data to a certainty of 95 percent.
The confidence intervals tend to be smaller for the larger data sets
and better model fits. OSHA's range of best risk estimates for a given
occupational Cr(VI) exposure overlap the 95 percent confidence bands
for each of the four supporting cohorts. This indicates that the range
of best estimates includes risks with a statistical precision that is
compatible with all the exposure-response data sets, including the
smaller Gerin and Alexander cohorts where the lung cancers did not show
a clear positive trend with cumulative Cr(VI) exposure.
The 95 percent confidence intervals from the four supporting
cohorts overlap those of either the Gibb or Luippold cohorts (or both).
The confidence intervals for estimates of the Mancuso cohort overlap
with those of the Gibb cohort but are higher than those of the Luippold
cohort. The risks projected from the Mancuso data set are likely
overestimated because they depend on air monitoring conducted near the
end of the study period when exposures were likely lower and because
the sampling method only captured highly soluble Cr(VI) compounds. The
Mancuso cohort was also probably exposed to significant
[[Page 59380]]
amounts of the more potent slightly soluble and insoluble chromates
(e.g., calcium chromate). The relative potency of Cr(VI) compounds is
further discussed in section VII.G.4. The confidence intervals for
estimates from the Hayes cohort overlap the Luippold cohort but are
lower than those of the Gibb cohort. The risks projected from the Hayes
cohort may be low because the cumulative exposure estimates rely on air
monitoring near the beginning of the study period when Cr(VI) levels
were likely higher. The confidence intervals for estimates from the
Gerin cohort also overlap those from the Luippold but not the Gibb
cohort. The confidence intervals for estimates from the Alexander
cohort overlap those from both featured cohorts.
While there is statistical consistency between the range of best
risk estimates based on the primary studies and those estimated from
the supporting data sets, the risk analysis does not account for
potential bias introduced by the lack of exposure data, inadequate
follow-up and other limitations in these weaker studies. Unfortunately,
the magnitude and direction of this potential bias cannot be reasonably
assessed and, thus, the impacts on the risk estimates are unclear.
It would be difficult to formally combine the data or the results
(e.g., parameter estimates) from the six studies considered for
quantitative analysis. The inclusion criteria (e.g., duration of
employment required for entry into the cohorts) differed from study to
study. Moreover, the reported cumulative exposure categories were based
on different lag periods before accumulation of exposure began.
Nevertheless, the lung cancer risks derived from all the data sets, as
a group, support the range of best estimates derived from the two
featured cohorts.
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 impact the degree of confidence in the OSHA
risk estimates. 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 VI.A.). Workers 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). 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 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. Gibb et al. reported that the full set of monitoring data
records was not accessible prior to 1971. 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.
The Exponent critique of the Gibb cohort suggested that the tape
samplers used in the Baltimore plant from the mid-1960s to 1985
resulted in reduction of Cr(VI) to Cr(III) and that Braver et al.
excluded these measurements from their analyses because of concerns
about underestimation of Cr(VI) concentration (Ex. 31-18-14). While
there may be some potential for Cr(VI) reduction on these tape
samplers, Gibb et al. reported that the tape measurements did not
significantly differ from personal breathing zone air measurements
``for approximately two-thirds of the job titles with sufficient number
of samples to make the comparison'' (Ex. 31-22-11, p. 118).
Furthermore, Gibb et al. reported that exposure estimates from the area
tape sampling system were adjusted to an equivalent personal exposure
estimate using job-specific ratios of the mean area and personal
breathing estimates determined during the 1978-1985 time period when
both were in operation (Ex. 31-22-11, p. 117). Any potential exposure
underestimation of Cr(VI) by the tape sampling system should be
minimized by this correction procedure. Braver et al. considered the
usual post-1960 Cr(VI) exposures of 31 ug/m3 to be ``less credible
because they were very low'' compared to prior time periods (e.g., pre-
1950s) and, therefore, excluded workers exposed after 1960 from their
exposure assessment (Ex. 7-17, p. 372). However, this exposure level
turned out to be very consistent with the more extensive Cr(VI)
concentrations later reported by Gibb et al. (Ex. 31-22-11) and Proctor
et al. (Ex. 35-61) for
[[Page 59381]]
chromate production plants in the 1960s and 1970s.
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 slightly 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.
Another type of uncertainty is associated with extrapolation from
one exposure pattern to another (e.g., different combinations of
exposure duration and Cr(VI) air concentrations). Both Gibb et al. and
Luippold et al. found that lung cancer mortality showed a significant
trend with cumulative Cr(VI) exposure, which is being employed by OSHA
as the exposure metric of choice in its quantitative risk assessments.
However, the Cr(VI) exposure levels experienced by the cohorts were
higher (e.g., 5 to 10,000 [mu]g/m3) than for some of the
lower exposure scenarios (e.g., 0.25 to 2.5 [mu]g/m3) of
interest to OSHA. The cohorts were also exposed for a considerably
shorter duration than a 45-year working lifetime. Uncertainties arise
when extrapolating risks for Cr(VI) concentrations and exposure
durations outside the experience of the cohort data, even when
cumulative exposures are similar.
There are several examples in which an increasing relative risk of
chronic disease has been observed to attenuate (e.g., the slope of the
exposure-response lessens) at high cumulative exposures (Ex. 35-55). A
variety of reasons can cause this behavior including the healthy worker
survivor effect previously discussed, a limit on the relative risk that
can be achieved for diseases with a high background rate (e.g., lung
cancer), and misclassification of exposure. Since the cumulative
exposure for a full working lifetime at the current OSHA PEL is higher
than observed in almost all workers from the Gibb cohort and most of
the Luippold cohort, it is possible that a linear relative risk model
might overpredict the excess risk at this exposure if there were a
significant attenuation in the slope of the exposure-response.
In order to evaluate the likelihood of an attenuated relative risk
of lung cancer at high cumulative Cr(VI) exposures, Environ fit the
Gibb and Luippold data sets to a power model of the form:
Relative Risk = E(1 + bdC)
where E was the expected number of lung cancer deaths, d is the
cumulative exposure, and b and c were parameters to be estimated (Ex.
36-2). The parameter, c, was allowed to be less than 1, which would
accommodate a decreasing slope in the exposure-response with increasing
cumulative exposure. Of course, the power model assumes a linear shape,
if c = 1. The power model fit to the two primary data sets produced
maximum likelihood estimates of 0.61 and 0.66 for the Gibb and Luippold
data sets, respectively. However, the power models did not
significantly improve the fit compared to the linear model (p = 0.41
and 0.14 for Gibb and Luippold, respectively). This is consistent with
the conclusions of NIOSH and Exponent who also reported that departure
from linearity in the exposure-response was not significant for these
data sets (Exs. 33-13; 33-12). In light of the above analyses, OSHA
does not find adequate reason to believe a linear relative risk model
overpredicts the lung cancer risk for a full working lifetime at the
OSHA PEL. This is especially true since this Cr(VI) exposure is well
within the range of cumulative exposures experienced by workers in the
Luippold cohort.
While the cumulative Cr(VI) exposure estimates determined from the
Gibb and Luippold cohorts are much more extensive than usually
available for a cancer cohort, they are still a primary source of
uncertainty in the assessment of risk. As occurs in many retrospective
cancer epidemiologic studies, it was difficult to reconstruct worker
exposure in the 1950s from the limited air monitoring data available
from the Painesville and Baltimore plants. It appears that the usual
airborne Cr(VI) exposure levels in some chromate production and
processing areas at these facilities dropped five to ten-fold from the
late 1940s to the mid-1960s with little documentation in the
intervening years. This required more indirect methods to complete the
job-exposure matrices for these cohorts. The need to reconstruct cohort
exposure in the absence of extensive air measurements combined with the
different procedures used to collect air samples at the two plants
could partially explain the slight but statistically different
exposure-specific risks between the Gibb and Luippold cohorts. Finally,
some uncertainty in risk is introduced when extrapolating cohort
exposures to higher Cr(VI) levels for shorter periods to an equivalent
cumulative exposure of lower intensity for a longer duration (e.g., 45
year exposure to 0.25 [mu]g/m3). Despite the uncertainties,
the exposure estimates from the Gibb et al. and Luippold et al. studies
are derived from the best available data and better than is generally
found in retrospective cohort studies. They are more than adequate to
assess occupational risk to
[[Page 59382]]
Cr(VI) and OSHA does not believe the potential inaccuracies in the
exposure assessment for either cohort 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. Linear and non-
linear risk models based on a Poisson distribution were applied to the
exposure-response data sets. Both Environ (Ex. 33-12) and NIOSH (Ex.
33-13) evaluated nonlinear models among the suite of models fit to the
Gibb et al. cohort data. These included quadratic, log-linear, log-
square-root, and log-quadratic models as well as models that included
cumulative dose raised to some power. Cox proportional hazard models
were also applied to the data. Linear models generally fit the
exposure-response data better than the nonlinear models. For most data
sets, there was no indication that any model more elaborate than a
linear model was necessary to describe the exposure-response patterns
observed in these cohorts.
The linear relative risk model was used to estimate excess lung
cancer risks at cumulative Cr(VI) exposures in the range of 0.01 to 2.3
mg/m3-yr (i.e., 0.25-52 [mu]g/m3 for 45 years)
which, to a large extent, overlap the cumulative exposures experienced
of workers in either the Gibb or Luippold cohorts. Certainly,
cumulative exposures above 0.1 mg/m3-yrs (e.g., 2.5 [mu]g/
m3 for 45 years) are within the exposure range of both
studies. Since risks were estimated at cumulative exposures generally
within the range of the data represented in the preferred cohorts, they
are less susceptible to dose-extrapolation uncertainties and less
susceptible to model misspecification. Thus, OSHA believes that the use
of a linear model is a reasonable and appropriate basis on which to
calculate lung cancer risks at the cumulative occupational exposures of
interest, especially given the consistency in the results from fitting
the linear model across most of the studies.
In their response to the OSHA Request For Information regarding
occupational exposure to Cr(VI), the Chrome Coalition submitted
comments, prepared by Exponent, suggesting that a threshold dose-
response model is an appropriate approach to estimate lung cancer risk
from Cr(VI) exposures (Ex. 31-18-1). Their arguments 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/
m3-yr (e.g., roughly equivalent to 20 [mu]g/m3
TWA for a 45 year working lifetime) and below ``a highest reported
eight hour average'' Cr(VI) concentration of 52 [mu]g/m3
(i.e., OSHA PEL); (2) the presumed existence of ``an overall reducing
capacity'' within the lung for extracellular reduction of Cr(VI) to
Cr(III) that must be exceeded before Cr(VI) can damage cellular DNA,
and (3) a reported dose rate effect for lung tumor development in rats
exposed to Cr(VI) by long-term, repeated intratracheal instillations.
The lack of a statistically significant result for a subset of the
entire cohort should not be construed to imply a threshold. As pointed
out in an earlier discussion (section VII.D) and by Crump et al., the
Luippold data set does not have the statistical power to detect small
increases in risk that may be associated with the lower cumulative
exposures in the cohort (Ex. 35-58). In their report, Exponent
acknowledges that the non-significant increase in lung cancer deaths in
the Luippold cohort below 1.25 mg Cr(VI)/m3-yr cumulative
exposure is consistent with predictions from a linear relative risk
model (Ex. 31-18-1, p.25).
The Chrome Coalition characterized the work of De Flora et al. as
providing convincing support for the existence of a threshold exposure
(i.e., exposure below which the probability of disease is zero) for
Cr(VI) carcinogenicity. De Flora et al. determined the amount of
soluble Cr(VI) reduced to Cr(III) in vitro by human bronchioalveolar
fluid and pulmonary alveolar macrophage fractions over a short period
(Ex. 31-18-7). These specific activities were used to estimate an
``overall reducing capacity'' of 0.9-1.8 mg Cr(VI) and 136 mg Cr(VI)
per day per individual for the two preparations, respectively. As
discussed in Health Effects section VI.A., cell membranes are permeable
to Cr(VI) but not Cr(III), so only Cr(VI) enters cells to any
appreciable extent. De Flora et al. 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 the threshold interpretation of De
Flora et al. 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 De Flora 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 De Flora data do not establish the dose range in which
the putative threshold would occur. It has already been shown that a
physiological concentration of ascorbate substantially reduces, but may
not eliminate, the uptake in cells treated with low M concentrations of
Cr(VI) for 24 hours (Ex. 35-68). OSHA does not believe that there is
sufficient scientific evidence to support the Chrome Coalition
conclusion that the De Flora data ``suggest a linear, non-threshold
model to predict cancer risk at low exposure levels [at least, those
being considered by OSHA] is overly conservative and inappropriate''
(Ex. 31-18-1, p.2).
The Chrome Coalition has stated that the intratracheal instillation
study in rats by Steinhoff et al. ``suggests that there is likely a
threshold exposure level below which there is no increase in lung
cancer risk, and that the threshold is compound-specific.'' (Ex. 31-18-
1, p. 2). The Steinhoff study is discussed in detail in section VI.B.
on carcinogenic effects. Briefly, the study showed that rats
intratracheally administered 1.25 mg/kg of soluble sodium dichromate or
slightly soluble calcium chromate once a week for 30 months developed
significant increases (about 17 percent incidence) in lung tumors (Ex.
11-7). The same total dose administered more frequently (e.g., five
times weekly) at a five-fold lower dose level did not increase lung
tumor incidence in the sodium dichromate-treated rats and significantly
increased lung tumor incidence (about 7.5 percent) in the calcium
chromate-treated rats by only about half as much as rats that received
the greater dose level.
OSHA does not believe that the accelerated tumor development at the
high Cr(VI) dose levels in the Steinhoff et al. study ``clearly support
that there is a threshold for Cr(VI) exposures'' or indicate that
``peak exposures high enough to overload the reductive capacity of the
lung may be a better
[[Page 59383]]
predictor of lung cancer risk than lifetime cumulative exposure'' as
stated by Chrome Coalition (Ex. 31-18-1, p. 31). Rather, OSHA believes
these findings should be interpreted to suggest that Cr(VI)-induced
carcinogenesis is 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. For example, the highest dose level (i.e., 1.25 mg/kg) in
the study was reported to cause moderate to severe lung damage,
including inflammation and hyperplasia. It is likely that these effects
caused a proliferative stimulus that accelerated the neoplastic
transformation and expansion of initiated (i.e., genetically altered)
cells. The Steinhoff et al. study also suggests that lung damage is not
an absolute requirement for Cr(VI)-induced tumorigenesis. This is
illustrated by the significant, but smaller, increased tumor incidence
in the animals receiving a lower dose level (i.e., 0.25 mg/kg) of
Cr(VI), as calcium chromate, that caused relatively minor non-
neoplastic changes in the lungs.
OSHA believes that the existence of dose rate effects is supported
by the available scientific evidence and may introduce uncertainty when
projecting lung cancer risk based on workers exposed to higher Cr(VI)
concentrations for shorter durations to workers exposed to the same
cumulative exposure but at substantially lower Cr(VI) concentrations
for substantially longer periods. However, the Steinhoff et al. study
instilled the Cr(VI) compounds directly on the trachea rather than
introduce the test compound by inhalation and was only able to
characterize a significant dose rate effect at one cumulative dose
level (e.g., 1.25 mg/kg). For these reasons, OSHA considers the data
inadequate to reliably determine the human exposures where a dose rate
effect might occur and to confidently predict its magnitude.
OSHA solicits comment on the whether the linear relative risk model
is the most appropriate approach on which to estimate risk associated
with occupational exposure to Cr(VI). OSHA is particularly interested
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 being used in the preliminary
assessment.
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.
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 nonsignificant 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
limited 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, it is reasonable to expect that the excess lung cancer
risks from Cr(VI) exposure predicted by the linear relative risk model
to 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 a heavy smoker. Because there were so few non-smokers in the study
cohorts (e.g., 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 this 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 . 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
[[Page 59384]]
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 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 racial 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 short-term employed workers have higher mortality rates than
workers with long-term employment status. This is possibly due to a
higher proportion of ill individuals and those with a less healthy
lifestyle (Ex. 35-60). As a result, exposure-response analyses based on
mortality of long-term healthy workers will tend underestimate the risk
to short-term workers and vice versa, even when their cumulative
exposure is similar. This might partially explain the higher risk
estimates from the Gibb data set relative to the Luippold data set for
the same cumulative exposures using similar risk models. The Gibb
cohort contained a higher proportion of workers with short duration of
employment, lower cumulative Cr(VI) exposure, and is arguably more
prone to mortality. On the other hand, the Luippold cohort consisted of
longer-term workers at higher cumulative exposures that may be more
prone to negative confounding as a result of the survivor effect. The
healthy worker survivor effect is thought to be less of a factor in
diseases with a multifactorial causation and long onset, such as
cancer.
4. Potency Considerations of Different Cr(VI) Compounds
An issue that needs to be addressed is whether the excess lung
cancer risks derived from epidemiologic data for chromate production
workers are representative of the risks for other Cr(VI)-exposed
workers (e.g., plating, painting, welding operations). Typically, OSHA
has used epidemiologic studies from one industry to estimate risk for
other industries. In many cases, this approach is acceptable because it
is exposure to a common agent of concern that 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 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 VI.B. of the Cancer Effects section and summarized
below, the scientific evidence indicates that the carcinogenic potency
of the highly water-soluble chromates is likely lower than the potency
of other less water-soluble Cr(VI) compounds. Therefore, OSHA believes
that the lung cancer risk of workers in other industries exposed to
equivalent levels of Cr(VI) will be of similar magnitude, or possibly
even greater in the case of some workers exposed to certain Cr(VI)
compounds, than the risks projected from chromate production workers in
the Gibb and Luippold cohorts.
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, it is likely that the Gibb and Luippold cohorts were
principally exposed to water-soluble Cr(VI). The Painesville plant used
a high-lime process known to form some less water-soluble Cr(VI)
compounds (Ex. 35-61). Less water-soluble chromates is a designation
that refers to all chromates not considered to be highly water soluble
and readily captured by an aqueous impinger sampling device. These
would include both slightly water-soluble chromates, such as calcium
and strontium chromate and the more water-insoluble chromates, such as
zinc and lead chromate. The 1953 USPHS survey confirmed 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 Painesville plant subsequently reduced and eliminated
exposure to Cr(VI) roasting residue through improvements in the
production process. The high-lime process was not used at the Baltimore
plant and the 1953 USPHS survey detected minimal levels of less soluble
Cr(VI) at this facility (Ex. 7-17). Proctor et al. estimated that a
proportion of the Luippold cohort prior to 1950 were probably exposed
to the less water-soluble Cr(VI) compounds, but that it would amount to
less than 20 percent of their total Cr(VI) exposure (Ex. 35-61). A
small proportion of workers in the Special Products Division of the
Baltimore plant may also have been exposed to less water-soluble Cr(VI)
compounds during the occasional production of these compounds over the
years.
As discussed in the preamble section VI.B on carcinogenic effects,
both water-soluble and insoluble forms of Cr(VI) compounds are regarded
as carcinogenic to the respiratory tract as a result of inhalation.
This is not only supported by epidemiologic studies of the chromate
production workers above, but also by studies of chromate pigment
workers exposed primarily to the insoluble zinc and lead chromates
(Exs. 7-36; 7-42; 7-49). The standardized lung cancer incidence and
mortality ratios reported among these pigment workers were relatively
high and clearly significant. Langard and Vigander found that the lung
cancer incidence among a cohort of workers exposed primarily to zinc
chromate, but also lead chromate, at a pigment production plant in
[[Page 59385]]
Norway was 44 times what would be expected from an age- and sex-
adjusted Norwegian population (Ex. 7-36). The Davies study found from
2.2-(p< 0.01) to 5.6-fold (p< 0.001) excess lung cancer mortality for
various cohorts of pigment workers exposed to both zinc and lead
chromate at two British factories (Ex. 7-42). Workers in jobs judged to
involve the highest Cr(VI) exposure had the highest risk of lung
cancer. A cohort study of workers exposed to the highly water-soluble
chromic acid during electroplating operations also reported excess lung
cancer mortality (Ex. 35-62). While the lung cancer mortality was
significantly elevated in pigment and electroplating cohorts, there was
inadequate exposure information for risk analysis.
The slightly water-soluble Cr(VI) compounds, calcium and strontium
chromate, led to significant increases in tumors when instilled in the
respiratory tract of experimental animals (Exs. 11-7; 11-2). Levy et
al. reported a bronchial carcinoma incidence of 43 percent (43/99) and
25 percent (25/100) after a single 2 mg intrabronchial instillation of
strontium chromate and calcium chromate, respectively (Ex. 11-2). This
compares with the non-significant bronchial carcinoma incidence of one
percent (1/100) in rats instilled with 2 mg of highly water-soluble
sodium dichromate in the same study. Steinhoff et al. reported a 7.5
percent tumor incidence (6/80, p< 0.01) following repeated intratracheal
instillations of 0.25 mg/kg slightly water-soluble calcium chromate in
rats (Ex. 11-7). The same dosing of the highly water-soluble sodium
dichromate produced no tumor incidence (0/80) in the same study. This
and other evidence led IARC to conclude that there was sufficient
evidence for carcinogenicity in experimental animals of the less water-
soluble strontium chromate, calcium chromate, zinc chromates, and lead
chromates but only limited evidence for carcinogencity in experimental
animals of the highly water-soluble chromic acid and sodium dichromate
(Ex. 18-1, p. 213). Because the above animal studies either used an
inadequate number of dose levels (e.g., single dose level) or employed
a less appropriate route of administration (e.g., tracheal
instillation), it was not possible to determine a reliable quantitative
estimate of risk for human workers breathing these chromates during
occupational exposure. IARC drew the overall conclusion that all Cr(VI)
compounds are carcinogenic to humans based on the combined results of
animal studies, human epidemiological evidence and other data relevant
to the carcinogenic mode of action.
Other studies reported that insoluble Cr(VI) compounds are retained
in the lung for longer periods and are considered a more persistent
source of locally available Cr(VI) for uptake into lung cells than
water-soluble Cr(VI) compounds. Bragt and Van Dura found that water-
soluble sodium chromate is more rapidly absorbed and cleared from the
lung than the highly insoluble lead chromate when intratracheally
instilled in rats (Ex. 35-56). On day 50 after instillation, 13.8
percent of the initial lead chromate remained in the lungs as opposed
to only 3.0 percent of the initial sodium chromate. Research at George
Washington University Medical Center showed that treatment of embryo
cells in culture with insoluble lead chromate particulates led to cell-
enhanced dissolution and uptake of Cr(VI) resulting in DNA damage and
neoplastic transformation (Exs. 35-104; 35-69; 35-132).
Internalization, dissolution, and uptake of lead chromate and the
resulting damage to DNA were later shown to also occur in normal human
lung epithelial cells (Exs. 35-66; 35-327). Elias et al. showed that a
wide range of insoluble lead and zinc chromate pigments could
morphologically transform normal mammalian cells into neoplastic cells
(Ex. 12-5). These studies have led the researchers to suggest that the
less water-soluble Cr(VI) compounds may be more carcinogenic in the
lung than the highly water-soluble Cr(VI) since these insoluble
chromate particulates provide a persistent source of high Cr(VI)
concentration within the immediate microenvironment of the lung cell
surface (Exs. 35-67; 35-149).
Experts have evaluated the combined epidemiologic, animal, and
mechanistic evidence and concluded that the less water-soluble
chromates are likely more carcinogenic than highly water-soluble Cr(VI)
compounds (Exs. 17-101; 17-5B). This is reflected in the lower
recommended ACGIH TLVs for insoluble Cr(VI) compounds (i.e., 10 mg/m3)
and certain slightly soluble Cr(VI) compounds (e.g., 1 mg/m3 for
calcium chromate; 0.5 mg/m3 for strontium chromate) than the
recommended TLV for the water-soluble Cr(VI) compounds (e.g., 50 mg/
m3). For all the reasons cited above, OSHA believes the lung cancer
risk for workers exposed to equivalent levels of Cr(VI) compounds other
than sodium chromate and sodium dichromate over a working lifetime is
likely to be similar in magnitude to the risks projected from the
chromate production workers in the Gibb and Luippold cohorts, or
possibly even greater in the case of inhaled slightly water-soluble and
insoluble Cr(VI) particulates.
OSHA seeks comment on whether its preliminary assessment of risk
based on the exposure-response data from the two cohorts of chromate
production workers is reasonably representative of the risks expected
from equivalent exposures to different Cr(VI) compounds encountered in
other industry sectors. Of particular interest is whether there is
convincing evidence that 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
the lung cancer risk for workers exposed at the same level and duration
to airborne Cr(VI) during welding operations, chromic acid aerosol in
electroplating operations, the less water soluble Cr(VI) particulates
encountered during pigment production and painting operations, or
Cr(VI) exposure in other important industry sectors and job categories.
H. Expert Peer Review of the OSHA Draft Preliminary Quantitative Risk
Assessment
OSHA contracted an independent organization known as Toxicology
Excellence for Risk Assessment (TERA) to organize an external
scientific peer review of the January 21, 2004 Draft Quantitative Risk
Assessment (Exs. 36-1-1; 36-1-2). TERA selected three peer reviewers
based on a high level of competence in occupational epidemiology and/or
risk assessment. The reviewers were screened to ensure no apparent
conflict of interest or involvement in the key studies that provided
the basis for the OSHA assessment. OSHA did not participate in the
selection process other than to examine reviewer credentials to confirm
their qualifications. The three peer reviewers selected by TERA were
Dr. David Gaylor, Dr. Allan Smith, and Dr. Irva Hertz-Picciotto.
Curriculum Vitae of the three reviewers have been submitted to the
docket (Ex. 36-1-3).
TERA provided the peer reviewers with a review package that
consisted of the draft quantitative risk assessment, copies of the key
studies, and a set of instructions and questions (Ex. 36-1-1). The
reviewers were asked to comment on several aspects of the draft OSHA
risk assessment including the suitability of the different data sets
for exposure-response analysis, the choice of exposure metric and risk
models, the appropriateness of the risk estimates, and the
characterization of key issues and uncertainties. The peer reviewers
filed written draft reports with TERA
[[Page 59386]]
which then reviewed the comments for completeness before passing the
reports on to OSHA (Ex. 36-1-4). OSHA requested clarification in
writing on some of the reviewer responses. These were addressed by the
peer reviewers in their final peer review reports or answered in an
attachment (Ex. 36-1-4-3). The clarification process with the reviewers
was handled by TERA.
The three peer reviewers agreed that the results from six
occupational cohorts under review were adequately evaluated as to their
suitability for exposure-response analysis and concurred that the Gibb
and Luippold cohorts provided the strongest data sets for quantitative
assessment. There was general agreement among the peer reviewers that
the risk models and statistical methodologies used in the OSHA
assessment were appropriately applied. Dr. Smith remarked that ``there
is no question in my mind that relative risk models are superior to
others when conducting quantitative cancer risk assessments on
epidemiological data'' (Ex. 36-1-4-2) and commended OSHA for supporting
a relatively straightforward [linear] model widely used in epidemiology
(Ex. 36-1-4-2). At his suggestion, OSHA expanded on reasons for using a
linear relative risk model to fit the epidemiological data. The
selection of the linear relative risk model was not solely based on
mathematical fit. Relative risk models inherently adjust for age-
related increases in cancer incidence. The linear relative risk model
has been extensively and successfully used to analyze other cancer
mortality data sets and is an accepted approach in carcinogen risk
assessment.
The peer reviewers were also in general agreement that cumulative
exposure based on time-weighted average air concentrations by job title
and employment history was a reasonable exposure metric to use. Dr.
Hertz-Picciotto stated ``the use of cumulative exposure constructed in
this way is currently the standard, and the use of individual job
histories is the best available method at this time (Ex. 36-1-4-4).''
She pointed out that the underlying assumption that exposure patterns
and dose rate differences at equivalent cumulative exposures do not
influence cancer risk is an uncertainty in the assessment. This is more
fully explained in section VII.G.1 on uncertainties with regard to
worker exposure.
Dr. Smith raised another limitation to the cumulative exposure
metric as it relates to relative risk. It has been shown, in some
instances, that relative risk of chronic disease will not continue to
rise at high cumulative exposure but will tend to stabilize or
attenuate. In the case of a significant attenuation, the excess risk at
high Cr(VI) exposures (e.g., working lifetime at the current OSHA PEL)
could be overestimated by a linear relative risk model. Environ
examined this possibility by fitting the Gibb and Luippold data sets to
a power model that requires the exposure-response to rise steeply at
low exposure and level out at high exposure (Ex. 36-2). The power model
did not significantly improve the fit compared to the linear relative
risk model for either data set. This analysis would not support a
significant attenuation in the relative risk of lung cancer with
increasing cumulative Cr(VI) exposure. Therefore, OSHA does not find
adequate reason to believe its linear relative risk model would
overpredict the lung cancer risk at the OSHA PEL or other cumulative
exposures in the range of interest. OSHA revised its preliminary
quantitative risk assessment to fully address this issue in section
VII.G.1.
The peer reviewers showed less enthusiasm for the highest reported
average monthly Cr(VI) air concentration as an appropriate exposure
metric or for an exposure threshold below which there exists no lung
cancer risk. Dr. Hertz-Picciotto remarked that ``the newly published
Crump et al. (2003) uses the monthly maximum [Cr(VI) concentration],
but fails to take duration into account, and the authors note
considerable variability was present in duration at the highest monthly
exposure'' and ``the inadequacy of the attempt to prove a threshold is
excellently presented [by OSHA]'' (Ex. 36-1-4-4). Dr. Gaylor stated ``a
threshold concentration or threshold cumulative exposure to Cr(VI)
below which no excess lung cancer is expected cannot be established
from the available information (Ex. 36-1-4-1).'' Dr. Smith added ``the
[OSHA] reasons given for dismissing Exponent's threshold inference are
valid. I would add [Exponent's] assessment ignores duration of
exposure. For example, it is unlikely one could detect increased lung
cancer risks in smokers whose `peak exposure' was a quarter pack per
day if they only smoked for three years. This would not mean that a
quarter pack per day is a threshold (Ex. 36-1-4-2).''
The peer reviewers found the range of excess lifetime risks of lung
cancer presented by OSHA to be sound and reasonable. These preferred
risk estimates were those bounded by the maximum likelihood estimates
determined from the featured Gibb and Luippold data sets. Dr. Gaylor
wrote ``the confidence limits are tighter for the Luippold study,
somewhat over a factor of two for the range from the lower to the upper
95% confidence limit, compared to a range of about 3.5 for the
confidence limits in the Gibb study. However, the Gibb cohort is larger
than the Luippold cohort. It appears reasonable to consider the two
studies jointly to provide estimates of lung cancer risk'' (Ex. 36-1-4-
1). Dr. Gaylor went on to point out that the range of maximum
likelihood between the featured data sets understates the [statistical]
uncertainty in the risk estimates. He recommended that the uncertainty
be expressed as the lower 95% confidence limit from the Luippold data
set and the 95% upper confidence limit for the Gibb data set. OSHA
agrees and has revised section VII.F to make clear that while the
maximum likelihood range represents the most likely estimates of lung
cancer risk, the 95% confidence bounds are the better representation of
statistical uncertainty.
Dr. Gaylor suggested that the OSHA assessment make clear that the
45-year working lifetime exposure should be regarded as a worst case
scenario and that the typical worker would be exposed to Cr(VI) for a
shorter period of time. Dr. Smith also questioned the need to estimate
risk from a 45-year working lifetime. He suggested that OSHA could
probably make more confident estimates of risk for shorter exposure
durations (e.g., ten years) within the range observed in the cohort
studies. This would avoid the uncertainties of an upward extrapolation.
OSHA does not disagree with these comments. However, the OSH Act is
clear on the agency statutory obligation to consider the risk of
material impairment from regular exposure to the hazardous agent for a
full working life. The risk of lung cancer from Cr(VI) exposures for
less than a full working lifetime are discussed in section VIII on
Significance of Risk and section IX on Benefits Analysis.
Dr. Hertz-Picciotto felt that OSHA may have overstated the
consistency in lung cancer risk between the two primary studies and the
four weaker supporting studies. She pointed out that two of the
supporting cohorts overlapped the featured cohorts and were not truly
independent data sets. She indicated that the weaker supporting studies
had serious bias that rendered the discussion of overlap in confidence
intervals to be relatively meaningless and, thus, prevented a
definitive evaluation of consistency. OSHA agrees that the magnitude
and direction of potential bias introduced by lack of exposure data,
inadequate follow-up, and other limitations in the
[[Page 59387]]
supporting studies prevents strong statements regarding consistency
among risks estimates. However, OSHA believes the finding that its risk
predictions based on the Gibb and Luippold data sets are within a
statistical precision that is compatible with other exposure-response
data sets enhances confidence in the estimates. OSHA notes that there
was no overlap in the Mancuso and Luippold cohorts, even though they
worked at the same plant, due to vastly different selection criteria
and exposure estimation based on different industrial hygiene surveys.
The Hayes and Gibb cohort have some overlap but the cohorts primarily
worked at different facilities and exposure estimates were, again,
based on different monitoring surveys. In the case of both cohort
pairs, statistical comparisons show that the risk estimates from one
data set would not be consistent with the other data set at the 95%
confidence level. OSHA believes the risks from the different cohorts
can be considered independent estimates. OSHA has revised sections
VII.E and VII.F to clarify the positions discussed above.
Dr. Smith suggested that OSHA consider presenting risk estimates
that can be readily calculated from the source data without use of a
complex mathematical model. He contends that this would allow the
reader to better understand how the risks relate to measures reported
in the published studies. He provided some illustrations of simple and
transparent risk estimations from the Gibb et al. study. OSHA agrees
there is merit to comparing risk estimates easily calculated from the
cohort mortality data with the more precise estimates determined from
the linear relative risk model as a kind of ``reality check''. OSHA has
included such calculations in sections VII.C.4 for the Gibb data set
and section VII.D for the Luippold data set.
OSHA does not agree with assertions by Dr. Smith that ``there is no
valid basis to conclude that more complex calculations [from
mathematical models], such as found in the source material and draft
[OSHA] document, have any greater validity than this estimate [directly
calculated from the published cohort data]'' and ``there is no gain in
validity in doing a full life table analysis but there is certainly a
loss in transparency (Ex. 36-1-4-2).'' OSHA believes excess risk
estimated from standard, well-supported mathematical model constructs
that incorporate the entire mortality data set is considerably more
accurate, more robust, more stable and more statistically rigorous than
a simple calculation from a single relative risk result determined from
a small subset of the cohort data as applied by Dr. Smith. The life
table analysis adjusts for both the increasing probability of
developing lung cancer with advancing age and the competing risk of
death from other causes. These age-related factors are not accounted
for in a simple relative risk calculation and may lead to a less
accurate risk estimate.
While the peer reviewers felt that most uncertainties in the risk
assessment were adequately characterized, they suggested certain topics
receive more attention. Dr. Hertz-Picciotto suggested that sensitivity
analyses on plausible alternate exposure assumptions for workers in the
Gibb and Luippold cohorts during the periods when there was very
limited air monitoring data ``would add concrete information on the
magnitude of uncertainty in the risk estimates (Ex. 36-1-4-4).''
Environ, while under contract with OSHA, had access to annual exposure
estimates on individual workers in the Gibb cohort. They explored the
feasibility of generating plausible alterative exposures using a
forward and reverse replacement scheme for the air concentrations
imputed during periods in the Gibb et al. study when air monitoring was
unavailable (Ex. 36-2). Unfortunately, lack of job title information
and job-specific monitoring data combined with apparent high job
transfer and turnover among workers made this approach impracticable
for estimating plausible exposures that could lead to a meaningful
analysis. OSHA did not have access to individual exposure data for the
Luippold cohort.
Dr. Hertz-Picciotto recommended that OSHA address the potential
impact on risk of the healthy worker survivor effect. The healthy
worker survivor effect refers to a common observation that long-term
workers have been found to have lower mortality than short-term
workers. 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. This healthy worker effect may partially
explain the higher risk estimates for the same cumulative exposures
from the Gibb cohort, which included a higher proportion of workers
with short exposure duration, relative to the Luippold cohort of
longer-term workers. The healthy worker survivor effect may have also
influenced risks estimated from the Mancuso cohort. OSHA agrees that
the healthy worker survivor effect contributes to the uncertainty in
the risk estimates and has included a discussion in section VII.G.3 on
issues and uncertainties and in the section VII.E.1 on the Mancuso data
set.
Dr. Smith thought that some important issues surrounding smoking
needed to be better addressed in the preliminary risk assessment
document. He agreed that OSHA adequately discussed the confounding due
to smoking but suggested that it be made clear that the linear relative
risk model, in the absence of any explicit interaction term between
smoking and Cr(VI), implicitly assumes a synergy (i.e., lung cancer
risk from smoking and Cr(VI) together is greater than the sum of the
risks from either agent alone) between the two exposures. OSHA believes
Dr. Smith has a valid point. Although the 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 the
background lung cancer rate reflects a mixture of smokers and non-
smokers, the expectation is that the projected OSHA risks from Cr(VI)
exposure are overestimated for a non-smoker to some unknown extent. By
the same token, the model may underestimate the risk from Cr(VI)
exposure to a heavy smoker. A discussion of this has been included in
section VII.G.3.
Finally, the peer reviewers believed that OSHA adequately presented
its position that workers in the Gibb and Luippold cohorts were
primarily exposed to the less carcinogenic, highly water-soluble Cr(VI)
compounds and that the lung cancer risks for workers exposed to
equivalent levels of other Cr(VI) compounds will be of a similar
magnitude and possibly greater in the case of certain less water-
soluble Cr(VI). However, the peer reviewers stated that they lacked the
expertise in toxicology and experimental carcinogenesis to critically
evaluate its consistency with the existing scientific data. OSHA has
made it clear in section VII.G.4 that the animal studies demonstrating
higher carcinogenic potency for sparingly water-soluble Cr(VI), such as
calcium chromate and strontium chromates, can not provide reliable
quantitative estimates of human risk. This is because the studies
employed an inadequate
[[Page 59388]]
number of dose levels or the studies employed routes of administration
(e.g., intratracheal instillation) less relevant to occupational
exposure.
I. Preliminary 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 four
other supporting data sets. 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. data sets and a linear relative risk model, OSHA
preliminarily 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 six 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. 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. 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.
Finally, as previously discussed, linear (and some non-linear) no-
threshold risk models adequately fit the existing exposure-response
data.
The Gibb and Luippold cohorts were predominantly exposed to water-
soluble chromates, particularly sodium dichromate. The scientific
evidence indicates that the water-soluble Cr(VI) compounds are
generally less potent carcinogens than slightly-water soluble and
water-insoluble Cr(VI) compounds. These less water-soluble Cr(VI)
compounds are retained in the lung for longer periods, are more likely
to concentrate at the lung cell surface, and are a more persistent
source of locally available Cr(VI) for uptake into target cells than
the highly water-soluble Cr(VI) compounds. Risks estimated from
chromate production workers primarily exposed to water-soluble
chromates in the Gibb and Luippold cohorts should adequately represent
risks to workers exposed to other water-soluble Cr(VI) compounds. OSHA
believes that workers exposed to equivalent levels of the potentially
more carcinogenic, less water-soluble Cr(VI) compounds may even be at
greater risk of lung cancer than predicted from the Gibb and Luippold
cohorts.
As with any risk assessment, there is some degree of uncertainty in
the projected risks that result 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 to higher Cr(VI) levels for shorter periods to an equivalent
cumulative exposure of lower intensity and longer duration of interest
to OSHA. The study cohorts were mostly 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 the 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 preliminary estimate of lung cancer risk from a 45 year
occupational exposure to Cr(VI) at an 8-hour TWA at the current PEL of
52 [mu]g/m3 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 uncertainty due to the
statistical nature of the analyses, or for other potential sources of
uncertainty or bias. The wider range of 62 to 493 per 1000 represents
the statistical uncertainty associated with OSHA's excess risk estimate
at the current 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 are shown in Table VI-8, together with the
uncertainty bounds for the primary and supporting studies at these
exposure concentrations. The excess lung cancer risks at alternate 8
hour TWA PELs under consideration by the Agency are shown in Table VI-
8. For example, OSHA s best estimate of excess risk from 45 years'
exposure at 1 [mu]g/m3 Cr(VI) is 2.1 to 4.6 per 1000; an
interval of 1.2- 16 per 1000 represents the statistical uncertainty of
OSHA s estimate. 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 VIII on the Significance of Risk and in Section IX. on the
Benefits Analysis.
VIII. 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, jointly
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 for the cause of worker
protection 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)
[[Page 59389]]
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
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 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 should be supported by
substantial evidence, the Agency ``is not required to support the
finding that a significant risk exists with anything approaching
scientific certainty''. 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 in ``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 preliminary quantitative
estimates of the excess lung cancer risk associated with currently
allowable Cr(VI) exposure concentrations and the expected impact of the
proposed PEL. OSHA has preliminarily determined that long-term exposure
at the current PEL causes significant risk to workers' health, and that
adoption of the proposed PEL will significantly reduce this risk.
A. Material Impairment of Health
As discussed in Section VI of this preamble, inhalation exposure to
Cr(VI) causes a variety of adverse health effects, including lung
cancer, nasal septum damage, and asthma. 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 Cr(VI) inhalation
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.
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).
While OSHA has relied primarily on the association between Cr(VI)
inhalation and lung cancer to demonstrate the necessity of the proposed
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 nasal passage atrophy, ulceration, and septum
perforation (Exs. 35-1; 7-3; 9-126; 35-10; 9-18; 3-84; 7-50; 31-22-12).
Septum ulcerations are often accompanied by swelling and bleeding, heal
slowly, and in some cases may progress to a permanent perforation that
can only be repaired surgically. Inhalation of Cr(VI) can also lead to
occupational 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 occupational asthma from Cr(VI) exposure, confirming Cr(VI)
as the sensitizing agent by bronchial challenge (Exs. 35-7; 35-12; 35-
16; 35-21).
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 current PEL, as well as the expected reduction of
risk that would occur with implementation of the proposed 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
preliminarily identified a range of expected risk from regular
occupational exposure at the current PEL (101-351 excess lung cancer
deaths per 1000 workers) and at the proposed PEL of 1 [mu]g/
m3 (2.1-9.1 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 on two extensively
studied worker populations,
[[Page 59390]]
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 preliminary 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. 25). 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 particularly 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 very strong basis for risk analysis, in that it
has high-quality documentation of worker Cr(VI) exposure and mortality,
a long period of followup, and a large proportion of relatively long-
term employees (55% > 5 years).
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 VII, the
Environ, Park et al., and linear Exponent models yield similar
predictions of excess risk from exposure at the current and proposed
PELs (see Tables VII-3 and VII-4). OSHA's preferred model predicts
about 350 excess lung cancers per 1000 workers exposed for a working
lifetime of 45 years at the current PEL (MLE 351, 95% CI 181-493) when
person-years of exposure are spread evenly across exposure groups (see
Table VII-3). Implementation of the proposed PEL is expected to reduce
this risk to about 10 excess lung cancers per 1000 workers (MLE 9.1,
95% CI 4-16).
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. The
linear models by all of the analyst groups 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 current PEL (MLE 101, 95% CI 62-
147), and two excess lung cancer deaths per 1000 workers exposed for 45
years at the proposed PEL (MLE 2.1, 95% CI 1.2-3.1).
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 current PEL and
2.1-9.1 per 1000 for 45 years' occupational exposure at the proposed
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 and the primary
supporting studies were submitted, which generally supported the
Agency's approach and results.
Although nasal damage and asthma are well-established effects of
occupational exposure to airborne Cr(VI), OSHA has preliminarily
determined that there are no adequate studies to support a quantitative
risk assessment for these effects. 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 with specific occupational exposure conditions, the Agency has
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
septum ulcerations 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 with ulcerations 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 appeared to develop over relatively long
periods of exposure (median time 172 days from hire date to diagnosis).
Another important study, Lindberg and Hedenstierna's 1983
examination of nasal effects among Swedish chrome platers,
characterizes the prevalence of nasal irritation, atrophy, ulceration,
and perforation among workers exposed to various concentrations of
Cr(VI) (Ex. 9-126). Workers' daily average exposure concentrations were
measured as 8-hour averages using personal air samplers, and estimates
of workers' peak exposures were derived from 6-hour average
concentrations collected with stationary equipment near the chrome
electroplating baths. Among 43 workers exposed almost exclusively to
Cr(VI), septum ulceration and perforation were not observed among those
exposed to peak exposures less than 20 [mu]g/m3 or those
exposed to 8-hour average concentrations less than 2 [mu]g/
m3, a result used by the EPA to identify a lowest-observed
adverse effect level (LOAEL) for their inhalation reference
[[Page 59391]]
concentration (Ex. 35-156). Nasal septum atrophy, a condition that can
progress to ulceration and perforation, was observed less frequently
among workers with 8-hour mean exposure concentrations less than 2
[mu]g/m3 and those with peak exposures less than 20 [mu]g/
m3 than among workers exposed to higher concentrations. It
is not clear whether workers who had nasal septum atrophy at these
exposure levels eventually developed ulcerations or perforations.
Although Lindberg and Hedenstierna's results suggest increasing risk of
nasal septum damage with increasing exposure concentrations, there are
considerable uncertainties associated with the cross-sectional study
design and the possible contribution of hand-to-nose transfer of Cr(VI)
to the observed nasal effects.
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 VIII-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 done in
significant risk determinations for previous standards, the Agency
preliminarily finds an excess lung cancer risk of approximately 100 to
350 per 1000 workers exposed at the current 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 proposed PEL of 1 [mu]g/m3 Cr(VI) is
expected to reduce these risks substantially, to below 10 excess lung
cancers per 1000 workers. However, even at the proposed PEL, the risk
posed to workers with a lifetime of regular exposure is still clearly
significant.
Table VIII-1.--Expected Excess Lung Cancer Deaths Per 1000 Workers
----------------------------------------------------------------------------------------------------------------
Cr(VI)
concentratin, 20-year 45-year
[mu]g/m3 exposure exposure
----------------------------------------------------------------------------------------------------------------
Current PEL............................................... 52 43-198 101-351
20 17-83 41-164
10 9-43 21-86
5.0 4.3-22 10-45
2.5 2.1-11 5.3-23
Proposed PEL.............................................. 1.0 0.85-4.4 2.1-9.1
0.5 0.43-2.2 1.1-4.6
0.25 0.21-1.1 0.53-2.3
----------------------------------------------------------------------------------------------------------------
Workers exposed to lower concentrations of Cr(VI) and for shorter
periods of time may also have significant excess cancer risk. OSHA's
estimates of risk are therefore proportional to concentration for any
given exposure duration; for example, workers exposed for 20 years to
10 [mu]g/m3 Cr(VI) have about ten times the risk of workers
exposed for 20 years to 1 [mu]g/m3 Cr(VI). The Agency's risk
estimates are also roughly proportional to duration for any given
exposure concentration, but not exactly proportional due to competing
mortality effects. 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 current PEL for five years are expected to die
from lung cancer as a result of their exposure. Those exposed to 5
[mu]g/m3 Cr(VI) for 5 years have an estimated excess risk of
1-6 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 current standard; even workers exposed for shorter periods at
levels below the current PEL are at substantial risk, and will benefit
from implementation of the proposed 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
[[Page 59392]]
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
VIII-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. For example, OSHA's best
estimate of excess lung cancer deaths per 1000 workers from regular
occupational exposure to Cr(VI) in the range of 2.5-5 [mu]g/
m3 is roughly comparable to the average number of fatal
injuries in high-risk occupations such as mining, assuming the same
duration of employment (see Table VIII-1). Regular exposures at higher
levels, including the current 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 proposed PEL of 1 [mu]g/m3 Cr(VI) the Agency's
estimate of excess lung cancer mortality falls much closer to the
private industry average fatal injury rate, given the same employment
time, but still exceeds the rates found in lower-risk industries such
as finance and health services.
Table VIII-2.--Fatal Inuries per 1000 Employees, by Industry
----------------------------------------------------------------------------------------------------------------
Over 1 year Over 20 years Over 45 years
----------------------------------------------------------------------------------------------------------------
All Private Industry...................................... 0.06 1.1 2.5
Coal Mining............................................... 0.41 8.3 18.6
Mining (General).......................................... 0.27 5.5 12.3
Construction.............................................. 0.19 3.9 8.7
Manufacturing............................................. 0.04 0.8 1.8
Wholesale Trade........................................... 0.04 0.8 1.7
Retail Trade.............................................. 0.03 0.6 1.4
Finance, Insurance, and Real Estate....................... 0.02 0.3 0.7
Health Services........................................... 0.01 0.2 0.4
----------------------------------------------------------------------------------------------------------------
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 VIII-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.
Table VIII-3.--Selected OSHA Risk Estimates (Excess Cancers per 1000 Workers)
----------------------------------------------------------------------------------------------------------------
Standard Risk at prior PEL Risk at current PEL Federal Register date
----------------------------------------------------------------------------------------------------------------
Ethylene Oxide................. 63-109 per 1000........ 1.2-2.3 per 1000....... June 22, 1984.
Asbestos....................... 64 per 1000............ 6.7 per 1000........... June 20, 1986.
Benzene........................ 95 per 1000............ 10 per 1000............ September 11, 1987.
Formaldehyde................... 0.4-6.2 per 1000....... .0056 per 1000......... December 4, 1987.
Formaldehyde................... * .0056 per 1000....... * < .0056 per 1000...... May 27, 1992.
Methylenedianiline............. ** 6-30 per 1000....... 0.8 per 1000........... August 10, 1992.
Cadmium........................ 58-157 per 1000........ 3-15 per 1000.......... September 14, 1992.
1,3-Butadiene.................. 11.2-59.4 per 1000..... 1.3-8.1 per 1000....... November 4, 1996.
Methylene Chloride............. 126 per 1000........... 3.6 per 1000........... January 10, 1997.
Chromium VI.................... ....................... 106-351 per 1000....... October 2004
----------------------------------------------------------------------------------------------------------------
* From information in December 4, 1987 Federal Register.
** No prior standard; reported risk is based on estimated exposures at the time of the rulemaking.
At 106-351 excess lung cancer deaths per 1000 workers, the
estimated risk from lifetime occupational exposure to Cr(VI) at the
current PEL is much higher than the estimated risk from permissible
exposures to other workplace carcinogens for which OSHA has performed
risk assessments (Table VIII-3, ``Risk at Current PEL''). The Cr(VI)
risk estimate is also higher than many risks the Agency has found to be
significant in previous rules (Table VIII-3, ``Risk at Prior PEL'').
The estimated risk from lifetime occupational exposure to Cr(VI) at the
proposed PEL is 2.2-9.1 excess lung cancer deaths per 1000 workers, a
range comparable to the risks from other carcinogenic exposures
remaining under recent rules (Table VIII-3, ``Risk at Current 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 preliminarily finds
that the risk of lung cancer posed to workers under currently
permissible levels of occupational Cr(VI) exposure is significant. The
proposed PEL of 1 [mu]g/m3 is expected to significantly
reduce risks to workers in Cr(VI)-exposed occupations. OSHA
additionally finds that nasal septum ulceration and
[[Page 59393]]
perforation can occur with significant frequency and seriousness in
exposure conditions allowed by the current rule. The proposed reduction
of the Cr(VI) PEL from 52 [mu]g/m3 to 1 [mu]g/m3
is expected to substantially reduce or eliminate workers' risk of these
adverse health effects.
IX. Summary of the Preliminary Economic Analysis and Initial Regulatory
Flexibility Analysis
A. Introduction
OSHA's Preliminary Economic and Initial Regulatory Flexibility
Analysis (PEA) addresses issues related to the costs, benefits,
technological and economic feasibility, and the economic impacts
(including small business impacts) of the Agency's Occupational
Exposure to Hexavalent Chromium rule. The full Preliminary Economic and
Regulatory Flexibility Analysis has been placed in the docket as Ex.
35-391. The analysis also evaluates regulatory alternatives to the
proposed rule. This rule is an economically significant rule under
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 Preliminary Economic and Regulatory Flexibility
Analysis is to:
Identify the establishments and industries potentially
affected by the proposed 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 proposed standard;
Assess the economic feasibility of the rule for affected
industries; and
Evaluate the principal regulatory alternatives to the
proposed rule that OSHA has considered.
The Full Preliminary 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. Regulatory Flexibility Analysis
Chapter VIII. Environmental Impacts
Chapter IX. Non Regulatory Alternatives.
These chapters are summarized in sections B to G of this Preamble
summary.
B. Introduction and Industrial Profile (Chapters I and II)
The proposed 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) can also lead to asthma. To protect exposed workers
from these effects, OSHA has set a Permissible Exposure Limit (PEL) of
1 [mu]g/m3 measured as an 8-hour time weighted average. OSHA
has also examined alternative PELs ranging from 20 [mu]g/m3
to 0.25 [mu]g/m3 measured as 8-hour time weighted averages.
OSHA's proposed 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 proposal requires employers to:
Monitor the exposure of employees (except in shipyards and
construction);
Establish regulated areas when exposures may reasonably be
expected to exceed the PEL (except in shipyards and constructions);
Implement engineering and work practice controls to reduce
employee exposures to Cr(VI);
Provide respiratory protection to supplement engineering
and work practice controls where they are not feasible, where such
controls are insufficient to meet the PELS, 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 PEL in general industry (In the shipyard and construction
sectors, medical exposure is only required for signs or symptoms of
Cr(VI) related disease);
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 proposing the
separate standards for general industry, construction and shipyard
employment, are more fully discussed the Summary and Explanation
Section of this Preamble.
Chapter II of the full PEA 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 analysis 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. One complication
with the use of the application group concept is that some firms may
have exposures in two or more different application groups. For
example, a large transportation equipment company may engage in
chromium electroplating, painting with paints that use chromium
pigments, and welding of metal containing chromium.
The most common reasons to encounter 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, such as stainless steel or other high chromium
steels, or with chromium coatings; 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 sharp declines 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 PEA. Painting activities in General
Industry primarily
[[Page 59394]]
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 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.
Table IX-1 shows the application groups analyzed in OSHA's PEA, as
well as the principle 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. (This
table provides the latest available data at the time this analysis was
produced. However, since the analysis was produced, there have been
changes to some of the affected industries. OSHA will continue to
incorporate more recent data as it becomes available.) As shown in the
table, there are a total of 38,000 to 55,000 establishments, depending
on the degree of overlap between application groups in some industries,
affected by the proposed standard.
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[[Page 59403]]
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Various types of welding applications account for the greatest
number of establishments and number of employees affected by the
proposed standard.
[[Page 59404]]
Table IX-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 was 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, and interested
parties.
In all sectors OSHA has used the best available information to
determine baseline exposures and technological feasibility. In a few
sectors this information has been difficult to obtain and OSHA has had
to rely on limited data in the industry or used analogous operations
from similar processes. In these cases OSHA (or its contractor)
discussed issues with industry experts and used their professional
judgment to determine technological feasibility. The sectors that fall
into the above categories are steel mills, welding in construction,
woodworking and catalyst users.
Data obtained for steel mills included several sources such as
NIOSH HHEs, IMIS exposure data and a site visit from IT Corporation, an
OSHA contractor. OSHA's contractor could only obtain permission to
conduct a site visit at a steel mill that used the teeming and primary
rolling method versus continuous casting which is now used in
approximately 95% of the steel mills. OSHA acknowledges this and uses
exposures from analogous operations with additional information from
industry experts. OSHA requests worker exposure information from steel
mills using the continuous casting process. Exposure information was
also limited for welding at construction sites. OSHA could use
analogous operations from welding in maritime in open spaces. This
could give a more detailed distribution for the baseline exposure
profile. OSHA requests comments on the use of the Maritime data as an
analogous operation for welding at construction sites.
In several sectors, such as woodworking and catalyst use, OSHA
anticipates that airborne exposures will be low. In these cases
exposure monitoring has been performed infrequently. OSHA then used
professional judgment or has calculated exposure using total dust
exposure to estimate employees' exposures to Cr(VI).
OSHA's analysis of technological feasibility analyzes employee
exposures at the operation or task level to the extent that such data
are available. There are a total of 380,000 workers exposed to Cr(VI),
of which 84,000 are exposed above the proposed PEL of 1 microgram per
cubic meter.
[[Continued on page 59405]]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
]
[[pp. 59405-59454]] Occupational Exposure to Hexavalent Chromium
[[Continued from page 59404]]
[[Page 59405]]
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[[Page 59406]]
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C. Technological Feasibility
In Chapter II of OSHA's PEA, OSHA also assesses the technological
feasibility of the proposed standard across a range of potential PELs
in all affected industry sectors.
Many employers, and some entire application groups already have
nearly all exposures below the proposed PEL. However, OSHA recognizes
that some employers in some application groups may not be able to
achieve the proposed PEL with engineering controls and work practices
for all job categories and may need to use respirators.
In general, OSHA considered the following kinds of possible
controls that could reduce employee exposures to Cr(VI): Local exhaust
ventilation (LEV) which could include the maintenance or upgrade of the
current LEV or installation of additional LEV; process enclosures that
would isolate the worker
[[Page 59407]]
from the exposure; process modifications that would reduce the
generation of Cr(VI) dust or fume in the work place; improved
housekeeping; improved work practices; and the supplemental use of
respiratory protection if engineering controls are not sufficient to
meet the proposed 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 what PELs they can achieve is based on information
collected by Shaw Environmental, Inc., consultant to OSHA, on current
exposure levels and associated existing controls, on the availability
of additional controls needed to reduce employee exposures and on other
evidence presented in the docket.
OSHA has determined that the primary controls most likely to be
effective in reducing employee exposure to Cr(VI) are LEV, process
enclosure and process modification, or substitution. In some cases,
firms need not improve their local exhaust systems, but instead must
spend more effort insuring that the exhaust system is working according
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.
Examples of processes that would need to improve, maintain, or install
LEV include hard chrome plating and welding processes that generate
large volumes of fume such as shielded metal arc welding (SMAW) and gas
metal arc welding (GMAW). (LEV is defined to include portable LEV
systems such as fume extraction guns (FEG).) Other sectors where new or
better maintained LEV may be needed are: painting and abrasive
blasting, chromate production, the production of pigments, catalyst,
dyes and plastic colorants.
OSHA estimates that process enclosures will be needed 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. For example, the packaging of chromic acid in small
bags is totally enclosed and therefore, employees only need to enter
the room during product upset or planned changes. This technology could
also be applied to other packaging operations involving similar sized
bags in other industries such as pigment manufacturing, catalyst
production and plastic colorants. Process modifications can also be
effective in reducing exposures in some industries. For example,
employers can significantly reduce employee exposure through the use of
automation in catalyst production, the use of fume suppressants in
electroplating and significant reduction of welding fume emission, by
up to 80 percent, is attainable using the pulsed arc GMAW welding
process as compared to the conventional short arc GMAW process.
OSHA recognizes that there are certain instances where the
supplemental use of respirators may be needed because engineering and
work practices are not sufficient to reduce airborne exposures below
the proposed PEL. For example, this is the case for hard chrome
electroplating in some circumstances. There are many factors that are
involved in the generation of Cr(VI) including the size of the part and
the thickness of the coating needed. In some worst case conditions,
respirators will be needed to supplement engineering controls. Welding
also includes many factors that contribute to Cr(VI) exposures; these
include type of welding, the base metal, the consumable, as well as the
environment in which the welding is being conducted. As a result,
engineering controls and work practices may not be sufficient in the
most severe conditions and therefore the supplemental use of
respirators will be needed. Table IX-3 shows OSHA's estimate of
respirator use by industry for each of the proposed PELs.
Table IX-3 identifies sectors where respirators will be needed for
some workers. Even at a PEL of 1 [mu]g/m\3\, a majority of exposed
workers in the chromium catalyst user application group will need
respirators, but this use is largely intermittent. As a result, workers
will not need to wear respirators on a daily basis.
PELs lower than 1 [mu]g/m3 could not be achieved by
means of engineering controls and work practices alone for some types
of welding (particularly GMAW and SMAW) and in hard chromium plating.
Based on this finding, OSHA has preliminarily determined that a PEL of
1 [mu]g/m3 is the lowest technologically feasible level.
For a complete analysis of technical feasibility please see the
Preliminary Economic Analysis, Chapter III, where feasibility is
reviewed for each industry/process by job category.
[[Page 59408]]
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[[Page 59409]]
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D. Costs
The costs employers are expected to incur to comply with the
proposed standard are $223 million per year. In addition, OSHA
estimates that employers will incur $67 million per year to comply with
the personal protective equipment and hygiene requirements already
present in existing generic standards. The proposed requirements to
provide protective clothing and equipment and hygiene
[[Page 59410]]
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 were 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 $67 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, by incurring the
obligation and expense of providing PPE to their employees, employers
are essentially transferring a benefit to employees $24 million per
year.
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 III of the full PEA.
Table IX-4 provides the annualized costs by provision and by industry.
Engineering control costs represent 45 percent of the costs of the new
provisions of the proposed standard, and respiratory protection costs
represent 19 percent of the costs of the new provisions of the proposed
standard.
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[[Page 59413]]
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Costs for the new provisions for General Industry are $179 million
per year, costs for constructions $35 million per year, and costs for
the shipyard sector and $9 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
[[Page 59414]]
general industry standard. OSHA seeks comment on the extent to which
welding, painting, and wood working done by construction firms might be
covered by the general industry standard.) Table IX-4 also shows the
costs by application group. The various types of welding represent the
most expensive application group, accounting for 47 percent of the
total costs.
OSHA also presents the distribution of compliance costs according
at the time they are imposed in Table IX-5. Because firms will have the
choice of whether to finance expenditures in order to spread out, for
example, startup costs over several 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 and the time distribution of imposed
costs, in addition to the annualized costs, is relevant when exploring
the question of economic feasibility and the overall impact of this
rulemaking.
E. Economic Impacts
To determine whether the proposed 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,
[[Page 59415]]
[GRAPHIC] [TIFF OMITTED] TP04OC04.019
OSHA developed quantitative estimates of the economic impact of the
proposed rule on the affected establishments. In this analysis,
compliance costs are compared with industry revenues and profits.
To assess the potential economic impacts of the proposed standard,
OSHA compared the anticipated costs of achieving compliance against
revenues and profits of entities affected by the rule. OSHA compared
the baseline financial data (from Table IX-1) with total annualized
costs of compliance by computing compliance costs as a percentage of
revenues. This impact assessment is presented in Table IX-6. This table
is considered a screening analysis because it measures costs as a
percentage of pre-tax profits and revenues but does not predict impacts
on pre-tax profits and sales.
[[Page 59416]]
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[[Page 59419]]
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This screening analysis is used to determine 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 will depend on the price elasticity of demand for the
services sold by establishments in that industry.
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 an establishment is 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 simply by raising the
prices they charge for that service; under this scenario, profit rates
are largely unchanged and the industry remains viable. 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 profits. 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 (Seventh Cir. 1993)).
Specifically if demand is completely inelastic (i.e., price
elasticity is 0), then the impact of compliance costs that amount to 1
percent of revenues would be a 1 percent increase in the price of the
product or service, with no decline in demand or in profits. Such a
situation is rare but might be approximately correct in situations in
which there are few, if any, substitutes for the product or service
offered by the affected sector or if the products or services of the
affected sector account for only a 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 worker health)
if the industry attempted to keep producing the same amount of goods
and services as previously. Under this scenario, if the costs of
compliance represent a large percentage of the sector's profits, some
establishments might be forced to 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 eye of the consumer, perfect
substitutes for the goods and services the affected establishments
produce or provide.
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.
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.
Table IX-6 provides costs as percentage of revenues and profits for
all affected establishments. OSHA believes that this is the best way to
examine its statutory responsibility to determine whether the standard
affects the viability of an industry as a whole. There is only one
industry where costs exceed one percent of revenues (chromium catalyst
production), and none in which costs exceed 1.5 percent of revenues. In
only four industries (electroplating, construction welding, chromium
catalyst production and chromium catalyst service) do compliance costs
exceed 10 percent of profits.
In the case of construction, such cost changes are unlikely to
significantly alter the demand for construction welding services which
are essential for many projects and not subject to foreign competition.
Independent electroplating shops have also been subject to annual
changes larger in magnitude than the
[[Page 59420]]
costs of hexavalent chromium. The required price increase to fully
restore profits of 0.93 percent is significantly less than the average
annual increase in price of electroplating services. While such an
additional price change might cause some small drop in the demand for
services, the historical data clearly show that such price changes can
be incurred without affecting the viability of the industry. Chromium
catalyst production and service companies are also unlikely to be
affected by costs of the relative magnitude found here. While there may
be a small long term shift from the use of chromium catalysts as a
result of the regulation, most companies are locked into the use of
specific catalyst without major new investments. As a result, while
there may be some long term shift away from the use of chromium
catalysts, a price change of one percent are unlikely to immediately
prompt such a change. This also means that the market for the services
of 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 preliminarily determines that the proposed
standard is economically feasible.
Table IX-7 shows costs as percentage of profits and revenues for
firms classified as small by the Small Business Administration and
Table IX-8 shows costs as a percentage of revenues and profits for
establishments with less than 20 employees. These Tables show greater
potential impacts, especially for small electroplating establishments.
Based on these results, OSHA has prepared an Initial Regulatory
Flexibility Analysis to examine the impacts on small businesses and how
they can be alleviated.
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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 current worker population. The industry by
industry exposure profile was given in Table IX-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 2,247 and
8,708 lung cancers attributable to Cr(VI) exposure will occur during
the working lifetime of the current worker population. Table IX-9 shows
the number of avoided lung cancers by PEL. At the proposed PEL of 1
[mu]g/m3, and estimated 1,970 to 7,500 lung cancers would be
prevented over the working lifetime of the current worker population.
Table IX-9.--Avoided Lung Cancers Estimates by PEL
--------------------------------------------------------------------------------------------------------------------------------------------------------
PEL ([mu]g/\3\m) 0.25 0.5 1 5 10 20
--------------------------------------------------------------------------------------------------------------------------------------------------------
Avoided Cancers (Total)................................. 2,147-8,270 2,078-7,968 1,970-7,500 1,440-5,233 1,052-3,649 585-1,864
Avoided Cancers (Annual)................................ 48-184 46-177 44-167 32-116 23-81 13-41
--------------------------------------------------------------------------------------------------------------------------------------------------------
Note that the Agency based these estimates on a worker that 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, or 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 estimates of the
number of avoided cancers, given the nature of the risk assessment
model. 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 that 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. OSHA intends to investigate the implications of alternative
exposure scenarios in the
[[Page 59429]]
course of further developing its economic benefits assessment.
For informational purposes only, OSHA has estimated the monetary
value of the benefits associated with the draft proposed 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
proposed 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% 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 bound values for nonfatal cases of
lung cancer avoided.
Using these assumptions, and latency periods of 10, 20 and 35 years
and possible increases in the value of life over time, OSHA estimated
the total annual benefits of the standard at various PELS in Table IX-
10, considering both the benefits from preventing fatal and non-fatal
cases of lung cancer.
Table IX-10.--Total Annual Lung Cancer Benefits
[Millions of 2003 Dollars]
--------------------------------------------------------------------------------------------------------------------------------------------------------
PEL ([mu]g/m\3\) 0.25 0.5 1 5 10 20
--------------------------------------------------------------------------------------------------------------------------------------------------------
Undiscounted............................................ $287-1,189 $278-1,145 $263-1,078 $192-753 $141-525 $78-269
Discount Rate = 3%...................................... 102-1,131 99-1,090 94-1,026 69-716 50-500 28-256
Discount Rate = 7%...................................... 27-773 26-745 25-701 18-490 14-342 8-175
--------------------------------------------------------------------------------------------------------------------------------------------------------
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 upperbound 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 upperbound 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.
Using National Institute for Occupational Safety and Health (NIOSH)
data, Ruttenberg and Associates (Ex. XXXX) 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 draft proposed 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.
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. (These benefits associated with dermatitis are
not included in the net benefits analysis, as these benefits largely
result from full compliance with existing requirements for PPE and
hygiene areas.)
Occupational exposure to Cr(VI) can lead to nasal septum
ulcerations and nasal septum perforations. As for 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/m\3\, 0.5 [mu]g/m\3\, 1.0 [mu]g/m\3\, 5.0 [mu]g/m\3\, 10.0
[mu]g/m\3\ and 20.0 [mu]g/m\3\. 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/
m\3\. 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/m\3\ and regular short-term exposures e.g. an hour
or so) were below 10 [mu]g/m\3\. Less than 10 percent of workers could
reasonably be expected to experience nasal tissue damage at a TWA
Cr(VI) below 2 [mu]g/m\3\ [and short-term exposures below 10 [mu]g/
m\3\]. It appears likely that nasal damage might be avoided completely
if all Cr(VI) [short-term and full shift] exposures were kept below 1
[mu]g/m\3\.
OSHA estimates that 5,387 nasal perforations/ulcerations occur
annually
[[Page 59430]]
under the current PEL. All of these are expected to be prevented under
the proposed PEL of 1 [mu]g/m\3\. 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 IX-11.
Table IX-11.--Annual Net Benefits and Cost Per Cancer Avoided by PEL
[Millions of 2003 Dollars]
--------------------------------------------------------------------------------------------------------------------------------------------------------
PEL ([mu]g/m\3\ ) 0.25 0.5 1 5 10 20
--------------------------------------------------------------------------------------------------------------------------------------------------------
Discount Rate = 3%
Costs (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Total Annual...................................... $524 $381 $212 $119 $91 $81
---------------------------------------------------
Net Benefits (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Minimum........................................... -422 -282 -119 -51 -41 -53
Maximum........................................... 606 708 813 596 408 174
Midpoint.......................................... 92 213 347 273 183 60
---------------------------------------------------
Cost Per Cancer Avoided (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Minimum........................................... 2.9 2.2 1.3 1.0 1.1 2.0
Maximum........................................... 11.0 8.3 4.8 3.7 3.9 6.2
Midpoint.......................................... 6.9 5.2 3.1 2.4 2.5 4.1
---------------------------------------------------
Discount Rate = 7%
Costs (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Total Annual...................................... 548 402 223 125 95 84
---------------------------------------------------
Net Benefits (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Minimum........................................... -521 -376 -198 -107 -82 -77
Maximum........................................... 224 342 477 363 246 90
Midpoint.......................................... -149 -17 139 128 82 7
---------------------------------------------------
Cost Per Cancer Avoided (Millions of 2003 Dollars)
--------------------------------------------------------------------------------------------------------------------------------------------------------
Minimum........................................... 3.0 2.3 1.3 1.1 1.2 2.0
Maximum........................................... 11.5 8.7 5.1 3.9 4.1 6.5
Midpoint.......................................... 7.2 5.5 3.2 2.5 2.6 4.2
--------------------------------------------------------------------------------------------------------------------------------------------------------
In addition to examining alternative PELs, OSHA also examined
alternatives to other provisions of the standard. These alternatives
are discussed in the Initial Regulatory Flexibility Analysis in the
next section.
As noted above, the OSH Act requires OSHA to set standards based on
eliminating risk to the extent feasible. Eliminating risk to the extent
feasible does not necessarily have anything to do with the results of a
benefit cost analysis. 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.
Incremental costs and benefits are those that are associated with
increasing stringency of the standard. Comparison of incremental
benefits and costs provides and 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 IX-12. Note that dermal benefits are
excluded since they do not vary with the PEL and hence, do not affect
the calculations.
Table IX-12.--Incremental Benefits, Costs, Net Benefits and Cost Per Cancer Avoided
----------------------------------------------------------------------------------------------------------------
2010 105 51 10.5 0.50.25
----------------------------------------------------------------------------------------------------------------
Discount Rate = 3%
----------------------------------------------------------------------------------------------------------------
Benefits...................... $133.0 $117.4 $167.4 $34.5 $22.3
Costs......................... -10.0 -28.0 -93.0 -169.0 -143.0
Net Benefits.................. 123.0 89.4 74.4 134.5 120.7
Cost Per Cancer Avoided....... 1.6 0.1 -0.7 -2.3 -1.7
-------------------------------
Discount Rate = 7%
----------------------------------------------------------------------------------------------------------------
Benefits...................... 86.2 76.4 109.1 22.5 14.5
Costs......................... -11.0 -30.0 -98.0 179.0 -146.0
[[Page 59431]]
Net Benefits.................. 75.2 46.4 11.1 156.5 131.5
Cost Per Cancer Avoided....... 1.6 0.1 -0.7 -2.3 -1.7
----------------------------------------------------------------------------------------------------------------
G. Initial Regulatory Flexibility Analysis
Reasons Why Action by the Agency Is Being Considered
Several well-conducted scientific investigations have found
increased lung cancer mortality among workers breathing Cr(VI) dusts
and mists in the workplace. The high rate of lung cancer mortality has
been documented in workers from several countries across multiple
industries that use a broad spectrum of Cr(VI) compounds. Many of the
studies found that the rate of lung cancer was greatest among workers
in jobs where Cr(VI) exposure was highest and in workers employed in
those jobs for the longest periods of time. These exposure-related
trends implicate Cr(VI) as a likely causative agent and suggest that
other known lung carcinogens to which the workers may be exposed, such
as cigarette smoke, are unlikely to account for the increased lung
cancers observed in the studies. The International Agency for Research
on Cancer, the U.S. Environmental Protection Agency, and the American
Conference of Governmental Industrial Hygienists have evaluated the
human, animal, and other experimental evidence and concluded that
Cr(VI) compounds are ``known'' or ``confirmed'' human carcinogens.
Two independent epidemiologic studies of workers from chromate
production plants in Baltimore, Maryland (Gibb et al., Ex. 31-22-11)
and Painesville, Ohio (Luippold et al., Ex. 33-10) were considered to
present the strongest data sets for quantitative risk assessment.
OSHA's analysis found that a linear, relative risk model provided the
best fit to the data (Ex. 33-15; Ex. 33-12). The Agency preliminarily
estimates that the excess lifetime lung cancer risk for workers exposed
at the current Permissible Exposure Limit (PEL) of 52 [mu]g/m\3\
Cr(VI), as an eight-hour time-weighted average for a 45-year working
lifetime, ranges from 106 to 351 excess lung cancers per thousand
workers exposed. OSHA applied the linear relative risk model to
preliminarily estimate excess lifetime lung cancer risks from 45-year
exposure at alternative PELs ranging from 0.25 [mu]g/m3 to
20 [mu]g/m3 (the range considered for the draft proposed
standard). The projected risks at these alternate PELs are between
four- and 200-fold lower than risks estimated at the current PEL. NIOSH
and the Exponent group have reported similar lung cancer risks based on
the Gibb (Ex. 33-13; Ex. 31-18-15-1) and the Luippold (Ex. 31-18-3)
data sets and a relative risk model. The risk estimates at the very
lowest Cr(VI) exposure levels under consideration (e.g., 0.25 to 2.5
[mu]g/m3) are considered to be somewhat more uncertain than
those projected at the higher Cr(VI) levels because they involve risk
model extrapolations below the range of exposures experienced by the
Gibb and Luippold worker cohorts.
Exposure to airborne Cr(VI) can cause other adverse effects to the
respiratory tract and the skin. Occupational surveys and medical
examinations have found nasal septum ulcerations and perforations (i.e.
``chrome holes'') among chromium production workers and chrome
electroplaters exposed repeatedly to relatively high levels of Cr(VI)
(e.g., 20 [mu]g/m\3\ to 50 [mu]g/m\3\). (Exs. 31-22-11; 9-126). Several
case reports have also documented occupational asthma triggered by
breathing Cr(VI) compounds in the workplace. Workers can also develop
an allergic reaction of the skin known as allergic contact dermatitis
as a result of repeated direct dermal contact with Cr(VI) solutions or
other Cr(VI)-containing materials. Allergic contact dermatitis is most
common on the hands and arms of workers who mix and use wet Cr(VI)-
containing cement. Dermal contact with Cr(VI) can also cause an
irritant dermatitis and ulceration of the skin called ``chrome
ulcers''. This type of dermatitis is not an allergic condition and
requires contact with a fairly concentrated form of Cr(VI). It has been
reported primarily in chromate production plants and chrome
electroplating facilities with poor industrial hygiene (work)
practices.
A full discussion of the health effects and risk assessment that
support the reasons why this action is being considered are given in
Section VI of the Preamble, Health Effects, and Section VII,
Quantitative Risk Assessment.
Objective of and Legal Basis for the Proposed Rule
The objective of the proposed rule is to reduce the numbers of
fatalities and illnesses occurring among employees exposed to Cr(VI) in
general industry, construction, and shipyard sectors. This objective
will be achieved by requiring employers to install engineering controls
where appropriate and to provide employees with the equipment,
respirators, training, medical surveillance, and other protective
measures to perform their jobs safely.
The legal basis for the rule is the responsibility given the U.S.
Department of Labor through the Occupational Safety and Health Act of
1970 (OSH Act). The OSH Act authorizes the Secretary of Labor to
promulgate occupational safety and health standards as necessary ``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). The legal authority can also be cited as
29 U.S.C. 655(b).
In addition to the statutory basis for a possible standard, the
legal basis for the action also involves litigation on the need for and
timetable for a Cr(VI) standard. See the Preamble Section III, for a
fuller discussion.
Description and Estimate of Affected Small Entities
Table IX-1 above provides an overview of the number of small
entities affected by the standard, by sector. Additional detail is
provided in the Full Preliminary Economic Analysis and Initial
Regulatory Flexibility Analysis (Ex. 35-391).
Summary of Reporting, Recordkeeping, and Other Compliance Requirements
Table IX-13 shows the costs of the proposed standard for entities
classified as small businesses by the SBA.
[[Page 59432]]
[GRAPHIC] [TIFF OMITTED] TP04OC04.032
[[Page 59433]]
[GRAPHIC] [TIFF OMITTED] TP04OC04.033
[[Page 59434]]
[GRAPHIC] [TIFF OMITTED] TP04OC04.034
Table IX-14 shows the unit costs these estimates are based on. (For
a full discussion of the engineering control costs, and of the basis
for the unit costs, see Chapter 3 of the Preliminary Economic Analysis
and Initial Regulatory Flexibility Analysis).
[[Page 59435]]
Table IX-14.--Unit Costs Applied in OSHA's Preliminary Analysis of the Proposed Standard
----------------------------------------------------------------------------------------------------------------
Escalation
factor Index used for price
Cost description Basis Base cost (October escalation Unit cost
2003 basis)
----------------------------------------------------------------------------------------------------------------
Cost per hour for an outside Estimate by In- $90.00 1 NONE.................. $90.00
industrial hygiene contractor. house CIH.
Cost of a personal sampling Gilian 3500; 680.00 1 NONE.................. 680.00
pump. Sensidyne, 16333
Bayvista Drive,
Clearwater, FL
33760.
Variable Cost per sample Estimate by In- 60.00 1 NONE.................. 60.00
(e.g., laboratory analysis). house CIH.
Flat Fee For Training Course.. Estimate by In- 400.00 1 NONE.................. 400.00
house CIH..
Cost of a calibration unit.... GILIBRATOR-2; 1,075.00 1 NONE.................. 1,075.00
Sensidyne, 16333
Bayvista Drive,
Clearwater, FL
33760.
Unit cost of OSHA-regulation July 1993 EMMED 3.03 1.2702 CPI--All items........ 3.84
warning signs with mounting Co, Inc. Catalog.
materials.
Cost of materials per Banana Oil Fit 0.07 1 NONE.................. 0.07
qualitative fit-testing. Test Kit; Lab
Safety Supply
Catalog 2003, PO
Box 1368,
Janesville, WI
53547-1368.
Unit cost per worker for an Allegro One- 1,473.33 1 NONE.................. 1,473.33
air-supplied respirator. Worker Full Face
Kit; Lab Safety
Supply Catalog
2003, PO Box
1368,
Janesville, WI
53547-1368.
Unit cost per employee for a MSA Ultra Twin 243.00 1 NONE.................. 243.00
full-face respirator. Full Face
Respirator; Lab
Safety Supply
Catalog 2003, PO
Box 1368,
Janesville, WI
53547-1368.
Unit cost per employee for a MSA Comfro 35.30 1 NONE.................. 35.30
half-mask respirator. Classic Half-
Mask Respirator;
Lab Safety
Supply Catalog
2003, PO Box
1368,
Janesville, WI
53547-1368.
Cost of replacement cartridges MSA P100 Filter 13.74 1 NONE.................. 13.74
cartridges per mask). (2 Cartridge:
Lab Safety
Supply Catalog
2003, PO Box
1368,
Janesville, WI
53547-1369.
Unit cost per employee for a Allegro Three 1,164.00 1 NONE.................. 1,164.00
blasting helmet air-supplied Person Air Pump,
respirator. Bullard 1/2''
Hose, 100'L,
Bullard Helmet w/
constant air
flow; Lab Safety
Supply Catalog
2003, PO Box
1368,
Janesville, WI
53547-1368.
Cost of materials to clean one Respirator 1.86 1 NONE.................. 1.86
respirator. Cleaning/Storage
Kit; Lab Safety
Supply Catalog
2003, PO Box
1368,
Janesville, WI
53547-1368.
Cost of PE coated Tyvek KAPPLER Poly-Coat 6.60 1 NONE.................. 6.60
coveralls. Coveralls; Lab
Safety Supply
Catalog 2003, PO
Box 1368,
Janesville, WI
53547- 1368.
Cost of Saranex coveralls..... Tychem QC 32.85 1 NONE.................. 32.85
Coveralls; Lab
Safety Supply
Catalog 2003, PO
Box 1368,
Janesville, WI
53547-1368.
Cost of Tyvek coveralls....... Tyvek Protective 4.50 1 NONE.................. 4.50
Wear Coveralls;
Lab Safety
Supply Catalog
2003, PO Box
1368,
Janesville, WI
53547-1368.
Cost of bib aprons............ Polypropylene Bib 0.58 1 NONE.................. 0.58
Apron; Lab
Safety Supply
Catalog 2003, PO
Box 1368,
Janesville, WI
53547-1368.
Cost of laundering uniforms Aramark 5.50 1 NONE.................. 5.50
for one employee per week. Cincinnati
Representative.
Cost of laundering uniforms Aramark 3.75 1 NONE.................. 3.75
for one employee per week. Cincinnati
Representative.
Cost of clear indirect vent Lab Supply 6.00 1 NONE.................. 6.00
goggles. Catalog 2003, PO
Box 1368,
Janesville, WI
53547-1368.
Cost of clear lens safety Lab Supply 5.00 1 NONE.................. 5.00
glasses. Catalog 2003, PO
Box 1368,
Janesville, WI
53547-1368.
Cost of grey lens safety Lab Supply 5.00 1 NONE.................. 5.00
glasses. Catalog 2003, PO
Box 1368,
Janesville, WI
53547-1368.
Cost of lined nitrile gloves.. Ansell Sol-Vex 2.50 1 NONE.................. 2.50
Flock Lined
Nitrile Gloves;
Lab Safety
Supply Catalog
2003, PO Box
1368,
Janesville, WI
53547-1368.
Cost of powder surgical N-Dex 4-mil 0.24 1 NONE.................. 0.24
nitrile gloves. powdered
disposable
Nitrile Lab
Gloves; Lab
Safety Supply
Catalog 2003, PO
Box 1368,
Janesville, WI
53547-1368.
[[Page 59436]]
Cost of rough PVC gloves...... BEST Super Flex 4.10 1 NONE.................. 4.10
PVC-gloves
Coated Gloves;
Lab Safety
Supply Catalog
2003, PO Box
1368,
Janesville, WI
53547-1368.
Unit cost of change rooms per Based upon Means 856.00 1.4742 CPI--All items........ 1,261.92
employee. Square Foot
Costs, 1989.
Cost per shower head.......... Based upon Means 3,590.00 1.4742 CPI--All items........ 5,292.39
Square Foot
Costs, 1989.
Cost per hand washing facility Glacier Bay 4 in 500.00 1 NONE.................. 500.00
Chrome Two
Handle Bar
Faucet, 40 in x
24In. White
Double Bowl
Utility Tub, 505
E. Kemper Rd.,
Cincinnati, OH
45246--Estimated
Installation
Cost.
Variable cost per shower Estimate......... 0.50 1 NONE.................. 0.50
(soap, clean towel, water,
etc.).
Variable cost per hand washing Kimberly-Clark 0.06 1 NONE.................. 0.06
facility (roll paper towels, OnePak
liquid soap, water). Dispenser,
WINDSOFT
Bleached White
Paper Roll
Towels; The
Betty Mills
Company, 60 East
3rd Ave, Ste
201, San Mateo,
CA 94401 (2003).
Unit cost of HEPA vacuums..... CONSAD (1993) 1,580.00 1.4742 CPI--All items........ 2,329.24
base price is
1991.
Unit cost of HEPA vacuum CONSAD (1993) 212.00 1.4742 CPI--All items........ 312.53
replacement filters. base price is
1991.
Unit cost of garbage bags and Estimate--Includi 500.00 1 NONE.................. 500.00
disposal. ng RCRA disposal.
Full cost of a comprehensive 1994 Quote from 282.00 1.4211 CPI--Medical Care 400.76
medical exam. two hospitals. Services.
Bethesda Care,
Cincinnati, OH
and Abington
Memorial
Hospital, Willow
Grove, PA.
Full cost of a limited medical 2003 cost of 125.00 1 NONE.................. 125.00
exam. physical exams
in Maryland (as
directed by
OSHA)..
Cost of additional medical Estimated to be 150.00 1.4211 CPI--Medical Care 213.17
testing after exam results equal to cost of Services.
are abnormal. limited medical
exam.
Cost of a partial 1994 Quote from 141.00 1.4211 CPI--Medical Care 200.38
comprehensive medical exam. two hospitals. Services.
Bethesda Care,
Cincinnati, OH
and Abington
Memorial
Hospital, Willow
Grove, PA--
Estimated half
of comprehensive
and/or limited
exam cost.
Cost of a partial medical exam 1994 Quote from 75.00 1.4211 CPI--Medical Care 106.59
two hospitals. Services.
Bethesda Care,
Cincinnati, OH
and Abington
Memorial
Hospital, Willow
Grove, PA--
Estimated half
of comprehensive
and/or limited
exam cost.
Cost per employee for training Estimate......... 2.00 1 NONE.................. 2.00
aids and materials.
Cost per employee for computer Estimate......... 1.00 1 NONE.................. 1.00
file space.
Cost of Medical History OSHA. Preliminary 25 1.4211 CPI--Medical Care 35.53
Questionnaire. Regulatory Services.
Impact and
Regulatory
Flexibility
Analysis of the
Proposed
Respiratory
Protection
Standard, 1994.
Cost of Medical Exam for OSHA. Preliminary 75 1.4211 CPI--Medical Care 106.58
Respirator Use. Regulatory Services.
Impact and
Regulatory
Flexibility
Analysis of the
Proposed
Respiratory
Protection
Standard. 1994.
Cost of Mop and Bucket........ The Home Depot. 62.92 1 NONE.................. 62.92
Contico, 35qt
Mop Bucket and
Wringer. Wilen,
16oz Cotton Cut-
End Mop.
Cost of Mop................... The Home Depot. 62.92 1 NONE.................. 62.92
Wilen, 16oz
Cotton Cut-End
Mop.
Cost of Mobile Shower Unit Ameri-can 42,960 1 NONE.................. 42,960
(construction). Engineering.
Basic 828
Decontamination
Trailer. 2003.
15886 Michigan
Road. Argos, IN
46501.
Cost of Change Area per Estimate......... 720 1 NONE.................. 300
employee (construction).
----------------------------------------------------------------------------------------------------------------
Source: U.S. Dept. of Labor, OSHA, Office of Regulatory Analysis, based on IT, 2004, Ex. 35-390.
[[Page 59437]]
Federal Rules That May Duplicate, Overlap, or Conflict With the
Proposed 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 fenceline 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 proposed standard would not be needed, or that some of the proposed
standard's provisions might not be needed.
OSHA has discussed EPA's MACT standard with EPA. The standards are
not duplicative or 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 proposed 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.
OSHA believes that chromium electroplaters can generally meet a PEL of
1 [mu]g/m3 without such major changes, and has not included
costs. This issue is discussed in detail in Chapter 2 of the full PEA.
However, OSHA welcomes comment on this issue.
OSHA examined the potential problem of overlapping jurisdiction for
CCA applicators, and found that there would indeed be overlapping
jurisdiction. For this proposed rule, OSHA had excluded CCA applicators
from the scope of the coverage of the proposed rule. OSHA has been
unable to find a case where a state, as a matter of law, bases
fenceline standards on OSHA PELs. OSHA notes that the OSHA PEL is
designed to addresses the risks associated with life long occupational
exposure only. OSHA welcomes comment on this issue.
OSHA has also examined other OSHA standards, and where standards
are overlapping, referred to them by reference in the proposed
standard. Existing OSHA standards that may duplicate the proposed
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 proposed
standard that OSHA is considering, with an emphasis on the those
suggested by the SBREFA Panel as potentially alleviating impacts on
small firms. (A discussion on the costs of some if these alternatives
to OSHA's proposed regulatory requirements for the hexavalent chromium
standard can be found in Section III.2 Costs of Regulatory Alternatives
in the final report by OSHA's contractor, IT (IT, 2004). In the IT
report, Tables III.42-III.51, costs are analyzed by regulatory
alternative and major industry sector at discount rates of 7 percent
and 3 percent).
Scope: The proposed standard covers exposure to all types of Cr(VI)
compounds in general industry, construction, and shipyard. Cement work
in construction is 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 has preliminarily 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.
As stated above, the proposed standard does not cover cement work
in construction. OSHA's preliminary 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 wet cement work in construction are
well below 0.25 [mu]g/3. Moreover, unlike other exposures in
construction, general industry or shipyards, exposures from cement work
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 wet cement in only minute quantities naturally.
Cement work also is found in the general industry setting, however the
data there indicate that, because of the volume of cement involved and
the nature of the work, airborne exposures are likely to be slightly
higher, with 3-5% of the exposures being greater than 0.25 [mu]g/
m3. Given these factors, the proposed standard excludes
cement work in construction. OSHA has made a preliminary determination
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 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 wet cement would depend on what requirements
were applied to wet cement workers. OSHA estimates that adding wet
cement to the scope of the standard would have costs of $33 million per
year. The cost of addressing the problem through existing standards
could range from $80 to $300 million per year. OSHA considered the
SBREFA Panel recommendation that sectors where there is little or no
known exposure to Cr(VI) be excluded from the scope of the standard.
OSHA has preliminarily 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.
Beyond the initial exposure assessment (required only in general
industry), very little would be required in workplaces where Cr(VI)
exposures are below the PEL and no hazard is present from skin or eye
[[Page 59438]]
contact with Cr(VI). Additional requirements would generally be limited
to housekeeping (in general industry) and hazard communication (warning
labels on containers of Cr(VI)-contaminated materials that are
consigned for disposal, training regarding the Cr(VI) standard). Where
exposures in general industry exceed the Action Level, periodic
monitoring would also be required. 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.
PELS: Section F of this preamble summary presented data on the
costs and benefits of alternative PELS for all industries. The full PEA
contains detailed data on the impacts of small firms at each level of
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 preliminarily 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 preliminarily not adopted
this approach because OSHA does not believe it would serve workers or
small businesses well. If an approach which requires a significant
number of workers to wear respirators on a regular basis were to be
adopted, that approach would result in many workers wearing respirators
with the associated risks, and in setting a lower PEL in accord with
the QRA's estimate that there is significant risk at PELS lower than
one.
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 the QRA. Here, it will only be noted that
this would suggest lower PELs than OSHA is setting in at least some
industries, and thus potentially increase impacts on 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 preliminarily decided to change its approach in these sectors.
OSHA is proposing 3 separate standards, one for general industry, one
for construction, and one for shipyards. In shipyard and construction,
OSHA will not require exposure monitoring of any kind; will not have an
action level; will require medical surveillance only for persons with
signs and symptoms; and will not require regulated areas. However,
employers must still meet the PEL with engineering controls and work
practices where feasible.
This approach reduces the specification oriented aspects of the
standard in these sectors, but may make it difficult for employers to
determine how to comply with the standard. OSHA is considering a more
specification oriented approach, similar to that used in the asbestos
in construction standard, and in ``control banding'' approaches used
abroad. Such an approach would require OSHA to specify what controls
would need to be used in various circumstances, and employers using
such controls would be considered to be in compliance with the
standard. OSHA does not have the information at this time to develop or
cost such an approach. OSHA welcomes comments on how it might develop
such an approach.
Timing of the Standard: The SBREFA Panel also recommended
considering a multi-year phase in of the standard. OSHA is examining
and soliciting comment on this issue. Such a phase-in would have
several advantages from a viewpoint of impacts on small businesses.
First, it would reduce 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 would also be useful in the electroplating
sector by allowing employers to coordinate their environmental and
occupational safety and health control strategies to minimize potential
costs. A differential phase-in for smaller firms would also aid very
small firms by allowing them to gain from the control experience of
larger firms. However a phase-in would also postpone the benefits of
the standard.
SBREFA Panel
Table IX-15 lists all of the SBREFA Panel recommendations and notes
OSHA responses to these recommendations.
Table IX-15.--SBREFA Panel Recommendations and OSHA Responses
------------------------------------------------------------------------
SBREFA panel recommendation OSHA response
------------------------------------------------------------------------
The Panel recommends that, as time OSHA has extensively reviewed
permits, OSHA revise its economic and its costs estimates, and
regulatory flexibility analyses as changed many of them in
appropriate to reflect the SERs' response to SER comments and
comments on underestimation of costs solicits comments on these
and that the Agency compare the OSHA revised cost estimates. A few
revised estimates to alternative examples of OSHA's cost
estimates provided and methodologies changes are given in the
suggested by the SERs. For those SER responses to specific issues,
estimates and methodological below (e.g., medical exams,
suggestions that OSHA does not adopt, training and familiarization).
the Panel recommends that OSHA explain
its reasons for preferring an
alternative estimate and solicit
comment on the issue.
The Panel recommends that, to the The PEA reflects OSHA's
extent time permits, OSHA should judgment on technological
carefully consider the ability of each feasibility and includes
potentially affected industry to meet responses to specific issues
any proposed PEL for CR(VI) and raised by the Panel and SERs.
solicit comment on the costs and OSHA will solicit comment on
technological feasibility of the PEL. the accuracy and
reasonableness of these
judgments.
The Panel recommends that OSHA OSHA has increased the
carefully review the basis for its estimated time for a limited
estimated medical surveillance medical exam from 1.5 hours to
compliance costs, consider these 3 hours and solicits comment
concerns raised by the SERs, and on all other cost projections
ensure that its estimates are revised, for medical surveillance. See
as appropriate and time permits, to Chapter IV OF THE PEA; COSTS
fully reflect the costs likely to be OF COMPLIANCE, COSTS BY
incurred by potentially affected PROVISION--Medical
establishments. Surveillance, for details of
OSHA's unit costs for medical
surveillance.
[[Page 59439]]
The Panel recommends that, as time OSHA revised the standard to
permits, OSHA consider alternatives relieve Construction and
that would alleviate the need for Shipyards from requirements
extensive monitoring on construction for exposure assessment; for
sites, and solicit comment on this General Industry, OSHA
issue. If OSHA does not adopt such believes that its unit cost
alternatives, then OSHA should estimates are realistic but
consider increasing the estimated will raise that as an issue.
costs of such monitoring in See CHAPTER IV OF THE PEA:
construction, and solicit comment on COSTS OF COMPLIANCE, COSTS BY
the costs of monitoring. PROVISION--Exposure Monitoring
(Initial and Periodic), for
details of OSHA's unit costs
for exposure monitoring in
general industry.
The Panel recommends that OSHA OSHA's proposed standard will
carefully review the basis for its permit hand washing as a
estimated hygiene compliance costs, hygiene option; OSHA's
consider the concerns raised by the analysis will also reflect,
SERs, and, to the extent time permits, where data confirm, any cost
ensure that its estimates are revised, premium related to handling
as appropriate, to fully reflect the contaminated waste water or
costs likely to be incurred by laundry, or where uncertainty
potentially affected establishments. exists, the issue will be
raised.
The Panel recommends that OSHA examine OSHA has recognized costs for
and solicit comment on this issue training and familiarization
[possible understates in the costs of to cover a better
regulated areas]. understanding of the costs of
regulated areas, and solicit
comment on the issue. See
CHAPTER IV OF THE PEA; COSTS
OF COMPLIANCE, COSTS BY
PROVISION--Communication of
Hazards to Employees--Training
and Familiarization, for
details of OSHA's unit costs
for this provision.
The Panel recommends that OSHA examine OSHA has examined and solicits
and solicit comment on these issues comment on this issue and the
[costs of laundering PPE]. cost OSHA has estimated. See
CHAPTER IV OF THE PEA; COSTS
OF COMPLIANCE, COSTS BY
PROVISION--Housekeeping,
Protective Work Clothing and
Equipments, and Table IV-8 for
details of OSHA's unit costs
for laundering PPE and other
related costs.
The Panel recommends that OSHA examine OSHA's analysis assumes that
whether its cost estimates reflect the employers will need time for
full costs of complying with the familiarization with the
hazard communication standard. standard, training on the
standard, and increased
initial supervision.
The Panel recommends that OSHA OSHA has reviewed and revised
thoroughly review the economic impacts many of its revenue and profit
of compliance with a proposed Cr(VI) estimates in the light of
standard and develop more detailed specific SER comments.
feasibility analyses where Examples of application groups
appropriate. The Panel also recommends with revised revenue and
that OSHA, to the extent permitted by profit estimates include Group
time and the availability of economic 4, Chromate Production; Group
data, reexamine its estimates of 5, Chromate Pigment Producers;
profits and revenues in light of SER and Group 17, Chromium Dye
comments, and update economic data to Producers. However, OSHA has
better reflect recent changes in the not updated revenue and profit
economic status of the affected impacts across the board--OSHA
industries, consistent with its estimates of costs, revenues,
statutory mandate. The Panel also and profits require consistent
recommends that OSHA examine, to the data sets which are not yet
extent feasible with the time available for more recent
available, the possibility that users years. OSHA's continues to
will substitute non-Cr(VI) products examine, and will solicit
for Cr(VI) products. The Panel comment on this issue.
recommends that OSHA solicit comment
on the extent to which foreign
competition may or may not impact what
is feasible for the industries
affected by this rule.
The Panel recommends that OSHA consider OSHA is reluctant to exempt
and solicit comments on selective industries where exposures are
exemption of some industries from the minimal because changes in
proposed standard, especially those technology could change
industries whose inclusion is not exposures in the future.
supported by the industry-specific However, OSHA is seeking
data or in which inhalation exposure comment on the issue of the
to Cr(VI) is minimal. scope of the standard and data
that would support not
covering certain sectors.
The Panel recommends that OSHA exempt OSHA has decided to exempt
applicators of CCA given that they are applicators of CCA in this
already regulated by EPA as pesticide proposal.
applicators under FIFRA. In addition,
OSHA should clarify and seek comment
as to why users of CCA-treated wood
should be covered under the Cr(VI)
proposal given that the use of CCA-
treated wood was previously excluded
by OSHA in its standard for inorganic
arsenic.
The Panel recommends that OSHA clearly The Quantitative Risk
explain the way that Cr(VI) exposure Assessment section of the
and risk for the worker cohort studies Preamble addresses this issue
used in the quantitative risk in detail, and OSHA is seeking
assessment were calculated, and should comments on this issue.
consider and seek comment as to
whether the major assumptions used in
these calculations are reasonable.
The Panel recommends that OSHA consider The Quantitative Risk
the available information on reduction Assessment of this Preamble
of inhaled Cr(VI) to Cr(III) in the addresses the issue of
body, to determine whether exposures possible threshold effects and
below a threshold concentration can be OSHA is seeking comments on
shown not to cause the genetic the issue.
alterations that are believed to cause
cancer. In addition, OSHA should
review epidemiological analyses
relevant to the question of threshold
dose, to determine whether such a dose
is identifiable from the available
human data. OSHA should further
consider and seek comment on these
findings in relation to the risk
assessment and the proposed PEL,
allowing for a higher PEL than those
presented in the draft standard if the
risk assessment so indicates.
[[Page 59440]]
The Panel recommends that OSHA should OSHA is required by law to set
clarify the meaning of the projected health standards so that they
lung cancer risk estimates used to avoid significant risk over a
support the proposed standard. In working lifetime. Both in the
particular, OSHA should explain these QRA and in the Benefits
estimates, which are based on a Chapter of the PEA, OSHA has
working lifetime of 45 years' exposure examined alternative exposure
at the highest allowable Cr(VI) scenarios. See VII.
concentration, and, where appropriate, Preliminary Quantitative Risk
note projected excess cancers that may Assessment in the Preamble and
result from shorter periods of CHAPTER VI of the PEA;
occupational Cr(VI) exposure. BENEFITS and NET BENEFITS,
Lung Cancers Avoided in this
PEA.
The Panel recommends that OSHA solicit OSHA has added information
information to better characterize the provided by firms in the
exposure patterns and Cr(VI) compounds shipyard industry since the
encountered in the maritime Panel meeting. (See Chapter II
environment, and should encourage of the PEA; PROFILE OF
input from marine chemists at AFFECTED INDUSTRIES,
appropriate points in the rulemaking. PROCESSES, AND APPLICATIONS
GROUPS, AFFECTED INDUSTRIES--
Welding and Painting and
Chapter III: Technological
Feasibility, Welding and
Painting). OSHA is soliciting
comment on shipyard issues and
from maritime chemists.
The Panel recommends that OSHA consider OSHA considered this
the appropriateness of separate PELs possibility and preliminarily
for specific Cr(VI) compounds, with decided against it, in part,
attention to the weight and extent of because it would require lower
the best available scientific evidence PELs with many persons in
regarding their relative carcinogenic respirators. OSHA is
potency. soliciting comment on this
issue.
The Panel recommends that OSHA solicit OSHA has eliminated the
information to better define requirement for monitoring in
construction activities likely to be the construction industry.
above and below the PEL (for initial OSHA has considered a control
exposure monitoring purposes) to banding approach to
minimize the amount of respiratory construction, but lacks the
protection that would need to be used data to fully implement this
for compliance. approach, and solicits comment
on the issue.
The Panel recommends that OSHA provide OSHA has removed the
a better explanation of how to requirement for exposure
implement an exposure assessment monitoring in construction and
program for construction activities. shipyards. The monitoring-
Also, OSHA should provide further related topics are further
explanation on monitoring-related discussed in the Preamble,
topics like the selection of sampling XVII. Summary and Explanation
and analytical methods, the selection of the Standard.
of plus-or-minus 25% as a confidence
interval, and the use of objective
data in lieu of monitoring.
The Panel recommends that OSHA consider OSHA has preliminarily left the
less frequent monitoring for exposures monitoring frequency
above the PEL, especially in unchanged, but has solicited
situations where the employer has comment on the issue.
already engineered down to the lowest
feasible level and is not able to
maintain levels below the PEL.
The Panel recommends that OSHA review OSHA has reviewed its
the technologies used to reduce Cr(VI) technological feasibility
exposure to ensure to ensure that they analysis and solicited comment
are available or reasonably on it.
anticipated to be available in the
future.
The Panel recommends that OSHA clarify The Summary and Explanation of
the purpose of the prohibition on the the Preamble explains further
use of employee rotation to meet the the prohibition on employee
PEL and take into account the needs rotation and the methods of
expressed by the SERs on the issue. compliance.
The Panel recommends that OSHA clarify ...............................
the methods of compliance section.
The Panel recommends that OSHA clarify OSHA has eliminated the
how to implement the use of regulated requirement for regulated
areas particularly for construction areas in construction and
activities. OSHA should better explain shipyards. The Summary and
how employers would delineate Explanation section of the
boundaries for regulated areas and Preamble explains the
should better clarify the use of regulated area requirements in
respiratory protection, personal General Industry.
protective clothing and equipment, and
hygiene facilities and practices in
regulated areas.
The Panel recommends that OSHA provide These issues are addressed in
a clearer explanation of why it is the Summary and Explanation
necessary to remove Cr(VI)- Section of the Preamble.
contaminated protective clothing and
wash hands prior to entering non-
Cr(VI) work areas and eating, drinking
or smoking and take into account lost
time and costs associated with
conducting such activities.
The Panel recommends that OSHA clarify ...............................
its definition of contaminated
clothing or waste, provide evidence
supporting the view that
``contaminated'' clothing presents a
hazard, and better explain the special
treatment of such items and why the
treatment is necessary.
The Panel recommends that OSHA clarify OSHA has changed the rule from
its definition of reasonably SBREFA draft in order to
anticipated skin and eye contact. clarify when PPE is required
The Panel recommends that OSHA clarify and to assure that it is not
the circumstances under which the required except where a dermal
proposed rule would require the use of hazard exists.
personal protective equipment to
prevent dermal exposures to solutions
containing Cr(VI). In particular, OSHA
should reconsider the requirements for
the use of dermal protection when the
PEL is exceeded; consider alternatives
that are more clearly risk based; and
determine whether the use of very
dilute Cr(VI) solutions, as used in
some laboratories, requires the use of
personal protective equipment..
[[Page 59441]]
The Panel recommends that OSHA provide OSHA has preliminarily dropped
a clearer explanation of the benefits routine medical surveillance
and the need for its proposed medical in the shipyard and
surveillance provisions. construction industries. The
The Panel recommends that OSHA provide Preamble Summary and
a clearer guidance as to which Explanation clarify what is
employees are intended to be covered required of medical
under the medical surveillance surveillance, and the extent
provisions and, in particular, how the to which the same medical
standard is intended to cover examination can be used to
employees who work for several meet the requirements of
different employers during the course different standards.
of a year.
The Panel recommends that OSHA clarify
the qualifications necessary to
provide a medical examination
(including what knowledge of Cr(VI) is
necessary) and what the elements of
such a medical examination should be.
The Panel recommends that OSHA design
the medical surveillance provisions to
be consistent with existing OSHA
standards (e.g., lead and arsenic)
wherever possible, in order to
minimize the need for duplicative
medical examinations. The Panel also
recommends that OSHA clarify that
differences in medical surveillance
requirements that may be unavoidable
across OSHA standards nevertheless
often will not require completely
separate medical examinations.
With respect to the EPA electroplating OSHA discusses the impact of
standards, the Panel recommends that EPA's electroplating standard
OSHA examine whether important costs in the PEA, (See Chapter II:
have been omitted, seek to develop Technological Feasibility,
alternatives that minimize these Electroplating and Chapter
costs, and seek comment on the issue. VIII: Environmental Impacts)
and seeks comments on this
issue.
With respect to possible dual OSHA preliminarily has decided
jurisdiction with FIFRA, the Panel to exclude CCA applicators
recommends that OSHA consider dropping from the scope of the
CCA applicators from the scope of the standard.
rule, and seek comment on this issue.
With respect to the issue of using OSHA OSHA solicits comment on the
PELs as a basis for fenceline ``fence line'' standard issue.
standards, the Panel recommends that
OSHA make clear the purpose of its
PELs, and explain that they are not
developed or examined in terms of
their validity as a basis for air
quality standards.
The Panel recommends that OSHA examine OSHA has preliminarily
whether existing standards are determined that, except for
adequate to cover occupational CCA applicators and wet cement
exposure to Cr(VI), and, if not, workers, other standards
develop the Cr(VI) standard in such a cannot provide the worker
way as to eliminate duplicative and protection needed, but has
overlapping efforts on the part of sought to avoid duplication of
employers. effort between standards.
The Panel recommends that OSHA consider OSHA has included an analysis
the scientific evidence in favor of a of the costs and benefits of a
higher PEL, analyze the costs and PEL of 20 in this Preamble
economic impacts of a PEL of 20 or summary, and has a full
greater, and solicit comment on this analysis of this option in the
option. PEA.
The Panel recommends that OSHA OSHA preliminarily determined
carefully examine the entire issue of that intermittent users need
intermittent exposures, consider not use engineering controls
options that can alleviate the burden to assure compliance with the
on such firms while meeting the PEL.
requirements of the OSH Act, and
solicit comment on such options.
Some SERs argued that some Cr(VI) OSHA has preliminarily
compounds offer lesser risks of cancer determined that all Cr(VI)
than others, and should be subject to compounds should have the same
different PELs. The Panel recommends PEL, but seeks comment on the
that OSHA consider these arguments and issue.
seek comment on the issue.
The Panel recommends that OSHA continue OSHA has preliminarily
to exempt wet cement from the scope of determined to exempt wet
the standard, and that if OSHA seeks cement from the scope of the
comment on this option, OSHA should standard, but has sought
note the Panel's recommendation and comment on the issue.
the reasons for the recommendation. OSHA has made a number of
The Panel also recommends that OSHA changes to the construction
seek ways of adapting the standard standard in this proposal,
better to the dynamic working including eliminating the
conditions of the construction exposure assessment
industry, examine the extent to which requirements, the regulated
Cr(VI) exposures are already covered area requirement, and the
by other standards, and seek comment action level. OSHA seeks
on these issues. The Panel also comment on its new approach.
recommends that OSHA consider the
alternative of developing a
construction standard in a separate
rulemaking.
The Panel recommends that OSHA OSHA has made a number of
consider, and solicit comment on, changes to the shipyard
approaches to their special problems; standard in this proposal,
that OSHA consider the possibility of including eliminating the
making the maritime proposed standard exposure assessment
more similar to the construction draft requirements, the regulated
standard, or consider the alternative area requirement, and the
of developing a maritime standard in a action level. OSHA has sought
separate rulemaking. comment on its new approach.
The Panel recommends that OSHA consider This option is discussed in the
and seek comment on multi-year phase- regulatory alternatives
in alternatives. section of the PEA, and OSHA
is seeking comments on this
alternative.
The Panel recommends that OSHA better OSHA has eliminated the action
explain the action level, including level in the construction and
its role in ensuring workers are shipyard standards, and
protected. explains its role in the
General Industry in the
Summary and Explanation of the
Preamble.
The Panel recommends that OSHA consider OSHA has preliminarily
the use of SECALs and solicit comment determined not to use SECALs,
on whether and in what industries they but solicits comments on this
are appropriate using the Cadmium issue.
standard as a model.
------------------------------------------------------------------------
[[Page 59442]]
X. OMB Review Under the Paperwork Reduction Act of 1995
The proposed standard for chromium (VI) contains collections of
information (paperwork) that are subject to review by the Office of
Management and Budget (OMB) under the Paperwork Reduction Act of 1995
(PRA95), 44 U.S.C. 3501 et seq, and its regulation at 5 CFR Part 1320.
PRA 95 defines collection of information to mean, ``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. Sec. 3502(3)(A)].
The title, description of the need for and proposed use of the
information, summary of the collections of information, description of
respondents, and frequency of response of the information collection
are described below with an estimate of the annual cost and reporting
burden has required by Sec. 1320.5(a) (1)(iv) and Sec. 1320.8(d)(2).
The reporting burden includes the time for reviewing instructions,
gathering and maintaining the data needed, and completing and reviewing
the collection of information.
OSHA invites comments on whether each proposed collection of
information:
(1) Ensures that the collection of information is necessary for the
proper performance of the functions of the agency, including whether
the information will have practical utility;
(2) Estimates the projected burden accurately, including the
validity of the methodology and assumptions used;
(3) Enhances the quality, utility, and clarity of the information
to be collected; and
(4) Minimizes the burden of the collection of information on those
who are to respond, including through the use of appropriate automated,
electronic, mechanical, or other technological collection techniques or
other forms of information technology, e.g., permitting electronic
submissions of responses.
Title: Chromium (VI) Standard for General Industry (Sec.
1910.1026), Shipyards (Sec. 1915.1026); and Construction (Sec.
1926.1126)
Description: The proposed Cr(VI) standard is an occupational safety
and health standard's information collection requirements are essential
components that will assist both employers and their employees in
identifying exposures as well as identifying means to take to reduce or
eliminate Cr(VI) overexposures.
Summary of the Collections of Information:
1910.1026(d)--Exposure Assessment
Paragraph (d)(5) of this section requires the employer to notify
employees of their exposure monitoring results within 15 working days
after the receipt for the exposure monitoring performed in this section
(Sec. 1910.1026(d)(2) Initial Exposure Monitoring, Sec.
1910.1026(d)(3) Periodic Monitoring, and Sec. 1910.1026 (d)(4)
Additional Monitoring).
Employers may notify each affected employee individually in writing
of the results or by posting the exposure-monitoring results in an
appropriate location that is accessible to all affected employees. If
the exposure monitoring results indicate that employee exposure is
above the PEL, the employer must include in the written notification
the corrective action being taken to reduce employee exposure to or
below the PEL.
1910.1026(g), 1915.1026(e), 1926.1126(e)--Respiratory
Protection
Paragraph (g)(2) in the general industry section, and paragraph
(e)(2) in the shipyards and construction sections require the employer
to institute a respiratory protection program in accordance with 29 CFR
1910.134. The Respiratory Protection Standard's (Sec. 1910.134)
information collection requirements require employers to: Develop a
written respirator program; conduct employee medical evaluations and
provide follow-up medical evaluations to determine the employee's
ability to use a respirator; provide the physician or other licensed
health care professional with information about the employee's
respirator and the conditions under which the employee will use the
respirator; and administer fit-tests for employees who will use
negative or positive-pressure, tight-fitting facepieces.
1910.1026(h), 1915.1026(f), 1926.1126(f)--Protective Work
Clothing and Equipment
Paragraph (h)(3)(iii) in the general industry section and
(f)(3)(iii) in the shipyards and construction sections require the
employer to inform any person who launders or cleans protective
clothing or equipment contaminated with chromium (VI) of the
potentially harmful effects of exposure to chromium (VI) and that the
clothing and equipment should be laundered or cleaned in a manner that
minimizes skin or eye contact with chromium (VI) and effectively
prevents the release of airborne chromium (VI) in excess of the PEL.
1910.1026(k), 1915.1026(h), and 1926.1126(h)--Medical
Surveillance
Paragraphs (k)(4) in the general industry section and (h)(4) in the
shipyards and construction sections require the employer to provide the
examining PLHCP with a copy of the standard. In addition, for each
employee receiving a medical examination, the employer must provide the
following information:
1. A description of the affected employee's former, current, and
anticipated duties as they relate to the employee's occupational
exposure to chromium (VI);
2. The employee's former, current and anticipated levels of
occupational exposure to chromium;
3. A description of any personal protective equipment used or to be
used by the employee, including when and for how long the employee has
used that equipment; and,
4. Information from records of employment-related medical
examinations previously provided to the affected employee currently
within the control of the employer.
Paragraphs (k)(5) in the general industry section, and (h)(5) in
shipyards and construction sections require the employer to obtain a
written medical opinion from the PLHCP, within 30 days for each medical
examination performed on each employee. The employer must provide the
employee with a copy the PLHCPs written medical opinion within two
weeks of receipt. This written opinion must contain the following
information:
1. The PLHCP's opinion as to whether the employee has any detected
medical condition(s) that would place the employee at increased risk of
material impairment to health from further exposure to chromium (VI);
2. Any recommended limitations upon the employee's exposure to
chromium (VI) or upon the use of personal protective equipment such as
respirators;
3. A statement that the PLHCP has explained to the employee the
results of the medical examination, including any medical conditions
related to chromium (VI) exposure that require further evaluation or
treatment, and any special provisions for use of protective clothing or
equipment.
1910.1026(l), 1915.1026(i), and 1926.1126(i)--Communication of
Chromium (VI) Hazards to Employees
Paragraph (l)(4) of the general industry section, and (i)(3) of the
shipyards and construction sections require that the employer provide
[[Page 59443]]
training for all employees who are exposed to airborne chromium (VI),
or who have skin or eye contact with chromium (VI). Employers must
maintain a record of the training provided. Also employers must provide
initial training prior to or at the time of initial assignment to a job
involving potential exposure to chromium (VI). However, employers do
not need to provide training to a new employee, if they can demonstrate
that a new employee has received training within the last 12 months
that addresses the elements specified in the paragraph and that the
employee can demonstrate knowledge of those elements. Employers must
provide training that is understandable to the employee and must ensure
that each employee can demonstrate knowledge of at least the following:
1. The health hazards associated with chromium (VI) exposure;
2. The location, manner of use, and release of chromium (VI) in the
workplace and the specific nature of operations that could result in
exposure to chromium (VI), especially above the PEL;
3. The engineering controls and work practices associated with the
employee's job assignment;
4. The purpose, proper selection, fitting, proper use, and
limitations of respirators and protective clothing;
5. Emergency procedures;
6. Measures employees can take to protect themselves from exposure
to chromium (VI), including modification of personal hygiene and habits
such as smoking;
7. The purpose and a description of the medical surveillance
program required by paragraph (k) of the general industry section and
paragraph (h) of shipyards and construction sections;
8. The contents of the standard; and
9. The employee s rights of access to records under 29 CFR
1910.1020(g).
1910.1026(m), 1915.1026(j), and 1926.1126(j)--Recordkeeping
Paragraph (m)(1) of the general industry section requires that
employers maintain an accurate record of all employee exposure-
monitoring records required in paragraph (d) of this section. The
record must include at least the following information:
1. The date of measurement for each sample taken;
2. The operation involving exposure to chromium (VI) that is being
monitored;
3. Sampling and analytical methods used and evidence of their
accuracy;
4. Number, duration, and the results of samples taken;
5. Type of personal protective equipment, such as respirators worn;
and,
6. The name, social security number, and job classification of all
employees represented by the monitoring, indicating which employees
were actually monitored.
Employers must maintain and make available employee exposure
monitoring records in accordance with 29 CFR 1910.1020.
Paragraph (m)(2) of the general industry section requires employers
who rely on historical monitoring data to maintain a record of
historical data. The record must include information that reflects the
following conditions:
1. The data were collected using methods that meet the accuracy
requirements of paragraph (d)(6) of the general industry section;
2. The processes and work practices that were in use when the
historical monitoring data were obtained are essentially the same as
those to be used during the job for which initial monitoring will not
be performed;
3. The characteristics of the chromium (IV) containing material
being handled when the historical monitoring data were obtained are the
same as those on the job for which initial monitoring will not be
performed;
4. Environmental conditions prevailing when the historical
monitoring data were obtained are the same as those on the job for
which initial monitoring will not be performed; and
5. Other data relevant to the operations, materials, processing, or
employee exposures covered by the exception.
This record must be maintained and must be made available in
accordance with 29 CFR 1910.1020.
Paragraph (m)(3) of the general industry section requires employers
who rely on objective data to satisfy initial monitoring requirements
to establish and maintain an accurate record of the objective data
relied upon. The record must include at least the following
information:
1. The chromium (VI)-containing material in question;
2. The source of the objective data;
3. The testing protocol and results of testing, or analysis of the
material for the release of chromium (VI);
4. A description of the operation exempted from initial monitoring
and how the data support the exemption; and
5. Other data relevant to the operations, materials, processing or
employee exposures covered by the exemption.
Employers must maintain this record for the duration of the
employer's reliance upon such objective data and must make such records
available in accordance with 29 CFR 1910.1020.
Paragraph (m)(4) of the general industry section, and paragraph
(j)(1) of the shipyard and construction sections, require employers to
establish and maintain an accurate record for each employee covered by
medical surveillance under paragraph (k) of the general industry
section, or paragraph (h) of the shipyard and construction sections.
This record must include the following information about the employee:
1. Name and social security number;
2. A copy of the PLHCP's written opinions as required by paragraph
(k)(5) of the general industry section, or paragraph (h)(5) for the
shipyard and construction sections;
3. A copy of the information provided to the PLHCP as required by
paragraph (k)(4) of the general industry section, or (h)(4) in the
shipyards and construction sections; Employers must ensure that medical
records are maintained and made available in accordance with 29 CFR
1910.1020.
Paragraph (m)(5) of the general industry section and paragraph
(j)(2) of the shipyards and construction sections require employers to
prepare a record at the completion of training that indicates the
identity of the individuals trained and the date the training was
completed. This record must be maintained for three years after the
completion of training. The employer must provide to the Assistant
Secretary or the Director, upon request, all materials relating to
employee information and training.
Respondents: Employers in general industry, shipyards or
construction whose employees work in jobs where there is a potential
for chromium (VI) exposure (38,391 businesses).
Frequency of Response: Frequency of response varies depending on
the specific collection of information.
Average Time Per Response: Varies from 5 minutes (.08 hour) for the
employer to provide a copy of the written physician's opinion to the
employee, to 12 hours to conduct exposure monitoring.
Total burden hours: 696,659.
Costs: (purchase of capital/startup costs): $30,793,697.
The Agency has submitted a copy of the information collection
request to OMB for its review and approval. Interested persons may
submit comments regarding the burden
[[Page 59444]]
estimates or other aspects of the information collection request to the
OSHA Docket Office, Docket No. H054A, Occupational Safety and Health
Administration, Room N-2625, 200 Constitution Avenue, NW., Washington,
DC 20210, and to the Office of Information and Regulatory Affairs,
Office of Management and Budget, New Executive Office Building, Room
10235, 725 17th Street, NW., Washington, DC 20503 (Attn: OSHA Desk
Officer (RIN 1218-AB45)). Comments submitted in response to this notice
will be summarized and/or included in the request for OMB approval of
the final information collection request, and they will also become a
matter of public record.
Copies of the referenced information collection request are
available for inspection and copying in the OSHA Docket Office and will
be provided to persons who request copies by telephoning Todd Owen at
(202) 693-1941. For electronic copies of the chromium (VI) information
collection request, contact the OSHA Web page on the Internet at http://www.osha.gov/
.
XI. Federalism
The Agency reviewed the proposed 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 proposal 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 proposed rulemaking does not
expand this limitation. OSHA has authority under Executive Order 13132
to propose a Cr(VI) standard because the problems addressed by these
requirements are national in scope.
As explained in section VIII 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 proposal 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 final requirements that result from this
proposal.
XII. State Plans
The 26 states and territories with their own OSHA-approved
occupational safety and health plans must adopt comparable provisions
within six months after the Agency publishes 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.
XIII. Unfunded Mandates
The Agency reviewed the proposed 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 IX of this preamble,
OSHA estimates that compliance with this proposal would require
private-sector employers to expend about $223 each year. However, while
this proposal 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 proposed provisions 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 to date, the Agency believes that few, if any, of the employers
affected by the proposal are state, local, and tribal governments.
Therefore, the proposed Cr(VI) requirements do not impose unfunded
mandates on state, local, and tribal governments.
XIV. 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 effect 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 proposed Cr(VI) standard is
economically significant under Executive Order 12866 (see section IX of
this preamble). However, after reviewing the proposed 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 proposed standard would require 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
[[Page 59445]]
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 proposed
rule than they are currently. Based on this preliminary determination,
OSHA believes that the proposed Cr(VI) standard does not constitute a
covered regulatory action as defined by Executive Order 13045.
XV. Environmental Impacts
The Agency reviewed the proposed 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 preliminary
determination that the proposed 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
proposed Cr(VI) standard would have no significant environmental
impacts.
XVI. Public Participation--Notice of Hearing
OSHA encourages members of the public to participate in this
rulemaking by submitting comments on the proposal, and by providing
oral testimony and documentary evidence at the informal public hearing
that the Agency will convene after the comment period ends. The Agency
invites interested persons having knowledge of, or experience with,
occupational exposure to Cr(VI) to participate in this process, and
welcomes any pertinent data and cost information that will provide it
with the best available evidence on which to develop the final
regulatory requirements. This section describes the procedures the
public must use to submit their comments to the docket in a timely
manner, and to schedule an opportunity to deliver oral testimony and
provide documentary evidence at informal public hearings on the
proposal. Comments, notices of intention to appear, hearing testimony,
and documentary evidence will be available for inspection and copying
at the OSHA Docket Office. You also should read the sections above
titled DATES and ADDRESSES for additional information on submitting
comments, documents, and requests to the Agency for consideration in
this rulemaking.
Written Comments. OSHA invites interested persons to submit written
data, views, and arguments concerning this proposal. In particular,
OSHA encourages interested persons to comment on the issues raised in
section II of this preamble. When submitting comments, parties must
follow the procedures specified above in the sections titled DATES and
ADDRESSES. The comments must clearly identify the provision of the
proposal you are addressing, the position taken with respect to each
issue, and the basis for that position. Comments, along with supporting
data and references, received by the end of the specified comment
period will become part of the record, and will be available for public
inspection and copying at the OSHA Docket Office.
Informal Public Hearing. Pursuant to section 6(b)(3) of the Act,
members of the public will have an opportunity to provide oral
testimony concerning the issues raised in this proposal at informal
public hearings. The hearings will commence at 9:30 a.m. on February 1,
2005. At that time, the presiding administrative law judge (ALJ) will
resolve any procedural matters relating to the proceeding. The
legislative history of section 6 of the OSH Act, as well as OSHA's
regulation governing public hearings (29 CFR 1911.15), establish the
purpose and procedures of informal public hearings.
Although the presiding officer at such hearings is an ALJ, and
questioning by interested persons is allowed on crucial issues, the
proceeding is informal and legislative in purpose. Therefore, the
hearing provides interested persons with an opportunity to make
effective and expeditious oral presentations in the absence of
procedural restraints or rigid procedures that could impede or protract
the rulemaking process. The hearing is an informal administrative
proceeding, rather than adjudicative one in which the technical rules
of evidence would apply; its primary purpose is to gather and clarify
information. The regulations that govern public hearings, and the pre-
hearing guidelines issued for this hearing, will ensure participants
fairness and due process, and also will facilitate the development of a
clear, accurate, and complete record. Accordingly, application of these
rules and guidelines will be such that questions of relevance,
procedure, and participation generally will favor development of the
record. Conduct of the hearing will conform to the provisions of 29 CFR
part 1911, ``Rules of Procedure for Promulgating, Modifying, or
Revoking Occupational Safety and Health Standards.''
Although the ALJs who preside over these hearings make no decision
or recommendation on the merits of OSHA's proposal, they do have the
responsibility and authority to ensure that the hearing progresses at a
reasonable pace and in an orderly manner. To ensure that interested
persons receive a full and fair informal hearing as specified by 29 CFR
part 1911, the ALJ has the authority and power to: Regulate the course
of the proceedings; dispose of procedural requests, objections, and
comparable matters; confine the presentations to matters pertinent to
the issues raised; use appropriate means to regulate the conduct of the
parties who are present at the hearing; question witnesses, and permit
others to question witnesses; and limit the time for such questioning.
At the close of the hearing, the ALJ will establish a post-hearing
comment period for parties who participated in the hearing. During the
first part of this period, the participants may submit additional data
and information to OSHA, while during the second part of this period,
they may submit briefs, arguments, and summations.
Notice of Intention to Appear to Provide Testimony at the Informal
Public Hearing. Interested persons who intend to provide oral testimony
at the informal public hearing must file a notice of intention to
appear by using the procedures specified above in the sections titled
DATES and ADDRESSES. This notice must provide the: Name, address, and
telephone number of each individual who will provide testimony;
capacity (e.g., name of the organization the individual is
representing; the individual's title and position) in which each
individual will testify; approximate amount of time required for each
individual's testimony; specific issues each individual will address,
including a brief statement of the position that the individual will
take with respect to each of these issues; and any documentary evidence
the individual will present, including a brief summary of the evidence.
The hearings are open to the public, and all interested persons are
welcome to attend. However, only a person who files a proper notice of
intention to appear may ask questions and participate fully in the
proceedings. While a person who did not file a notice of intention to
appear may be allowed to testify at the hearing if time permits, this
determination is at the discretion of the presiding ALJ.
Hearing Testimony and Documentary Evidence. Any person requesting
more than 10 minutes to testify at the informal public hearing, or who
intends to submit documentary evidence at the hearing, must provide the
complete text
[[Page 59446]]
of the testimony and the documentary evidence as specified above in the
DATES and ADDRESSES sections. The Agency will review each submission
and determine if the information it contains warrants the amount of
time requested. If OSHA believes the requested time is excessive, it
will allocate an appropriate amount of time to the presentation, and
will notify the participant of this action, and the reasons for the
action, prior to the hearing. The Agency may limit to 10 minutes the
presentation of any participant who fails to comply substantially with
these procedural requirements; in such instances, OSHA may request that
the participant return for questioning at a later time.
Certification of the Record and Final Determination After the
Informal Public Hearing. Following the close of the hearing and post-
hearing comment period, the presiding ALJ will certify the record to
the Assistant Secretary of Labor for Occupational Safety and Health;
the record will consist of all of the written comments, oral testimony,
and documentary evidence received during the proceeding. OSHA will
review the proposed Cr(VI) standard in light of all the evidence
received as part of the record, and will make its decisions based on
substantial evidence in the record as a whole.
XVII. Summary and Explanation of the Standards
OSHA believes that, based on currently available information, the
proposed requirements set forth in this notice are necessary and
appropriate to provide adequate protection to employees exposed to
Cr(VI). OSHA has considered responses to the RFI as well as numerous
reference works, journal articles, and other data obtained by the
Agency in the development of this proposed standard.
The language of the standards and the order of the various
provisions are generally consistent with drafting in other recent OSHA
health standards, such as the methylene chloride, formaldehyde, and
cadmium standards. OSHA believes that a similar style should be
followed from standard to standard when possible in order to facilitate
uniformity of interpretation of similar provisions. This approach is
also consistent with Section 6(b)(5) of the OSH Act, which states that
health standards shall consider ``experience gained under this and
other health and safety laws.''
(a) Scope and Application
OSHA is proposing to issue separate standards addressing hexavalent
chromium exposure in general industry, construction, and shipyards. The
standard for shipyards would also apply to marine terminals and
longshoring. The standards are intended to provide equivalent
protection for all workers, while accounting for the different work
activities, anticipated exposures, and other conditions in these
sectors. The proposed standards for construction and shipyards are very
similar to each other, but differ in some respects from the proposed
standard for general industry. This summary and explanation will
describe the proposed standard for general industry and will note
differences between it and the proposed standards for construction and
shipyards.
Based on the record developed to date, OSHA believes that certain
activities in construction and shipyards are different enough to
warrant requirements that are somewhat modified from those proposed for
general industry. This preliminary determination is consistent with the
recommendation of the Maritime Advisory Committee on Occupational
Safety and Health (MACOSH), which has recommended that a separate
standard be developed for maritime. The proposed standards do not cover
the agricultural sector. OSHA is not aware of significant exposures to
Cr(VI) in agriculture. The Agency is interested in any evidence
indicating that significant exposures to Cr(VI) occur in sectors not
covered under the proposed standards. Accordingly, the subject has been
raised in the ``Issues'' section of this proposal.
The proposed standard applies to occupational exposures to
hexavalent chromium (also referred to as chromium (VI) or 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 stakeholders have argued that specific Cr(VI) compounds should
be excluded from this rulemaking and addressed in a separate standard.
Notably, after OSHA was initially petitioned to issue a Cr(VI)
standard, the Color Pigments Manufacturers Association (CPMA) submitted
a cross-petition calling for a separate standard for lead chromate
pigments (Ex. 2). CPMA argued that differences in the bioavailability
and toxicity of lead chromate when compared to other Cr(VI) compounds
warranted a separate standard (Ex. 2, p. 5). CPMA stated:
Simply put, there are no studies which show a link between lead
chromate pigments in a finished form and cancer caused by exposure
to Chromium VI. To the contrary, studies of lead chromate workers in
the manufacture of lead chromate pigments alone do not show any
increased risk of cancer (Ex. 2, p. 5).
Because CPMA deemed that lead chromate pigments posed little threat to
employee health, and because of concern about adverse economic impacts
associated with regulation, the Association considered that ``* * * no
good purpose would be served by additional restrictions on lead
chromate pigments'' (Ex. 2, p. 6). This position was reiterated in
CPMA's response to the RFI (Ex. 31-15, p. 6).
In its response to the RFI, the Boeing Company also expressed the
view that OSHA should consider the bioavailability of different Cr(VI)
compounds (Ex. 31-16, p. 8). Boeing indicated that exposures to
strontium chromate and zinc chromate used in aerospace manufacturing
are not equivalent to Cr(VI) exposures in other industries. The
findings of two epidemiological studies of Cr(VI)-exposed aerospace
workers were said to support this conclusion.
OSHA has proposed a rule that covers all Cr(VI) compounds because
the Agency believes the evidence supports this approach. As discussed
in Section VI.A of this preamble, absorption of Cr(VI) from the lung
into the bloodstream is greatly dependent on the solubility of the
Cr(VI) compound. Insoluble chromates are poorly absorbed and as a
result remain in the lungs for a longer period of time (Ex. 35-87).
While in the lungs, insoluble Cr(VI) particulates can come into contact
with the epithelial cell surface, resulting in uptake into cells (Exs.
35-68; 35-67). Cellular uptake leads to DNA damage, apoptosis, and
neoplastic transformation (Ex. 35-119). Less water-soluble chromates
(e.g., lead chromate) appear to be more potent carcinogens than more
soluble chromates (e.g., sodium chromate). (For a detailed discussion,
see Section VI.B.8 of this preamble.)
Experimental studies involving Syrian hamster embryo cells support
the belief that cytotoxicity and neoplastic transformation occur when
exposures involve lead chromate pigments (Ex. 12-5). Evidence indicates
that even chromates that are encapsulated in a paint matrix may be
released in the lungs (Ex. 31-15, p. 2). OSHA therefore sees no reason
to exempt these
[[Page 59447]]
compounds from the current Cr(VI) rulemaking.
OSHA believes this view is consistent with the epidemiological
studies involving chromate pigment production workers and aerospace
workers. While co-exposures to other Cr(VI) compounds do not allow for
specific findings related to lead chromate exposure, OSHA has found
that epidemiological studies of workers in the chromate pigment
production industry have consistently shown excess risks for lung
cancer (see Section VI.B.2 of this preamble). The studies of aerospace
workers did not find an increased risk of lung cancer. However, this is
not convincing evidence that aerospace workers are not at risk from
Cr(VI) exposure. The small cohort size, lack of smoking data,
relatively young age of the population, and number of members lost to
follow-up in the study reported by Alexander et al. (Ex. 31-16-3) and
the lack of exposure information in the report of Boice et al. (Ex. 31-
16-4) do not allow for any broad conclusions regarding aerospace
workers to be reached on the basis of these two studies. OSHA's
preliminary conclusion that Cr(VI) compounds should be addressed
collectively under a single standard is consistent with the findings of
IARC, NTP, and NIOSH. These organizations have each found Cr(VI)
compounds to be carcinogenic, without exception. Although ACGIH has
issued different TLVs for soluble and insoluble Cr(VI) compounds, and
for certain specific compounds, the TLV for insoluble Cr(VI) compounds
is five-fold lower than the TLV for soluble Cr(VI) compounds. This is
consistent with OSHA's preliminary finding that less soluble Cr(VI)
compounds, to the extent that they differ from more soluble Cr(VI)
compounds, are more potent carcinogens and pose a greater risk to the
health of workers.
The proposed standard applies to occupational exposure in which
Cr(VI), in any quantity, is present in an occupationally related
context. Exposure of employees to the ambient environment, which may
contain small concentrations of Cr(VI) unrelated to the job, is not
subject to this standard.
The proposed standard for construction does not cover exposure to
Cr(VI) in 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 cement is generally less than 20
[mu]g/g (Ex. 9-57). While the Cr(VI) in cement may represent a dermal
hazard, the evidence obtained by OSHA thus far indicates that the
Cr(VI) concentration is generally so low that the proposed PEL could
not be reached without exceeding OSHA's current PEL for Particulates
Not Otherwise Regulated (PNOR). The PEL for PNOR (15 [mu]g/
m3 for total dust) thus is at least as protective as the
proposed Cr(VI) PEL in limiting the Cr(VI) inhalation exposure of
cement workers. OSHA's preliminary exposure profile indicates that no
employees are exposed to levels of Cr(VI) above 0.25 [mu]g/
m3 as an 8-hour TWA during cement work in construction.
Because airborne exposures to Cr(VI) during cement work in construction
are expected to be minimal, and because of the economic burden of
applying the ancillary provisions of the proposed standard to workers
exposed to portland cement in the construction environment, OSHA has
preliminarily concluded that exposures to Cr(VI) from portland cement
are best addressed by providing guidance to employers rather than
including portland cement in the construction rule.
OSHA has proposed to cover exposures to Cr(VI) in portland cement
in general industry. The Agency's preliminary exposure profile
indicates that some employees in general industry are exposed to
airborne Cr(VI) levels associated with a significant risk of lung
cancer as a result of work with portland cement. OSHA's preliminary
findings show that nearly 2500 workers in general industry are exposed
to Cr(VI) levels between 0.25 [mu]g/m3 and 0.5 [mu]g/
m3 as an 8-hour TWA. Because of the evidence of higher
airborne Cr(VI) exposures in general industry than in construction, and
because lower burdens are anticipated in the more stable work
environments found in general industry, the Agency believes it is
appropriate to cover Cr(VI) exposures from portland cement under the
general industry proposed standard. OSHA is interested in comments and
information regarding this preliminary determination, and has included
this topic in the ``Issues'' section of this preamble.
This proposal 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 proposes to specifically
exclude those exposures regulated by EPA from coverage under the
standard.
The manufacture of pesticides containing Cr(VI) is not considered
pesticide application, and is covered under this proposed standard. The
use of wood treated with pesticides containing Cr(VI) is also covered.
In this respect, the proposed 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. The
record in this rulemaking indicates that work with wood treated with
pesticides containing Cr(VI) can involve significant Cr(VI) exposures.
OSHA's exposure profile for woodworking indicates that over 30% of
current employee Cr(VI) exposures exceed the proposed PEL. OSHA
therefore believes it appropriate to include these activities under the
scope of the proposed standard.
(b) Definitions
``Action level'' is defined as an airborne concentration of Cr(VI)
of 0.5 micrograms per cubic meter of air (0.5 [mu]g/m3)
calculated as an eight-hour time-weighted average (TWA). The action
level triggers requirements for exposure monitoring and medical
surveillance in general industry workplaces. In this proposal, as in
other standards, the action level has been set at one-half of the PEL.
Because of the variable nature of employee exposures to airborne
concentrations of Cr(VI), maintaining exposures below the action level
provides reasonable assurance that employees will not be exposed to
Cr(VI) at levels above the PEL on days when no exposure measurements
are made. Even when all measurements on a given day may fall below the
PEL (but are above the action level), there is some chance that on
another day, when exposures are not measured, the employee's actual
exposure may exceed
[[Page 59448]]
the PEL. When exposure measurements are above the action level, the
employer cannot be reasonably confident that employees may not be
exposed to Cr(VI) concentrations in excess of the PEL during at least
some part of the work week. Therefore, requiring periodic exposure
measurements when the action level is exceeded provides the employer
with a reasonable degree of confidence in the results of the exposure
monitoring.
The action level is also intended to encourage employers to lower
exposure levels in order to avoid the costs associated with the
exposure monitoring and medical surveillance provisions. Some employers
would be able to reduce exposures below the action level in all work
areas, and other employers in some work areas. As exposures are
lowered, the risk of adverse health effects among workers decreases.
OSHA s preliminary risk assessment indicates that significant risk
remains at the proposed PEL of 1.0 [mu]g/m3. Where there is
continuing significant risk, the decision in the Asbestos case
(Building and Construction Trades Department, AFL-CIO v. Brock, 838 F.
2d 1258, (D.C. Cir 1988)) indicated 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's preliminary
conclusion is that the action level will result in a very real and
necessary, but non-quantifiable, further reduction in risk beyond that
provided by the PEL alone. OSHA's choice of proposing an action level
of one-half of the PEL is based on the Agency's successful experience
with 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).
As discussed under the requirements for exposure monitoring, OSHA
has not proposed an action level for construction and shipyards. This
definition is therefore not included in the proposed standards for
construction and shipyards.
``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 preliminary 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 VI 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 proposed 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. Every spill or leak is not necessarily an emergency. The
exposure to Cr(VI) must be unexpected and significant.
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. The particular
circumstances of the release itself, such as the quantity involved,
confined space considerations, and the adequacy of ventilation will
have an impact on employee safety. In addition, factors such as the
knowledge of employees in the immediate work area, 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. Those instances that
constitute an emergency trigger certain requirements in this proposed
standard (e.g., medical surveillance) that are discussed later in this
section.
``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.
``Physician or other licensed health care professional (PLHCP)''
refers to an individual who is legally permitted to provide some or all
of the health care services required by this section. This definition
is included because the proposed standard requires that all medical
examinations and procedures be performed by or under the supervision of
a PLHCP.
Any professional may perform the medical examinations and
procedures provided under the standard when they are licensed by state
law to do so. The Agency recognizes that this means that the personnel
qualified to provide the required medical examinations and procedures
may vary from state to state, depending on state licensing laws. This
provision grants the employer the flexibility to retain the services of
a variety of qualified licensed health care professionals, provided
that these individuals are licensed to perform the specified service.
OSHA believes that this flexibility will reduce cost and compliance
burdens for employers and increase convenience for employees. The
approach taken in this proposed standard is consistent with the
approach OSHA has taken in other recent standards, such as those for
methylene chloride (29 CFR 1910.1052), bloodborne pathogens (29 CFR
1910.1030), and respiratory protection (29 CFR 1910.134).
``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 proposed a requirement for regulated areas in
construction and shipyards. This definition is therefore not included
in the proposed 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)
OSHA proposes to set an 8-hour time-weighted average (TWA) exposure
limit of 1 microgram of Cr(VI) per cubic meter of air (1 [mu]g/
m3). This limit means that over the course of any 8-hour
work shift, the average exposure to Cr(VI) cannot exceed 1 [mu]g/
m3. The proposed limit applies to Cr(VI), as opposed to the
current PEL which is measured as CrO3. The current PEL of 1
milligram per 10 cubic meters of air (1 [mu]g/10 m3, or 100
[[Page 59449]]
[mu]g/m3) reported as CrO3 is equivalent to a
limit of 52 [mu]g/m3 as Cr(VI). The current PEL is enforced
as a TWA in construction and as a ceiling (a level not to be exceeded
at any time) in general industry.
OSHA proposes a new PEL of 1 [mu]g/m3 because the Agency
has preliminarily determined that occupational exposure to Cr(VI) at
the current PEL results in a significant risk of lung cancer among
exposed workers, and that compliance with the proposed standard will
substantially reduce that risk. OSHA's preliminary risk assessment,
presented in Section VII of this preamble, indicates that the most
reliable lifetime estimate of risk from a 45 year exposure to Cr(VI) at
the current PEL is 101 to 351 excess deaths from lung cancer per 1000
workers. As discussed in Section VIII of this preamble, this clearly
represents a risk of material impairment of health that is significant
within the context of the Benzene decision. OSHA believes that lowering
the PEL to 1 [mu]g/m3 would reduce the lifetime excess risk
of death from lung cancer to between 2.1 and 9.1 per 1000 workers.
OSHA considers the level of risk remaining at the proposed PEL to
be significant. However, as discussed in Section IX of this preamble,
the proposed PEL is set at the lowest level that the Agency believes to
be feasible in all affected industry sectors. As guided by the 1988
Asbestos decision, OSHA is proposing additional requirements to further
reduce the remaining risk. OSHA anticipates that the ancillary
provisions in the proposed standard will further reduce the risk beyond
the reduction that would be achieved by the proposed PEL alone.
OSHA believes that it is appropriate to establish a single PEL that
applies to all Cr(VI) compounds. OSHA's preferred estimates of risk
supporting the proposed PEL are derived from worker cohorts that were
predominantly exposed to soluble sodium chromate. The evidence reviewed
by OSHA indicates that similar doses of less soluble chromates result
in higher numbers of lung tumors when compared to more soluble
compounds such as sodium chromate (see Section VI of this preamble).
Thus, any variation in toxicological effect due to solubility is
expected to result in a higher level of risk than is indicated by
OSHA's preliminary risk estimates. OSHA consequently believes that the
Agency's findings regarding significance of risk are valid regardless
of the solubility of the Cr(VI) compound. However, the available
evidence is not sufficient to make quantitative estimates of risk for
each individual Cr(VI) compound. OSHA is therefore proposing a single
PEL for all Cr(VI) compounds. The Agency seeks comment on whether
different PELs for different Cr(VI) compounds should be set and how
such determinations should be made, and has included this topic in the
``Issues'' section of the preamble.
(d) Exposure Monitoring
The proposed general industry standard imposes monitoring
requirements 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 assessment of employee exposures to Cr(VI)
include: 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.
Paragraph (d)(1) contains proposed general requirements for
exposure monitoring. 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 can be 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.
OSHA proposes that employers who have workplaces covered by the
general industry standard determine if any of their employees are
exposed to Cr(VI) at or above the action level. Further obligations
under the standard would be 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.
Initial monitoring need not be conducted under two circumstances.
First, where the employer has previously monitored for Cr(VI) in the
past 12 months and 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 used and prevailing in the employer's current operations,
and where that monitoring satisfies all other requirements of this
section, including the accuracy and confidence requirements, the
employer may rely on such earlier monitoring results to satisfy the
initial monitoring requirements of this section. This provision is
designed to make it clear that OSHA does not intend to require
employers who have recently performed appropriate employee monitoring
to conduct ``initial'' monitoring. OSHA anticipates that this provision
will reduce the compliance burden on employers, since monitoring for
tasks that involve essentially the same exposures would
[[Page 59450]]
not be required. The Agency believes allowing the use of 12 month old
data is appropriate; samples taken earlier than 12 months previously
may not adequately represent current workplace conditions. The 12 month
limit is consistent with the Methylene Chloride standard (29 CFR
1910.1052).
Second, where the employer has objective data demonstrating that a
particular product or material containing Cr(VI) or a specific process,
operation, or activity involving Cr(VI) cannot release dust, fumes, or
mist in concentrations at or above the action level under any expected
conditions of use, the employer may rely upon such data to satisfy
initial monitoring requirements. The data must reflect workplace
conditions closely resembling the processes, types of material, control
methods, work practices, and environmental conditions in the employers'
current operations.
Objective data demonstrate that the work operation or the product
may not reasonably be foreseen to release Cr(VI) in airborne
concentrations at or above the action level under the expected
conditions of use that will cause the greatest possible release, or in
any plausible accident. The objective data may include monitoring data,
or mathematical modeling or calculations based on the chemical and
physical properties of a material. For example, data collected by a
trade association from its members that meet the definition of
objective data may be used. When using the term ``objective data'',
OSHA is referring to employers' reliance on manufacturers' worst case
studies, laboratory studies, and other research that demonstrates,
usually by means of exposure data, that meaningful exposures cannot
occur. OSHA has allowed employers to use objective data in other
standards such as those for formaldehyde (29 CFR 1910.1048) and
asbestos (29 CFR 1910.1001) in lieu of initial monitoring and hence,
from most of the provisions of these standards.
Paragraph (d)(3) contains requirements for periodic monitoring. The
requirement for continued monitoring depends on the results of initial
monitoring. If the initial monitoring indicates that employee exposures
are below the action level, no further monitoring would be 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 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 proposed rule 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 later, the employer may
discontinue monitoring for those employees whose exposures are
represented by such monitoring. Similarly, if periodic monitoring
measurements indicate that exposures are below the PEL but above the
action level, and those results are confirmed by consecutive
measurements taken at least seven days later, 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 exceed the action level but are below the
PEL, employers should continue to monitor employees to ensure that
exposures remain 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 proposed frequency of six months for subsequent
periodic monitoring for exposures above the action level but 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). The
proposed requirement for periodic monitoring is also consistent with
OSHA's Standards Improvement Project (SIPs) proposal for monitoring
frequency (67 FR 66494, 66504 (8/31/02)).
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. The Agency
intends for this provision to encourage employers to control their
employees' exposures to Cr(VI) below the action level, thus maximizing
the protection of employees' health.
Under paragraph (d)(4), 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). 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. 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 is necessary so that the employer can take appropriate action to
protect exposed employees, such as instituting additional engineering
controls or providing appropriate respiratory protection.
Under paragraph (d)(5) of the general industry standard, employers
are to notify each affected employee of their monitoring results within
15 working days after the receipt of the results. 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
[[Page 59451]]
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.
The proposal would require that all affected employees be notified
of the monitoring results. When using the term ``affected employees''
in this context, OSHA is not referring only to the employee(s) actually
subject to personal monitoring. Affected employees include all
employees represented by the employee(s) sampled.
Individual notification in writing or posting would be acceptable
under the proposed rule. This is consistent with other OSHA standards
such as those for methylenedianiline (29 CFR 1910.1050), butadiene (29
CFR 1910.1051), and methylene chloride (29 CFR 1910.1052). In addition,
the SIPs proposal (67 FR 66494, 66508 (10/31/02)) allows for employer
choice of notification method. The Cr(VI) proposal is also consistent
with SIPs in that SIPs specifies 15 working days after the receipt of
monitoring results as the appropriate time to notify employees in
general industry (67 FR 66494, 66508 (10/31/03)).
Under paragraph (d)(6), the employer would be required 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% percent for airborne concentrations at or above the action
level. Many laboratories presently have methods to measure Cr(VI) at
the proposed action level with at least the required degree of
accuracy. One example of an acceptable method of monitoring and
analysis is OSHA method ID215. Rather than specifying a particular
method that must be used, OSHA proposes to take a performance approach
and instead allows the employer to use any method as long as the chosen
method meets the accuracy specifications.
Paragraph (d)(7) requires the employer to provide affected
employees or their designated representatives an opportunity to observe
any monitoring of employee exposure to Cr(VI). 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 applicable 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).
The proposed construction and shipyard standards for Cr(VI) do not
include provisions for exposure monitoring. OSHA recognizes that in
these sectors in many instances the results of exposure monitoring
required under this proposed standard would not be available until
after operations involving Cr(VI) exposure have been completed. For
example, a welding task may be finished in a single day. If air
monitoring is performed, the task would be completed before the
employer is informed of the monitoring results. Therefore, the employer
would not be in a position to make use of the monitoring results to
determine appropriate control measures for that task. In other cases,
the workplace conditions in construction and shipyard worksites may
vary to such a great extent that it may be difficult to accurately
characterize employee exposure from one day to the next. For example, a
stainless steel welder may work outdoors on a windy day one day and in
an enclosed environment the next day. Personal monitoring for Cr(VI)
exposure on a given day may not accurately reflect these changing
conditions. OSHA has therefore proposed a performance-oriented
requirement for construction and shipyard employers. Rather than
include specific requirements for exposure monitoring for these
employers, OSHA proposes to allow construction and shipyard employers
the flexibility to assess Cr(VI) exposures in any manner they choose.
Thus, construction and shipyard employers could use historical data,
objective data, or employee monitoring to determine employee exposures.
Because the obligation to comply with the PEL would remain, whatever
method the employer chooses would have to be sufficient to ensure that
no employee is exposed to an airborne concentration of Cr(VI) in excess
of the PEL.
In some cases, the employer may choose not to perform any
monitoring. For example, certain tasks (e.g., abrasive blasting of
materials coated with Cr(VI); welding, cutting, or torch burning of
stainless steel or of materials coated with Cr(VI); or spray
application of Cr(VI) containing paints or coatings) frequently entail
exposures to Cr(VI) above the proposed PEL. OSHA estimates that
approximately 43% of the exposures in construction welding and 17.9% of
the exposures in shipyard welding are greater than the proposed PEL of
1 [mu]g/m3. A construction or shipyard employer has the
option of assuming the employee is exposed above the PEL and providing
appropriate protective measures as prescribed by the standard.
Similarly, an employer may not find it necessary to perform
exposure monitoring where exposures are well below the PEL. For
example, there are several construction application groups (e.g.,
industrial rehabilitation and maintenance, hazardous waste site work,
and refractory restoration and maintenance) where a large percentage of
exposures are either below 0.25 [mu]g/m3 or below the limit
of detection for Cr(VI). In these situations, employers may be
relatively assured that employees' exposure are well below the PEL and
would therefore not need to conduct exposure monitoring.
This approach is 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. The Agency seeks comment as to whether this performance-
oriented approach to exposure monitoring is appropriate in construction
and shipyard workplaces, and has included this topic in the ``Issues''
section of this preamble.
(e) Regulated Areas
Under paragraph (e), general industry employers must 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, and would be required to
include the warning signs specified in paragraph (l)(2) of the proposed
standard. Access to regulated areas is limited to persons authorized by
the employer and required by work
[[Page 59452]]
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 entering the area to be properly protected, the number of
persons given access to the area should 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 proposal to as few employees as possible.
In keeping with the performance orientation of this proposed
standard, OSHA has not specified how employers are to demarcate
regulated areas. The demarcation should effectively warn employees not
to enter the area unless they are authorized, and then only if they are
using the proper personal protective equipment. The demarcation must
include display of warning signs at all approaches to the regulated
areas, consistent with the requirements of paragraph (l)(2) of this
proposed standard. In many cases these warning signs alone will be
sufficient to identify the boundaries of the regulated area.
Access to the regulated area is restricted to ``authorized
persons''. For the purposes of this proposed standard, these are
persons required by their job duties to be present in the area, as
authorized by the employer. In addition, persons exercising the right
to observe monitoring procedures are also allowed to enter regulated
areas. Employees in some workplaces may designate a union
representative to observe monitoring; this person would be allowed to
enter the regulated area. Persons authorized under the OSH Act, such as
OSHA compliance officers, are also allowed access to regulated areas.
OSHA has not included a requirement for regulated areas in
construction and shipyard workplaces, due to the expected difficulties
in establishing regulated areas in construction and shipyard
workplaces. For example, several small entity representatives (SERs)
from the construction and shipyard industries who participated in the
SBREFA review noted that in their work settings regulated areas would
be particularly problematic and might require that the entire worksite
be designated as a regulated area. They also noted that due to the
changing nature of the work site (namely construction sites) the
demarcation of the regulated area would have to be changed each day as
the work progressed (e.g., Exs. 34-6, 34-14). The same rationale
applies to shipyards. The Agency seeks comment as to whether a
requirement for the establishment of regulated areas would be
appropriate for construction or shipyard workplaces and how such areas
could be established, and has included this topic in the ``Issues''
section of this preamble.
(f) Methods of Compliance
The proposed standard requires employers to 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, or if employees are not exposed above the PEL for 30
or more days per year. Employers would be required to institute
engineering controls and work practices to reduce exposure to the
lowest feasible level even if these measures alone would not reduce the
concentration of airborne Cr(VI) to or below the PEL. The employer
would then be required to supplement these controls with respirators to
ensure that employees are not exposed to Cr(VI) above the PEL.
Primary reliance on engineering controls and work practices is
consistent with good industrial hygiene practice and with OSHA'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 continually and
inexpensively, allow for predictable performance levels, and can
efficiently remove toxic substances 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.
For these reasons, engineering controls are preferred by OSHA.
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.
[[Page 59453]]
Work practices 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 provides
further support for ensuring 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.
OSHA has traditionally relied less on respiratory protection in the
hierarchy of controls because the use and efficacy of respirators
depends to a great extent on human behavior. Often work is strenuous,
and the increased breathing resistance of the respirator reduces its
acceptability to employees. Respirators can limit an employee's vision
and ability to communicate. In some difficult and dangerous jobs,
effective vision or communication is vital to a safe, efficient
operation. Voice communication when using a respirator can be difficult
and fatiguing. In any event, movement of the jaw in speaking can cause
a temporary breaking of the face-to-facepiece seal, thereby reducing
the efficiency of the respirator and decreasing the employee's
protection. Skin irritation can result from wearing a respirator in
hot, humid conditions. Such irritation can cause considerable distress
to workers and may disrupt work schedules. To be used effectively,
respirators must be individually selected; fitted and periodically
refitted; conscientiously and properly worn; regularly maintained,
including filter changes; and replaced as necessary. In some
workplaces, these preconditions for effective respirator use can be
difficult to achieve. It is more difficult to assure that each employee
is wearing a respirator correctly than to ascertain that engineering
controls are operational. Thus, OSHA has concluded that reliance upon
respirators should be minimized when engineering and work practice
controls are found to be effective.
OSHA has proposed an exception to the general requirement for
primary reliance on engineering and work practice controls for those
employers who do not have employee exposures above the PEL for 30 or
more days per year (12 consecutive months) from a particular process or
task. Thus, if an employee is exposed to Cr(VI) on only 29 days during
any 12 consecutive months from a particular process or task, even if
the exposure is above the PEL on all of these days, the employer would
not be required by this proposed standard to implement engineering and
work practice controls to control exposures to the PEL. The burden
would be on the employer to show that exposures do not exceed the PEL
on 30 or more days per year. OSHA believes this provision would provide
needed flexibility to employers, while still protecting workers.
Under the proposed exception, the employer's obligation to
implement engineering and work practice controls to comply with the PEL
would not be triggered until an employee in a process or task is
exposed above the PEL on 30 or more working days during a year. Where
the exposure is for fewer than 30 working days, the employer could use
any combination of controls to prevent employees from being exposed
above the PEL, including respirators alone. The employer may use this
exception if he or she has a reasonable basis for believing that
employees in a process or task will not be exposed above the PEL for 30
or more days per year (12 consecutive months). OSHA intends for this
exception to be process- or task-based, i.e., it is specific to a
process where engineering controls might be implemented to reduce
exposures below the PEL. For example, an employer might have two
processes, A and B, where A involved an ongoing process in the facility
with exposures above the PEL for more than 30 days and another process,
B, only resulted in exposures above the PEL between 10 and 29 days. The
fact that the employer had employees exposed above the PEL for more
than 30 days in process A would not be used to determine that
engineering and work practice controls had to be used for process B.
OSHA intends this exception to be similarly applied by process or task
in the construction and shipyard environments where employees may move
from one work site to another.
OSHA has proposed this exception because the Agency 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 of exposure, it may not be economically
feasible or cost effective to invest the monies needed to install
engineering controls or to institute work practices to control Cr(VI)
to the PEL. Without such an exception, employers would be required to
implement feasible engineering controls or 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 and work practice controls in such
circumstances may not be justified. Consequently, incorporating an
exception is a reasonable way to lessen the burden on employers while
still protecting employees. OSHA's proposed exception for fewer than 30
working days per year is consistent with the standards for lead (29 CFR
1910.1025) and cadmium (29 CFR 1910.1027), both of which incorporate
similar provisions.
In proposing this exception, OSHA intends to provide relief
exclusively to employers whose employees are exposed to Cr(VI) only for
short periods (in terms of days and weeks) and otherwise are not
exposed to Cr(VI) above the PEL. Where the employee has other exposures
above the PEL, the employer would be obligated to achieve the PEL by
means of engineering and work practice controls. The Agency believes
the proposed 30-working-day exclusion would make the standard more
flexible in workplaces where exposure days are extremely limited.
In order for this exception to apply, the proposed standard states
that the employer must have a ``reasonable basis for believing that no
employees in a
[[Page 59454]]
process or task will be exposed above the PEL for 30 or more days''.
Historical data, objective data, or exposure monitoring data may all
provide a reasonable basis for believing that employees will not be
exposed above the PEL for 30 or more days per year. Other information,
such as production orders showing that processes involving Cr(VI)
exposures are conducted on fewer than 30 days per year, may also serve
as a reasonable basis for believing that employees will not be exposed
above the PEL for 30 or more days per year.
In order to take advantage of the proposed exception, the employer
would have the burden to demonstrate that his or her employees in a
process or task will not be exposed above the PEL for more than 30 days
per year. The burden of proof is placed on the employer because the
employer has access to needed information about employee exposure
levels and processes and tasks at the worksite. Where existing
information is inadequate, the employer is also in the best position to
develop the necessary information. The obligation to demonstrate that a
reasonable basis exists for believing that employees in a process or
task will not be exposed above the PEL for more than 30 days per year
is the same for general industry, construction, and shipyard employers.
Paragraph (f)(2) of the proposed rule (paragraph (d)(2) of the
construction and shipyard proposals) would prohibit the employer from
using employee rotation as a means of compliance with the PEL. Worker
rotation reduces the exposures to individual employees, but increases
the number of employees exposed. Since OSHA has made a preliminary
determination that Cr(VI) is carcinogenic, the Agency considers it
inappropriate to place more workers at risk. Since no threshold has
been established for the carcinogenic effects of Cr(VI), it is prudent
to limit the number of workers exposed at any concentration. This
provision does not, however, prohibit worker rotation when it is
conducted for reasons other than compliance with the PEL. For example,
an employer may rotate workers in order to provide cross-training on
different tasks, or to allow workers to alternate physically demanding
tasks with less strenuous activities. OSHA does not intend for this
provision to be interpreted as a general prohibition on employee
rotation where workers are exposed to Cr(VI). This proposed provision
is consistent with other OSHA standards such as those for butadiene (29
CFR 1910.1051), methylene chloride (29 CFR 1910.1052), and cadmium (29
CFR 1910.1027).
(g) Respiratory Protection
When engineering controls and work practices cannot reduce employee
exposure to Cr(VI) to within the PEL, OSHA proposes that the employer
must protect employees' health through the use of respirators.
Specifically, respirators would be required as supplementary protection
to reduce employee exposure during the installation and implementation
of engineering and work practice controls; during work operations where
engineering and work practice controls are not feasible; when all
feasible engineering and work practice controls have been implemented,
but are not sufficient to reduce exposure to or below the PEL; during
work operations where employees are exposed above the PEL for fewer
than 30 days per year, and the employer has elected not to implement
engineering and work practice controls to achieve the PEL; and during
emergencies.
These limitations on the required use of respirators are generally
consistent with other OSHA health standards, such as those for
butadiene (29 CFR 1910.1051) and methylene chloride (29 CFR 1910.1052).
They reflect the Agency's determination, discussed in the section on
methods of compliance, that respirators are inherently less reliable
than engineering and work practice controls. OSHA has therefore
proposed to allow reliance on respirators only in certain designated
situations.
In those circumstances where engineering and work practice controls
cannot be used to achieve the PEL (e.g., in emergencies, or during
periods when equipment is being installed), or where engineering
controls may not be reasonably necessary (e.g., where employees are
exposed above the PEL for fewer than 30 days per year), OSHA recognizes
that respirators may be essential to reduce worker exposure, and
provision is made for their use as primary controls. In other
circumstances, where feasible work practices and engineering controls
alone cannot reduce exposure levels to the PEL, respirators also may be
used for supplemental protection. In these situations, the burden of
proof is placed on the employer to demonstrate that engineering and
work practice controls are not feasible.
OSHA anticipates that engineering and work practice controls will
be in place by the effective dates specified in paragraph (n) of this
proposal (paragraph (k) for construction and shipyards). The Agency
realizes that in some cases employers may commence operations that
involve employee Cr(VI) exposures after that date, may install new or
modified equipment, or make other workplace changes that result in new
or additional exposures to Cr(VI). In these cases, a reasonable amount
of time may be needed before appropriate engineering controls can be
installed and proper work practices implemented. When employee
exposures exceed the PEL in these situations, employers are expected to
provide respiratory protection to protect workers.
Respiratory protection is also required during work operations
where engineering and work practice controls are not feasible. OSHA
anticipates that there will be very few situations where no engineering
and work practice controls are feasible to limit employee exposure to
Cr(VI). In other cases, some engineering and work practice controls may
be feasible, but these controls may not be capable of lowering employee
exposures to or below the PEL. For example, tasks such as stainless
steel welding or abrasive blasting may present certain difficulties
when performed in confined spaces. In these cases, the employer would
be required to provide respiratory protection. In any event, the
employer must always install engineering controls and implement work
practice controls when such controls are feasible to reduce exposures,
even if these controls cannot reduce exposures below the PEL.
The requirement to provide respiratory protection when feasible
engineering controls are not sufficient to reduce exposures to within
the PEL would also apply in instances where effective engineering
controls have been installed and are being maintained or repaired. In
these situations, controls may not be effective while maintenance or
repair is underway. Where exposures exceed the PEL, the employer would
be required to provide respirators.
As discussed earlier with regard to methods of compliance, OSHA is
proposing an exemption from the general requirement for use of
engineering and work practice controls where employee exposures do not
exceed the PEL on 30 or more days per year. Where this exception
applies, the employer would then be required to provide respiratory
protection to achieve the PEL. OSHA also believes that emergencies are
situations where respirators must be used to protect employees. Since
an emergency, by definition, involves or is likely to involve an
uncontrolled release of Cr(VI), it is important to protect
[[Continued on page 59455]]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
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[[pp. 59455-59474]] Occupational Exposure to Hexavalent Chromium
[[Continued from page 59454]]
[[Page 59455]]
employees from the significant exposures that may occur.
Whenever respirators are used to comply with the requirements of
the standard, OSHA proposes that the employer implement a comprehensive
respiratory protection program in accordance with the Agency's
Respiratory Protection standard (29 CFR 1910.134). The respiratory
protection program is designed to ensure that respirators are properly
used in the workplace, and are effective in protecting workers. The
program must include procedures for selecting respirators for use in
the workplace; medical evaluation of employees required to use
respirators; fit testing procedures for tight-fitting respirators;
procedures for proper use of respirators in routine and reasonably
foreseeable emergency situations; procedures and schedules for
maintaining respirators; procedures to ensure adequate quality,
quantity, and flow of breathing air for atmosphere-supplying
respirators; training of employees in the proper use of respirators;
and procedures for evaluating the effectiveness of the program. In
addition, this provision will serve as a reminder to employers covered
by the Cr(VI) rule that they must also comply with the Respiratory
Protection standard when respirators are provided to employees.
OSHA has proposed to revise the Respiratory Protection standard to
include assigned protection factors (68 FR 34036 (6/6/03)). The
proposed revision includes a table which indicates the level of
respiratory protection that a given respirator or class of respirators
is expected to provide, and will apply to employers whose employees use
respirators for protection against Cr(VI) when it becomes a final rule
(68 FR 34036, 34115 (6/6/03)).
(h) Protective Work Clothing and Equipment
The proposed standard would require that the employer provide
protective clothing and equipment at no cost to employees where a
hazard is present or is likely to be present from skin or eye contact
with Cr(VI). The employer would also be required to ensure that
employees use the clothing and equipment provided. The intent of this
provision is to prevent the adverse health effects associated with
dermal exposure to Cr(VI) (described in Section VI.D of this preamble)
and the potential for inhalation of Cr(VI) that may be deposited on
employees' street clothing. The proposed requirements for protective
clothing and equipment are similar to those in other OSHA health
standards such as those for cadmium (29 CFR 1910.1027) and
methylenedianiline (29 CFR 1910.1050), and are based upon widely
accepted principles and conventional practices of industrial hygiene.
The proposed requirements are also consistent with Section 6(b)(7) of
the OSH Act which states that, where appropriate, standards shall
prescribe suitable protective equipment to be used in connection with
hazards.
OSHA has proposed a standard that will cover payment for personal
protective equipment in all workplaces (64 FR 15401 (3/31/99)). The
Agency is incorporating the record of that rulemaking into the Cr(VI)
rulemaking and will give due consideration to all relevant comments.
Criteria for determining when a hazard is present or is likely to
be present from skin or eye contact with Cr(VI) are not specified. When
evaluating the potential for hazardous eye or skin contact with Cr(VI),
OSHA anticipates that the employer will assess the workplace in a
manner consistent with the current requirements of the Agency's
standards for use of personal protective equipment in general industry
(29 CFR 1910.132) and shipyards (29 CFR 1915.152). These standards
require the employer to assess the workplace to determine if hazards
(including hazards associated with eye and skin contact with chemicals)
are present, or are likely to be present.
As described in the non-mandatory appendices providing guidance on
hazard assessment for these standards (29 CFR 1910 Subpart I Appendix
B; 29 CFR 1915 Subpart I Appendix A), the employer should ``exercise
common sense and appropriate expertise'' in assessing hazards. The
recommended approach involves a walk-through survey to identify sources
of hazards to workers. Review of injury/accident data is also
recommended. Information obtained during this process provides a basis
for the evaluation of potential hazards.
Based on the results of this assessment, the employer must
determine what clothing and equipment is necessary to protect employees
from Cr(VI) hazards. The proposed requirement is performance-oriented,
and is designed to allow the employer flexibility in selecting the
clothing and equipment most suitable for his or her particular
workplace. The type of protective clothing and equipment needed to
protect employees from Cr(VI) hazards will depend on the potential for
exposure and the conditions of use in the workplace. Examples of
protective clothing and equipment include, but are not limited to
gloves, aprons, coveralls, foot coverings, and goggles. Ordinary street
clothing and work uniforms or other accessories that do not serve to
protect workers from Cr(VI) hazards are not considered protective
clothing and equipment under this proposed standard.
The employer must exercise reasonable judgment in selecting the
appropriate clothing and equipment to protect employees from Cr(VI)
hazards. This provision is consistent with OSHA's current standards for
provision of personal protective equipment (e.g., 29 CFR 1910.132, 29
CFR 1915.152, 29 CFR 1926.95). For example, a worker who is
constructing a home foundation using wood treated with chromated copper
arsenate, leather gloves may be all that is necessary to prevent
hazardous Cr(VI) exposure. In other situations, such as when a worker
is performing abrasive blasting on a structure covered with Cr(VI)-
containing paint, more extensive measures such as coveralls, head
coverings, and goggles may be needed. Where exposures to Cr(VI) are
minute, no protective clothing or equipment may be necessary. Many
Cr(VI) compounds are acidic or alkaline (e.g., chromic acid, portland
cement), and these characteristics may also influence the choice of
protective clothing and equipment. For example, a chrome plater may
require an apron, gloves, and goggles to protect against possible
splashes of chromic acid that could result in both Cr(VI) exposure and
chemical burns.
OSHA has not proposed a threshold concentration of Cr(VI) for
determining when a substance would be covered under the rule. In some
OSHA standards an exemption from certain requirements based on
percentage composition has been included. For example, the standard for
formaldehyde requires that the employer prevent eye and skin contact
with liquids containing one percent or more formaldehyde (29 CFR
1910.1048(h)(1)(i)). Contact with liquids containing less than one
percent formaldehyde is exempt from this provision. Such exemptions
have been included so that coverage would not be extended to trivial
exposures that were not associated with adverse health effects.
A similar exemption has not been included in this proposed standard
because adverse health effects have been shown to occur as a result of
dermal contact to relatively low concentrations of Cr(VI). For example,
exposures to portland cement have been associated with allergic contact
dermatitis, even though Cr(VI) concentrations in the cement were
reported to be below 10 [mu]g/
[[Page 59456]]
g (i.e., 0.001%) (Ex. 35-326). OSHA is not aware of any evidence that
would allow establishment of a threshold concentration of Cr(VI) below
which adverse dermal effects would not occur.
Paragraph (h)(2) (paragraph (f)(2) of the proposals for
construction and shipyards) contains proposed requirements for removal
and storage of protective clothing and equipment. The employer must
ensure that all protective clothing and equipment contaminated with
Cr(VI) is removed at the completion of the work shift or at the
completion of tasks involving Cr(VI) exposure. Where employees must
change their clothes (i.e., take off their street clothes), removal of
protective clothing and equipment must occur in change rooms provided
in accordance with paragraph (i) of this section (paragraph (g) of the
construction and shipyard proposals). This provision is intended to
reduce Cr(VI) contamination of the workplace, and limit Cr(VI)
exposures outside the workplace. Wearing contaminated clothing outside
the work area could lengthen the duration of exposure, and could carry
Cr(VI) from regulated areas to other areas of the workplace. In
addition, contamination of personal clothing could result in Cr(VI)
being carried to employees' cars and homes, increasing the worker's
exposure as well as exposing other individuals to Cr(VI) hazards.
Contaminated protective clothing and equipment must be removed at
the end of the work shift or at the completion of tasks involving
Cr(VI) exposure, whichever comes first. This language is intended to
convey that protective clothing contaminated with Cr(VI) must generally
not be worn when tasks involving Cr(VI) exposure have been completed
for the day. For example, if employees perform work tasks involving
Cr(VI) exposure for the first two hours of a work shift, and then
perform tasks that do not involve Cr(VI) exposure, they must remove
their protective clothing after the exposure period to avoid the
possibility of increasing the duration of exposure and contamination of
the work area from Cr(VI) residues on the protective clothing. If,
however, employees are performing tasks involving Cr(VI) exposure
intermittently throughout the day, or if employees are exposed to other
contaminants where their protective clothing and equipment is needed,
this provision does not prevent them from wearing the clothing and
equipment until the completion of their shift.
To limit exposures outside the workplace, OSHA proposes that the
employer ensure that Cr(VI)-contaminated protective clothing and
equipment be removed from the workplace only by those employees whose
job it is to launder, clean, maintain, or dispose of such clothing or
equipment. Furthermore, the proposed standard would require that
clothing and equipment that is to be laundered, cleaned, maintained, or
disposed of be placed in closed, impermeable containers. This provision
is intended to assure that contamination of the change room is
minimized and that employees who later handle these items are
protected. Those cleaning the Cr(VI)-contaminated clothing and
equipment will be further protected by the requirement that warning
labels be placed on containers to inform them of the potential hazards
of exposure to Cr(VI).
The proposed standard requires that the employer clean, launder,
repair and replace protective clothing as needed to ensure that the
effectiveness of the clothing and equipment is maintained. This
provision is necessary to ensure that clothing and equipment continue
to serve their intended purpose of protecting workers. This would also
prevent unnecessary exposures outside the workplace from employees
taking contaminated clothing and equipment home for cleaning.
In keeping with the performance-orientation of the proposed rule,
OSHA does not specify how often clothing and equipment should be
cleaned, repaired or replaced. The Agency believes that appropriate
time intervals may vary widely based on the types of clothing and
equipment used, Cr(VI) exposures, and other circumstances in the
workplace. The obligation of the employer, as always, is to keep the
clothing and equipment in the condition necessary to perform its
protective functions.
Removal of Cr(VI) from protective clothing and equipment by
blowing, shaking, or any other means which disperses Cr(VI) in the air
would be prohibited. Such actions would result in unnecessary exposure
to airborne Cr(VI) as well as possible dermal contact.
The proposal would require that the employer inform any person who
launders or cleans protective clothing or equipment contaminated with
Cr(VI) of the potentially harmful effects of exposure to Cr(VI), and
the need to launder or clean contaminated clothing and equipment in a
manner that effectively prevents skin or eye contact with Cr(VI) or the
release of airborne Cr(VI) in excess of the PEL. This provision is
intended to ensure that persons who clean or launder Cr(VI)-
contaminated items are aware of the associated hazards, and can then
take appropriate protective measures.
The proposed standard would require employers to provide protective
clothing and equipment at no cost to employees. The Agency believes
that the employer is generally in the best position to select and
obtain the proper type of protective clothing and equipment. OSHA also
believes that by providing and owning protective clothing and
equipment, the employer will be in a better position to maintain
control over the inventory of protective clothing and equipment,
conduct periodic inspections, and, when necessary, repair or replace it
to maintain its effectiveness. The protective clothing and equipment at
issue is designed and intended for work use. As discussed above,
employees must remove contaminated clothing and equipment at the end of
the work shift or the completion of tasks involving Cr(VI) exposure,
whichever comes first. Employees may not remove contaminated clothing
and equipment from the worksite, except for the employees whose job it
is to launder, clean, maintain, or dispose of such clothing or
equipment. The employer is responsible for cleaning or disposing of the
protective clothing and equipment and retains complete control over it.
The Agency is seeking comment on the proposed provision, and has
included this topic in the ``Issues'' section of this preamble.
(i) Hygiene Areas and Practices
The proposed standard would require employers to provide hygiene
facilities and to assure employee compliance with basic hygiene
practices that serve to minimize exposure to Cr(VI). The proposal
includes requirements for change rooms and washing facilities, ensuring
that Cr(VI) exposure in eating and drinking areas is minimized, and a
prohibition on certain practices that may contribute to Cr(VI)
exposure. OSHA believes that strict compliance with these provisions
would substantially reduce employee exposure to Cr(VI).
Several of these provisions are presently required under other OSHA
standards. For example, OSHA's current standard addressing sanitation
in general industry (29 CFR 1910.141) requires that whenever employees
are required by a particular standard to wear protective clothing
because of the possibility of contamination with toxic materials,
change rooms equipped with storage facilities for street clothes and
separate storage facilities for protective clothing shall be provided.
The sanitation standard also includes
[[Page 59457]]
provisions for washing facilities, and prohibits storage or consumption
of food or beverages in any area exposed to a toxic material. Similar
provisions are in place for construction (29 CFR 1926.51). The hygiene
provisions of this paragraph are intended to augment the requirements
established under other standards with additional provisions applicable
specifically to Cr(VI) exposure.
In workplaces where employees must change their clothes to use
protective clothing and equipment, OSHA believes it is essential to
have change rooms with separate storage facilities for street and work
clothing to prevent contamination of employees' street clothes. This
provision will minimize employee exposure to Cr(VI) after the work
shift ends, because it reduces the duration of time they may be exposed
to contaminated work clothes. Potential exposure resulting from
contamination of the homes or cars of employees is also avoided. Change
rooms also provide employees with privacy while changing their clothes.
OSHA intends the proposed requirement for change rooms to apply to all
covered workplaces where employees must change their clothes (i.e.,
take off their street clothes) to use protective clothing and
equipment. In those situations where removal of street clothes would
not be necessary (e.g., in a workplace where only gloves are used as
protective clothing), change rooms would not be required.
Paragraph (i)(3) (paragraph (g)(3) of the proposals for
construction and shipyards) contains proposed requirements for washing
facilities. The employer is to provide readily accessible washing
facilities capable of removing Cr(VI) from the skin and is to ensure
that affected employees use these facilities when necessary. Also, the
employer is to ensure that employees who have skin contact with Cr(VI)
wash their hands and faces at the end of the work shift and prior to
eating, drinking, smoking, chewing tobacco or gum, applying cosmetics,
or using the toilet.
Washing reduces exposure by diminishing the period of time that
Cr(VI) is in contact with the skin. Although engineering and work
practice controls and protective clothing and equipment are designed to
prevent hazardous skin and eye contact from occurring, OSHA realizes
that in some circumstances these exposures will occur. For example, a
worker who wears gloves to protect against hand contact with Cr(VI) may
inadvertently touch his face with the contaminated glove during the
course of the day. The intent of this provision is to have employees
wash in order to mitigate the adverse effects when skin and eye contact
does occur. At a minimum, employees are to wash their hands and faces
at the end of the shift because washing is needed to remove any
residual Cr(VI) contamination. Likewise, washing prior to eating,
drinking, smoking, chewing tobacco or gum, applying cosmetics or using
the toilet also protects against further Cr(VI) exposure.
OSHA has made a preliminary determination that washing facilities
would be sufficient to allow employees to remove significant levels of
Cr(VI) contamination that may occur under the proposed standard. A
requirement for provision and use of showers has not been included in
the proposal. Some other health standards, such as the standards for
cadmium (29 CFR 1910.1027) and lead (29 CFR 1910.1025), have included
requirements for showers. OSHA requests information and comment as to
whether provisions for showers should be included in a final Cr(VI)
standard, and has included this topic in the ``Issues'' section of this
preamble.
To minimize the possibility of food contamination and to reduce the
likelihood of additional exposure to Cr(VI) through inhalation or
ingestion, OSHA believes it is imperative that employees have a clean
place to eat. Where the employer chooses to allow employees to eat at
the facility, the proposal would require the employer to ensure that
eating and drinking areas and surfaces are maintained as free as
practicable of Cr(VI). Employers would also be required to assure that
employees do not enter eating or drinking areas wearing protective
clothing, unless properly cleaned beforehand. This is to further
minimize the possibility of contamination and reduce the likelihood of
additional Cr(VI) exposure from contaminated food or beverages.
Employers are given discretion to choose any method for removing
surface Cr(VI) from clothing and equipment that does not disperse the
dust into the air or onto the employee's body. For example, if a worker
is wearing coveralls for protection against Cr(VI) exposure, thorough
HEPA vacuuming of the coveralls could be performed prior to entry into
a lunchroom.
The employer is not required to provide eating and drinking
facilities to employees. Employees may consume food or beverages off
the worksite. However, where the employer chooses to allow employees to
consume food or beverages at a worksite where Cr(VI) is present, OSHA
intends to ensure that employees are protected from Cr(VI) exposures in
these areas.
Proposed paragraph (i)(5) (paragraph (g)(5) in the construction and
shipyard proposals) specifies certain activities that would be
prohibited. These activities would include eating, drinking, smoking,
chewing tobacco or gum, or applying cosmetics in regulated areas, or in
areas where skin or eye contact occurs. Products associated with these
activities, such as food and beverages, could not be carried or stored
in these areas. This provision is intended to protect employees from
additional sources of exposure to Cr(VI). Because the construction and
shipyard proposals do not include requirements for regulated areas,
reference to regulated areas is omitted in the proposed regulatory text
for these standards.
(j) Housekeeping
The proposed standard includes housekeeping provisions that would
require the employer to maintain surfaces as free as practicable of
Cr(VI), promptly clean Cr(VI) spills and leaks, use appropriate
cleaning methods, and properly dispose of Cr(VI)-contaminated waste.
These provisions are exceptionally important because they minimize
additional sources of exposure that engineering controls generally are
not designed to address. Good housekeeping is a cost effective way to
control employee exposures by removing accumulated Cr(VI) that can
become entrained by physical disturbances or air currents and carried
into an employee's breathing zone, thereby increasing employee
exposure. Contact with contaminated surfaces may also result in dermal
exposure to Cr(VI). The proposed provisions are consistent with
housekeeping requirements in other OSHA standards, such as those for
cadmium (29 CFR 1910.1027) and lead (29 CFR 1910.1025).
Cr(VI) deposited on ledges, equipment, floors, and other surfaces
should be removed as soon as practicable, to prevent it from becoming
airborne and to minimize the likelihood that skin contact will occur.
When Cr(VI) is released into the workplace as a result of a leak or
spill, the proposal would require the employer to promptly clean up the
spill. Measures for clean-up of liquids should provide for the rapid
containment of the leak or spill to minimize potential exposures.
Clean-up procedures for dusts must not disperse the dust into the
workplace air. These work practices aid in minimizing the number of
employees exposed, as well as the extent of any potential Cr(VI)
exposure.
[[Page 59458]]
The proposed standard would require that, where possible, surfaces
contaminated with Cr(VI) be cleaned by vacuuming or other methods that
minimize the likelihood of Cr(VI) exposure. OSHA believes vacuuming to
be the most reliable method of cleaning surfaces on which dust
accumulates, but equally effective methods may be used. Shoveling, dry
or wet sweeping, and brushing would be permitted only if the employer
shows that vacuuming or other methods that are usually as efficient as
vacuuming are not effective under the particular circumstances found in
the workplace. The proposal would also require that vacuum cleaners be
equipped with HEPA filters to prevent the dispersal of Cr(VI) into the
workplace. The use of compressed air for cleaning would only be allowed
when used in conjunction with a ventilation system designed to capture
the dust cloud created by the compressed air. This provision is also
intended to prevent the dispersal of Cr(VI) into the workplace.
Cleaning equipment is to be handled in a manner that minimizes the
reentry of Cr(VI) into the workplace. For example, cleaning and
maintenance of HEPA-filtered vacuum equipment should be done carefully
to avoid exposures to Cr(VI). Filters need to be changed and the
contents of bags disposed of properly to avoid unnecessary Cr(VI)
exposures.
The proposal would also require that items contaminated with Cr(VI)
and consigned for disposal be collected and disposed of in sealed
impermeable bags or other closed impermeable containers. These
containers would include warning labels to inform individuals who
handle these items of the potential hazards. By alerting employers and
employees who are involved in disposal to the potential hazards of
Cr(VI) exposure, they will be better able to implement protective
measures.
No housekeeping provision has been included in the proposals
covering construction or shipyards. OSHA has made a preliminary
determination that a specific housekeeping provision is not appropriate
because of the difficulties of performing housekeeping related to
Cr(VI) exposure in the construction and shipyard environments. For
example, in shipyard and particularly in construction work environments
the generally dusty nature of outdoor work settings is likely to make
it difficult to distinguish Cr(VI)--contaminated dusts from other dirt
and dusts commonly found at the work site. The same control measures
that apply to general industry are likely to be more difficult to
implement and burdensome in these environments.
This preliminary determination differs from OSHA's determination in
the standards for lead in construction (29 CFR 1926.62) and cadmium in
construction (29 CFR 1926.1127), where the Agency included housekeeping
provisions. In these rulemakings, OSHA did not find housekeeping
provisions to present the difficulties anticipated with Cr(VI). The
Agency believes that Cr(VI)-contaminated dusts will not generally be as
easily identified as lead- or cadmium-contaminated dusts. Welding, in
particular, could result in deposition of minute quantities of Cr(VI)
that would be difficult for a construction or shipyard employer to
identify. OSHA seeks comment on this preliminary finding, and has
included this topic in the ``Issues'' section of this preamble.
Construction and shipyard employers would still need to comply with
the general housekeeping requirements found at 29 CFR 1926.25 (for
construction) or 29 CFR 1915.91 (for shipyards). These standards
include general provisions for keeping workplaces clear of debris, but
do not contain the more specific requirements found in the proposed
Cr(VI) standard for general industry (such as those addressing cleaning
methods) that are designed to limit Cr(VI) contamination of the
workplace.
(k) Medical Surveillance
OSHA proposes to require that each employer covered by this rule
make medical surveillance available at no cost, and at a reasonable
time and place, for all employees who are experiencing signs or
symptoms of the adverse health effects associated with Cr(VI) exposure,
or who are exposed in an emergency. In addition, general industry
employers would be required to provide medical surveillance for all
employees exposed to Cr(VI) at or above the PEL for 30 or more days a
year. The required medical surveillance must be performed by or under
the supervision of a physician or other licensed health care
professional.
The purpose of medical surveillance for Cr(VI) is, where reasonably
possible, to determine if an individual can be exposed to the Cr(VI)
present in his or her workplace without experiencing adverse health
effects; to identify Cr(VI)-related adverse health effects so that
appropriate intervention measures can be taken; and to determine the
employee's fitness to use personal protective equipment such as
respirators. The proposal is consistent with Section 6(b)(7) of the OSH
Act which requires that, where appropriate, medical surveillance
programs be included in OSHA health standards to aid in determining
whether the health of workers is adversely affected by exposure to
toxic substances. Other OSHA health standards have also included
medical surveillance requirements.
The proposed standard is intended to encourage participation by
requiring that medical examinations be provided by the employer without
cost to employees (also required by section 6(b)(7) of the Act), and at
a reasonable time and place. If participation requires travel away from
the worksite, the employer would be required to bear the cost.
Employees would have to be paid for time spent taking medical
examinations, including travel time. OSHA is proposing that medical
surveillance be provided to employees in general industry exposed at or
above the PEL for 30 or more days a year in order to focus on those
workers at greatest risk. Employees exposed below the PEL, or exposed
for only a few days in a year, will be at lower risk of developing
Cr(VI)-related disease. OSHA believes that these cutoffs, based both on
exposure level and on the number of days an employee is exposed to
Cr(VI), are a reasonable and administratively convenient basis for
providing medical surveillance benefits to Cr(VI)-exposed workers. In
past health standards, OSHA has used 30 days above the action level for
triggering medical surveillance. Because of the large reduction in the
PEL down to 1 [mu]g/m3 OSHA believes that 30 days above the
PEL may be more reasonable since exposures above the PEL are more
likely to result in adverse health effects that might benefit from
medical surveillance. OSHA is seeking comment on the appropriateness of
this trigger for medical surveillance, and whether the Agency should
consider a trigger at the action level or an alternative trigger.
OSHA has not included exposure above the PEL for 30 or more days
per year as a trigger for medical surveillance in the construction or
shipyard Cr(VI) proposals. As discussed earlier, OSHA has not proposed
to require exposure monitoring for construction or shipyard employment
because of the difficulties in conducting such monitoring in these work
settings. While OSHA assumes that some monitoring will be conducted in
order for employers to know when or if they are above the PEL, OSHA
also assumes that certain employers will not conduct exposure
monitoring and may choose to presume that certain work processes or
practices are above the PEL or rely on historical or objective data to
show exposure levels. However, if medical surveillance for individual
[[Page 59459]]
employees is triggered by exposures above the PEL for 30 days or more,
these employers would be forced to do monitoring in order to determine
which employees are exposed above the PEL for 30 days or more. This
would have the effect of re-introducing an exposure monitoring burden
that the Agency is attempting to relieve.
Some employees may exhibit signs and symptoms of the adverse health
effects associated with Cr(VI) exposure even when not exposed above the
PEL for 30 or more days per year. These employees could be especially
sensitive, may have been unknowingly exposed, or may have been exposed
to greater amounts than the exposure assessment suggests. OSHA has
therefore proposed that employees who experience signs or symptoms of
the adverse health effects associated with Cr(VI) exposure be subject
to medical surveillance. Signs and symptoms that may warrant
surveillance include dermatitis, chrome holes, and nasal septum ulcers
or perforations. Thus, the proposal would protect all employees exposed
to Cr(VI) in unusual circumstances even if they fall outside the
criteria for routine medical surveillance.
Appropriate surveillance would be required to be made available for
employees exposed in an emergency regardless of the airborne
concentrations of Cr(VI) normally found in the workplace. Emergency
situations involve uncontrolled releases of Cr(VI), and the significant
exposures that occur in these situations justify a requirement for
medical surveillance. The proposed requirement for medical examinations
after exposure in an emergency is consistent with the provisions of
several other OSHA health standards, including the standards for
methylenedianiline (29 CFR 1910.1050), butadiene (29 CFR 1910.1051),
and methylene chloride (29 CFR 1910.1052).
OSHA has made a preliminary determination not to include eye or
skin contact as a basis for medical surveillance. OSHA believes that
compliance with the proposed provisions for protective work clothing
and equipment, hygiene areas and practices, and other protective
measures will minimize the potential for adverse eye and skin effects.
When such health effects occur, OSHA believes that trained employees
will be able to detect these conditions, report them to their employer,
and obtain medical assistance. In such situations, affected employees
would be provided medical surveillance on the basis that they are
experiencing signs or symptoms of Cr(VI)-related health effects.
OSHA has proposed that the medical examinations provided under the
rule be performed by or under the supervision of a physician or other
licensed health care professional (PLHCP). The Agency considers it
appropriate to allow any professional to perform medical examinations
and procedures provided under the standard when they are licensed by
state law to do so. This provision provides flexibility to the
employer, and would reduce cost and compliance burdens. The proposed
requirement is consistent with the approach of other recent OSHA
standards, such as those for methylene chloride (29 CFR 1910.1052),
bloodborne pathogens (29 CFR 1910.1030), and respiratory protection (29
CFR 1910.134).
The proposed standard also specifies how frequently medical
examinations are to be offered to those employees covered by the
medical surveillance program. Employers would be required to provide
all covered employees with medical examinations whenever an employee
shows signs or symptoms of Cr(VI) exposure; within 30 days after an
emergency resulting in an uncontrolled release of Cr(VI); and within 30
days after a PLHCP's written medical opinion recommends an additional
examination. In addition, employers in general industry would be
required to provide covered employees with examinations within 30 days
after initial assignment unless the employee has received a medical
examination provided in accordance with the standard within the past 12
months; annually; and at the termination of employment, unless an
examination has been given less than six months prior to the date of
termination.
Signs or symptoms may indicate that adverse health effects
attributable to Cr(VI) exposure are occurring. In such situations OSHA
believes it would be appropriate to evaluate the employee's condition
to determine if exposure to Cr(VI) is the cause of the condition, and
to determine if protective measures are necessary. Emergency situations
may involve high or unknown exposures, and OSHA believes that a medical
examination is necessary to evaluate the possible adverse effects of
these exposures.
In addition to medical evaluations after exposures in an emergency
or when signs or symptoms occur, OSHA is proposing that additional
examinations be offered following a PLHCP's recommendation that
additional exams are necessary. A PLHCP may recommend additional
evaluations in order to follow developments in a worker's condition, or
to allow for specialized evaluation. For example, if nasal ulceration
is identified in a Cr(VI)-exposed worker, a PLHCP may recommend follow-
up examinations to ensure that treatment and workplace interventions
are successful in addressing the condition, or a worker who exhibits
dermatitis may be referred to a dermatologist for testing to determine
if they are sensitized to Cr(VI).
The proposed requirement for general industry that a medical
examination be offered at the time of initial assignment is intended to
achieve the objective of determining if an individual will be able to
work in the job involving Cr(VI) exposure without adverse effects. It
also serves the useful function of establishing a health baseline for
future reference. Where an examination that complies with the
requirements of the standard has been provided in the past 12 months,
that previous examination would serve these purposes, and an additional
examination would not be needed.
OSHA believes that the provision of medical surveillance on an
annual basis in general industry is an appropriate frequency for
screening employees for Cr(VI)-related diseases. The main goal of
periodic medical surveillance for workers is to detect adverse health
effects at an early and potentially reversible stage. The proposed
requirement for annual examinations is consistent with other OSHA
health standards, including those for cadmium (29 CFR 1910.1027),
formaldehyde (29 CFR 1910.1048), and methylene chloride (29 CFR
1910.1052). Based on the Agency's experience, OSHA believes that annual
surveillance would strike a reasonable balance between the need to
diagnose health effects at an early stage, and the limited number of
cases likely to be identified through surveillance. The proposed
requirement for general industry that the employer offer a medical
examination at the termination of employment is intended to assure that
no employee terminates employment while carrying an active, but
undiagnosed, disease.
The examination to be provided by the PLHCP is to consist of a
medical and work history; a physical examination of the skin and
respiratory tract; and any additional tests considered appropriate by
the PLHCP. Special emphasis is placed on the portions of the medical
and work history focusing on Cr(VI) exposure, health effects associated
with Cr(VI) exposure, and smoking. The physical exam focuses on organs
and systems known to be susceptible to Cr(VI) toxicity. The information
obtained will allow the PLHCP to assess
[[Page 59460]]
the employee's health status, identify adverse health effects related
to Cr(VI) exposures, and determine if limitations should be placed on
the employee's exposure to Cr(VI).
The proposal does not indicate specific tests that must be included
in the medical examination. OSHA does not believe that any particular
tests are generally applicable to all employees covered by the medical
surveillance requirements, and the Agency proposes to give the
examining PLHCP the flexibility to determine any appropriate tests to
be selected for a given employee. For example, tests for dermal
sensitization exist, but they are not recommended as a screening tool
because they are capable of sensitizing persons who had not been
affected previously. These tests should be considered by the PLHCP if a
medical history indicating probable sensitization exists or if the
employee experiences signs or symptoms indicative of sensitization.
Radiological examinations and pulmonary function tests may also be
useful in evaluating possible effects of Cr(VI). OSHA believes that the
PLHCP is in the best position to decide which medical tests are
necessary for each individual examined. Where specific tests are deemed
appropriate by the PLHCP, the proposed standard would require that they
be provided.
OSHA is aware that certain methods are available for evaluating
Cr(VI) exposures based on analysis of chromium in urine or blood.
However, the Agency is not aware of evidence indicating that these
methods adequately characterize Cr(VI) exposures in most occupational
environments. OSHA has also found no medical justification for routine
urine or blood analysis for the detection of Cr(VI)-related health
effects. Therefore, no requirement for such analysis is proposed.
The proposed standard would require the employer to ensure the
PLHCP has a copy of the standard, and to provide the following
information: a description of the affected employee's former and
current duties as they relate to Cr(VI) exposure; the employee's
former, current, and anticipated exposure level; a description of any
personal protective equipment used or to be used by the employee,
including when and for how long the employee has used that equipment;
and information from records of employment-related medical examinations
previously provided to the affected employee, currently within the
control of the employer. Making this information available to the PLHCP
will aid in the evaluation of the employee's health in relation to
assigned duties and fitness to use personal protective equipment, when
necessary.
The results of exposure monitoring are part of the information that
would be supplied to the PLHCP responsible for medical surveillance.
These results contribute valuable information to assist the PLHCP in
determining if an employee is likely to be at risk of harmful effects
from Cr(VI) exposure. A well-documented exposure history would also
assist the PLHCP in determining if a condition (e.g., dermatitis) may
be related to Cr(VI) exposure.
The proposed rule would require employers to obtain from the
examining PLHCP a written opinion containing the results of the medical
examination with regard to Cr(VI) exposure, the PLHCP's opinion as to
whether the employee would be placed at increased risk of material
health impairment as a result of exposure to Cr(VI), and any
recommended limitations on the employee's exposure or use of personal
protective equipment. The PLHCP would also need to state in the written
opinion that these findings were explained to the employee. The purpose
of requiring the PLHCP to supply a written opinion to the employer is
to provide the employer with a medical basis to aid in the
determination of placement of employees and to assess the employee's
ability to use protective clothing and equipment. The employer must
obtain the written opinion within 30 days of the examination; OSHA
believes this will provide the PLHCP sufficient time to receive and
consider the results of any tests included in the examination, and
allow the employer to take any necessary protective measures in a
timely manner. The proposed requirement that the opinion be in written
form is intended to ensure that employers and employees have the
benefit of this information.
The PLHCP would not be allowed to include findings or diagnoses
which are unrelated to Cr(VI) exposure in the written opinion provided
to the employer. OSHA has proposed this provision to reassure employees
participating in medical surveillance that they will not be penalized
or embarrassed by the employer's obtaining information about them not
directly pertinent to Cr(VI) exposure. The employee would be informed
directly by the PLHCP of all results of his or her medical examination,
including conditions of non-occupational origin. The employer would
also be required to provide a copy of the PLHCP's written opinion to
the employee within two weeks after receiving it, to ensure that the
employee has been informed of the result of the examination in a timely
manner.
In some OSHA health standards, a provision for medical removal
protection (MRP) has been included. MRP typically requires that the
employer temporarily remove an employee from exposure when such an
action is recommended in a written medical opinion. During the time of
removal, the employer is required to maintain the total normal
earnings, as well as all other employee rights and benefits. However,
MRP is not intended to serve as a worker's compensation system. The
primary reason MRP has been included in these previous standards has
been to encourage employee participation in medical surveillance. By
protecting employees who are removed on a temporary basis from economic
loss, this potential disincentive to participating in medical
surveillance is alleviated.
The proposed rule does not include a provision for MRP, because
OSHA has made a preliminary determination that MRP is not reasonably
necessary or appropriate for Cr(VI)-related health effects. The Agency
believes that Cr(VI)-related health effects generally fall into one of
two categories: Either they are chronic conditions that temporary
removal from exposure will not remedy (e.g., lung cancer, respiratory
or dermal sensitization), or they are conditions that can be addressed
through proper application of control measures and do not require
removal from exposure (e.g., irritant dermatitis). Since situations
where temporary removal would be appropriate are not anticipated to
occur, OSHA does not believe that MRP is necessary. The Agency seeks
comment on this preliminary determination, and has included this topic
in the ``Issues'' section of this preamble.
(1) Communication of Hazards to Employees
The proposed standard includes requirements intended to ensure that
the dangers of Cr(VI) exposure are communicated to employees by means
of signs, labels, and employee information and training. These proposed
requirements would parallel the existing requirements of OSHA's Hazard
Communication standard (29 CFR 1910.1200). The hazard communication
requirements of the proposed rule are designed to be substantively as
consistent as possible with the Hazard Communication standard, while
including additional specific requirements needed to protect employees
exposed to Cr(VI).
The proposed standard would require that all approaches to
regulated areas be
[[Page 59461]]
posted with legible and readily visible warning signs stating: Danger;
Chromium (VI); Cancer Hazard; Can Damage Skin, Eyes, Nasal Passages,
and Lungs; Authorized Personnel Only; Respirators Required in this
Area. Such warning signs would be required wherever a regulated area
exists, that is, wherever the PEL is exceeded in general industry.
Because the construction and shipyard proposals do not include
requirements for regulated areas, no provision is included for warning
signs in the proposed regulatory text for the construction and shipyard
standards.
The signs are intended to serve as a warning to employees who
otherwise may not be aware that they are entering a regulated area, and
to remind employees of the hazards of Cr(VI) so that they take
necessary protective steps before entering the area. These signs are
intended to supplement the training that employees receive regarding
the hazards of Cr(VI), since even trained employees need to be reminded
of the locations of regulated areas and of the precautions necessary
before entering these dangerous areas.
In some instances, regulated areas are permanent, because the
employer is unable to reduce Cr(VI) exposures in that area below the
PEL with engineering controls. In those cases, the signs serve to warn
employees not to enter the area unless they are authorized and are
wearing respirators. In other cases, such as emergency situations and
maintenance operations, regulated areas may be established temporarily.
The use of warning signs is particularly important in these situations
to make employees who are regularly scheduled to work at these sites
aware of the hazards. Access is limited to authorized personnel to
ensure that those entering the area are adequately trained and
equipped, and to limit exposure to only those whose presence is
absolutely necessary.
The proposed standard specifies the wording of the warning signs
for regulated areas in order to ensure that the proper warning is given
to employees. OSHA believes that the use of the word ``Danger'' is
appropriate, based on the evidence of the toxicity and carcinogenicity
of Cr(VI). ``Danger'' is used to attract the attention of workers in
order to alert them to the fact that they are entering an area where
the PEL may be exceeded and to emphasize the importance of the message
that follows. The use of the word ``Danger'' is also consistent with
other OSHA health standards dealing with carcinogens such as cadmium
(29 CFR 1910.1027), methylenedianiline (29 CFR 1910.1050), asbestos (29
CFR 1910.1001), and benzene (29 CFR 1910.1028).
The proposed standard would also require that the sign indicate
that respirators are required in the area. Regulated areas are areas
demarcated by the employer where the employee's exposure to airborne
concentrations of chromium (VI) exceeds, or can reasonably be expected
to exceed the PEL (definition of a regulated area). The employer has
made the determination that such areas are regulated on the basis of
his/her own exposure assessments of the employees in the area. Since
the employer has determined that such areas are not able to be reduced
below the PEL, respirators are required as a means of control to
protect the employees in those areas. The sign also serves as a means
to warn other employees not in the regulated area not to enter, or if
those other employees enter the area, they need to protect themselves
in situations where excessive exposures can occur.
The proposal would require that warning labels be affixed to all
bags or containers of contaminated clothing and equipment that are to
be removed from the workplace for laundering, cleaning, or maintenance.
Containers of waste, scrap, debris, and any other materials
contaminated with Cr(VI) that are consigned for disposal would also
need to be labeled. The labels must state: Danger; Contains Chromium
(VI); Cancer Hazard; Can Damage Skin, Eyes, Nasal Passages, and Lungs.
The purpose of this requirement is to ensure that all affected
employees, not only those of a particular employer, are apprised of the
hazardous nature of Cr(VI) exposure. These proposed requirements are
consistent with the mandate of Section (6)(b)(7) of the OSH Act, which
requires that OSHA health standards prescribe the use of labels or
other appropriate forms of warning to apprise employees of the hazards
to which they are exposed. Because the construction and shipyard
proposals do not include disposal requirements, no provision is
included in the construction and shipyard proposals for placing warning
labels on containers of waste, scrap, debris, and other materials
contaminated with Cr(VI).
Information and training is essential to inform employees of the
hazards to which they are exposed and to provide employees with the
necessary understanding of the degree to which they themselves can
minimize potential health hazards. As part of an overall hazard
communication program, training serves to explain and reinforce the
information presented on labels and in material safety data sheets.
These written forms of communication will be successful and relevant
only when employees understand the information presented and are aware
of the actions to be taken to avoid or minimize exposures, thereby
reducing the possibility of experiencing adverse health effects.
OSHA proposes that employers provide training for all employees who
are exposed to airborne Cr(VI) or who have skin or eye contact with
Cr(VI), ensure that employees participate in the training, and maintain
a record of the training provided. Training would be provided to all
employees exposed to Cr(VI), and would not be limited to only those
exposed above the PEL or action level. This proposed requirement is
consistent with the Hazard Communication standard (29 CFR 1910.1200),
which requires training for all employees exposed to hazardous
chemicals and defines this to include potential (e.g., accidental or
possible) exposure. This training would allow employees to make efforts
to avoid exposures altogether or mitigate those exposures that do
occur.
The employer is to provide initial training prior to or at the time
of initial assignment to a job involving potential exposure to Cr(VI).
An employer who is able to demonstrate that a new employee has received
training within the last 12 months is allowed to use that training for
purposes of initial training required by the standard, provided the
previous training has addressed the elements specified in the training
provisions of the proposal, and the employee is able to demonstrate
knowledge of those elements. In cases where understanding of some
elements is lacking or inadequate, the employer would be required to
provide training only in those elements. This allowance for prior
training is intended to ensure that employees receive sufficient
training, without requiring unnecessary repetition of that training.
The training requirements in this standard are performance-
oriented. The proposed standard lists the subjects that must be
addressed in training, but not the specific ways that this is to be
accomplished. Hands-on training, videotapes, slide presentations,
classroom instruction, informal discussions during safety meetings,
written materials, or any combination of these methods may be
appropriate. Such performance-oriented requirements are intended to
encourage employers to tailor training to the needs of their
workplaces, thereby resulting in the most effective training program in
each specific workplace.
[[Page 59462]]
OSHA believes that the employer is in the best position to
determine how the training can most effectively be accomplished. The
Agency has therefore laid out the objectives to be met to ensure that
employees are made aware of the hazards associated with Cr(VI) in their
workplace and how they can help to protect themselves. The specifics
regarding how this is to be achieved are left up to the employer.
In order for the training to be effective, the employer must ensure
that it is provided in a manner that the employee is able to
understand. Employees have varying educational levels, literacy, and
language skills, and the training must be presented in a language and
at a level of understanding that accounts for these differences in
order to meet the proposed requirement that individuals being trained
understand the specified elements. This may mean, for example,
providing materials, instruction, or assistance in Spanish rather than
English if the workers being trained are Spanish-speaking and do not
understand English. The employer would not be required to provide
training in the employee's preferred language if the employee
understood both languages; as long as the employee is able to
understand the language used, the intent of the proposed standard would
be met.
In order to ensure that employees comprehend the material presented
during training, it is critical that trainees have the opportunity to
ask questions and receive answers if they do not fully understand the
material that is presented to them. When videotape presentations or
computer-based programs are used, this requirement may be met by having
a qualified trainer available to address questions after the
presentation, or providing a telephone hotline so that trainees will
have direct access to a qualified trainer.
Under the proposal, the employer would be required to ensure that
each employee can demonstrate knowledge of the specified elements. This
could be determined through methods such as discussion of the required
training subjects, written tests, or oral quizzes.
The frequency of training under the proposed standard would be
determined by the needs of the workplace. Individuals would need to be
trained sufficiently to understand the specified elements. Additional
training is needed periodically to refresh and reinforce the memories
of individuals who have previously been trained, and to ensure that
these individuals are informed of new developments in the workplace
that may result in new or additional exposures to Cr(VI). For example,
training after new control measures are implemented would generally be
necessary in order to ensure that employees are able to properly use
the new controls that are introduced. Employees would likely be
unfamiliar with new work practices undertaken, with the operation of
new engineering controls, or the use of new personal protective
equipment; training would rectify this lack of understanding.
Additional training would ensure that employees are able to actively
participate in protecting themselves under the conditions found in the
workplace, even if those conditions change.
(m) Recordkeeping
The proposed standard for general industry would require employers
to maintain exposure monitoring, medical surveillance, and training
records. Because the proposed construction and shipyard standards do
not include requirements for exposure monitoring, no provision for
retention of exposure monitoring records is included in the proposed
regulatory texts for construction and shipyards. However, the record
retention requirements of OSHA's standard on access to medical and
exposure records (29 CFR 1910.1020) apply to any exposure records that
construction and shipyard employers produce.
The recordkeeping requirements are proposed in accordance with
section 8(c) of the OSH Act, which authorizes OSHA to require employers
to keep and make available records as necessary or appropriate for the
enforcement of the Act or for developing information regarding the
causes and prevention of occupational injuries and illnesses. The
proposed recordkeeping provisions are also consistent with the OSHA's
standard addressing access to employee exposure and medical records (29
CFR 1910.1020).
The proposal would require that records be kept of environmental
monitoring results that identify the monitored employee and accurately
reflect the employee's exposure. The employer would be required to keep
records for each exposure measurement taken. Specifically, records must
include the following information: The date of measurement for each
sample taken; the operation involving exposure to Cr(VI) that was
monitored; sampling and analytical methods used and evidence of their
accuracy; the number, duration, and results of samples taken; the type
of personal protective equipment used; and the name, social security
number, and job classification of all employees represented by the
monitoring, indicating which employees were actually monitored.
Most of OSHA's substance-specific standards require that exposure
monitoring and medical surveillance records include the employee's
social security number. OSHA has included this requirement in the past
because social security numbers are particularly useful in identifying
employees, since each number is unique to an individual for a lifetime
and does not change when an employee changes employers. When employees
have identical or similar names, identifying employees solely by name
makes it difficult to determine to which employee a particular record
pertains. However, based on privacy concerns, OSHA is examining
alternatives to requiring social security numbers for employee
identification. In its Standards Improvement Project proposal, the
Agency requested public comment on the necessity, usefulness, and
effectiveness of social security numbers as a means of identifying
employee records, and any privacy concerns or issues raised by this
requirement, as well as the availability of other effective methods of
identifying employees for OSHA recordkeeping purposes (67 FR 66493 (19/
31/02)). OSHA intends for the requirements of the Cr(VI) standard to
conform with any final determination made through the Standards
Improvement Project.
The proposal would allow the employer to rely on Cr(VI) monitoring
results obtained in the past 12 months when the data were obtained
during operations conducted under workplace conditions closely
resembling the employer's current operations. Where historical
monitoring data are used, the proposal would require that records of
these data be maintained. The records of historical data must
demonstrate that exposures on a particular job will be below the action
level by showing that the work being performed, Cr(VI)-containing
material being handled, and environmental conditions at the time the
historical data were obtained are the same as those on the job for
which monitoring was not performed. The records must also demonstrate
that the data were obtained using a method sufficiently accurate to be
allowed under the standard. Other data relevant to operations,
materials, processing, or employee exposures must also be included in
records.
A provision allowing the use of objective data in place of initial
monitoring is included in this proposed standard. Objective data are
information demonstrating that a particular product or material cannot
release Cr(VI) in
[[Page 59463]]
concentrations at or above the action level under any expected
conditions of use, even under conditions of worst-case release. Where
objective data are used to satisfy initial monitoring requirements, the
proposal would require employers to establish and maintain accurate
records of the objective data relied upon. Since the use of objective
data exempts the employer from requirements for conducting periodic
monitoring and certain other provisions of the proposal due to the low
level of potential exposure, it is critical that this determination be
carefully documented. The record would be required to include
identification of the Cr(VI)-containing material in question; the
source of the objective data; the testing protocol and results of
testing, or analysis of the material for the release of Cr(VI); a
description of the operation exempted from initial monitoring and how
the data support the exemption; and any other data relevant to the
operations, materials, processing or employee exposures covered by the
exemption.
Compliance with the requirement to maintain a record of objective
data protects the employer at later dates from the contention that
initial monitoring was not conducted in an appropriate manner. The
record would also be available to employees so that they can examine
the determination made by the employer. The employer would be required
to maintain the record for the duration of the employer's reliance upon
the objective data.
In addition to records relating to employee exposures to Cr(VI),
the proposal would require the employer to establish and maintain an
accurate medical surveillance record for each employee subject to the
medical surveillance requirements of the standard. OSHA believes that
medical records, like exposure records, are necessary and appropriate
both to the enforcement of the standard and to the development of
information regarding the causes and prevention of occupational
illnesses. Good medical records, including the record of the
examination at termination of employment itself, can be useful to the
Agency and others in enumerating illnesses and deaths attributable to
Cr(VI), in evaluating compliance programs, and in assessing the
accuracy of the Agency's risk estimates. Furthermore, medical records
are necessary for the proper evaluation of the employee's health.
The medical surveillance records would be required to include the
following information: The name, social security number, and job
classification of the employee; a copy of the PLHCP's written opinions;
and a copy of the information provided to the PLHCP. This information
includes the employee's duties as they relate to Cr(VI) exposure,
Cr(VI) exposure levels, and descriptions of personal protective
equipment used by the employee.
The employer would be required under the proposal to maintain
records of employees' Cr(VI)-related training. At the completion of
training, the employer would be required to prepare a record that
indicates the identity of the individuals trained and the date the
training was completed. The record would need to be maintained for
three years after the completion of training. In addition, the employer
would need to provide materials relating to employee information and
training to OSHA or NIOSH, if requested.
OSHA believes that a three year retention period for training
records is reasonable. Since OSHA is not proposing specific intervals
for periodic retraining, but is making retraining contingent upon the
need to maintain employee understanding of safe use and handling of
Cr(VI) and workplace changes which result in significant increases in
employee exposures to Cr(VI), it is appropriate to have records of
training to allow employers to determine when and how employees have
been trained. The proposed requirement to provide training materials
upon request is necessary to allow for evaluation of training programs,
and is consistent with the other OSHA standards such as those for
bloodborne pathogens (29 CFR 1910.1030) methylene chloride (29 CFR
1910.1052), butadiene (29 CFR 1910.1051), and methylenedianiline (29
CFR 1910.1050).
All medical and exposure records developed under the Cr(VI) rule
would be made available to employees and their designated
representatives in accordance with OSHA's standard on access to records
(29 CFR 1910.1020). The medical and exposure records standard requires
that exposure records be kept for at least 30 years and that medical
records be kept for the duration of employment plus thirty years. It is
necessary to keep these records for extended periods because of the
long latency period commonly associated with cancer. Cancer often
cannot be detected until 20 or more years after first exposure. The
extended record retention period is therefore needed because diagnosis
of disease in employees is assisted by, and in some cases can only be
made by, having present and past exposure data as well as the results
of present and past medical examinations.
(n) Dates
OSHA proposes that the final Cr(VI) rule become effective 60 days
after its publication in the Federal Register. This period is intended
to allow affected employers the opportunity to familiarize themselves
with the standard. Employer obligations to comply with most
requirements of the final rule would begin 90 days after the effective
date (150 days after publication of the final rule). This is designed
to allow employers sufficient time to complete initial exposure
assessments, establish regulated areas, obtain appropriate work
clothing and equipment, and comply with other provisions of the rule.
Additional time would be allowed for the employer to establish
change rooms and to implement engineering controls. Change rooms would
be required no later than one year after the effective date of the
standard, and engineering controls would need to be in place within two
years after the effective date. This is to allow affected employers
sufficient time to design and construct change rooms (where necessary),
and to design, obtain, and install the necessary control equipment.
OSHA solicits comment on the adequacy of these proposed start-up dates.
In particular, the Agency is aware that in some cases employers may be
required to reevaluate modified ventilation systems for compliance with
regulations governing discharges of Cr(VI) to the environment. OSHA
would like to ensure that employers are provided sufficient time to
complete this process, and has included this topic in the ``Issues''
section of this preamble.
XVIII. Authority and Signature
This document was prepared under the direction of John L. Henshaw,
Assistant Secretary of Labor for Occupational Safety and Health, U.S.
Department of Labor, 200 Constitution Avenue, NW., Washington, DC
20210.
The Agency issues the proposed sections under the following
authorities: Sections 4, 6(b), 8(c), and 8(g) of the Occupational
Safety and Health Act of 1970 (29 U.S.C. 653, 655, 657); section 107 of
the Contract Work Hours and Safety Standards Act (the Construction
Safety Act) (40 U.S.C. 333); section 41, the Longshore and Harbor
Worker's Compensation Act (33 U.S.C. 941); Secretary of Labor's Order
No. 5-2002 (67 FR 65008); and 29 CFR Part 1911.
[[Page 59464]]
List of Subjects in 29 CFR Parts 1910, 1915, 1917, 1918, and 1926
Cancer, Chemicals, Hazardous substances, Health, Occupational
safety and health, Reporting and recordkeeping requirements.
Signed at Washington, DC, this 21st day of September, 2004.
John L. Henshaw,
Assistant Secretary of Labor.
XIX. Proposed Standards
Chapter XVII of Title 29 of the Code of Federal Regulation is
proposed to be amended as follows:
PART 1910--[AMENDED]
Subpart Z--[Amended]
1. The authority citation for Subpart Z of Part 1910 is revised to
read as follows:
Authority: Secs. 4, 6, 8 of the Occupational Safety and Health
Act of 1970 (29 U.S.C. 653, 655, 657: Secretary of Labor's Order No.
12-71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), 1-90 (55
FR 9033), 6-96 (62 FR 111), 3-2000 (65 FR 50017), or 5-2002 (67 FR
65008), as applicable; and 29 CFR part 1911.
All of subpart Z issued under section 6(b) of the Occupational
Safety and Health Act, --except those substances that have exposure
limits listed in Tables Z-1, Z-2, and Z-3 of 29 CFR 1910.1000. The
latter were issued under Sec. 6(a) (29 U.S.C. 655(a)).
Section 1910.1000, Tables Z-1, Z-2 and Z-3 also issued under 5
U.S.C. 553, Section 1910.1000 Tables Z-1, Z-2, and Z-3 not issued
under 29 CFR part 1911 except for the arsenic (organic compounds),
benzene, and cotton dust listings.
Section 1910.1001 also issued under Sec. 107 of the Contract
Work Hours and Safety Standards Act (40 U.S.C. 3704) and 5 U.S.C.
553.
Section 1910.1002 also issued under 5 U.S.C. 553 but not under
29 U.S.C. 655 or 29 CFR part 1911.
Sections 1910.1018, 1910.1029 and 1910.1200 also issued under 29
U.S.C. 653.
Section 1910.1030 also issued under Pub. L. 106-430, 114 Stat.
1901.
Sec. 1910.1000 [Amended]
2. In Sec. 1910.1000, Table Z-2, the entry for Chromic acid and
chromates 1.0 mg/10 m3 is removed and the following entry
added in its place:
Sec. 1910.1000 Air contaminants.
* * * * *
Table Z-2
----------------------------------------------------------------------------------------------------------------
Acceptable maximum peak above the
acceptable ceiling average
Substance 8-hour time Acceptable ceiling concentration for an 8-hr shift
weighted average concentration ---------------------------------------
Concentration Maximum duration
----------------------------------------------------------------------------------------------------------------
* * * * * * *
Chromium (VI) compounds (as Cr);
see 1910.1026.
* * * * * * *
----------------------------------------------------------------------------------------------------------------
* * * * *
3. A new Sec. 1910.1026 is added to read as follows:
Sec. 1910.1026 Chromium (VI).
(a) Scope. This standard applies to occupational exposures to
chromium (VI) in all forms and compounds in general industry, except
exposures that occur in the application of pesticides (e.g., the
treatment of wood with preservatives).
(b) Definitions. For the purposes of this section the following
definitions apply:
Action level means a concentration of airborne chromium (VI) of 0.5
microgram per cubic meter of air (0.5 [mu]g/m3) calculated
as an 8-hour time-weighted average (TWA).
Assistant Secretary means the Assistant Secretary of Labor for
Occupational Safety and Health, U.S. Department of Labor, or designee.
Chromium (VI) [hexavalent chromium or Cr(VI)] means chromium with a
valence of positive six, in any form and in any compound.
Director means the Director of the National Institute for
Occupational Safety and Health (NIOSH), U.S. Department of Health and
Human Services, or designee.
Emergency means any occurrence that results, or is likely to
result, in an uncontrolled release of chromium (VI). 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.
Employee exposure means the exposure to airborne chromium (VI) that
would occur if the employee were not using a respirator.
High-efficiency particulate air [HEPA] filter means a filter that
is at least 99.97 percent efficient in removing mono-dispersed
particles of 0.3 micrometers in diameter or larger.
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 paragraph (k) of this
section.
Regulated area means an area, demarcated by the employer, where an
employee's exposure to airborne concentrations of chromium (VI)
exceeds, or can reasonably be expected to exceed, the PEL.
This section means this chromium (VI) standard.
(c) Permissible exposure limit (PEL). The employer shall ensure
that no employee is exposed to an airborne concentration of chromium
(VI) in excess of 1 microgram per cubic meter of air (1 [mu]g/m\3\),
calculated as an 8-hour time-weighted average (TWA).
(d) Exposure assessment. (1) General. The employer shall determine
the 8-hour TWA exposure for each employee on the basis of a sufficient
number of personal breathing zone air samples to accurately
characterize full shift exposure on each shift, for each job
classification, in each work area. Where an employer does
representative sampling instead of sampling all employees in order to
meet this requirement, the employer shall sample the employee(s)
expected to have the highest chromium (VI) exposures.
(2) Initial exposure monitoring. (i) Except as provided for in
paragraphs (d)(2)(ii) and (d)(2)(iii) of this section, each employer
who has a workplace or work operation covered by this section shall
determine if any employee may be
[[Page 59465]]
exposed to chromium (VI) at or above the action level.
(ii) Where the employer has monitored for chromium (VI) in the past
12 months, and 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
used and prevailing in the employer's current operations, and where
that monitoring satisfies all other requirements of this section,
including the accuracy and confidence levels of paragraph (d)(6) of
this section, the employer may rely on such earlier monitoring results
to satisfy the requirements for initial monitoring.
(iii) Where the employer has objective data demonstrating that a
material containing chromium (VI) or a specific process, operation, or
activity involving chromium (VI) cannot release dust, fumes, or mist of
chromium (VI) in concentrations at or above the action level under any
expected conditions of use, the employer may rely upon such data to
satisfy initial monitoring requirements. 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.
(3) Periodic monitoring. (i) If initial monitoring or periodic
monitoring indicates that employee exposures are below the action
level, the employer may discontinue monitoring for those employees
whose exposures are represented by such monitoring.
(ii) If initial monitoring or periodic monitoring reveals employee
exposures to be at or above the action level, the employer shall
perform periodic monitoring at least every six months.
(iii) If initial monitoring reveals employee exposures to be at or
above the PEL, the employer shall perform periodic monitoring at least
every three months.
(iv) If periodic monitoring indicates that employee exposures are
below the action level, and the result is confirmed by the result of
another monitoring taken at least seven days later, the employer may
discontinue the monitoring for those employees whose exposures are
represented by such monitoring.
(4) Additional monitoring. The employer shall perform additional
monitoring when there has been any change in the production process,
raw materials, equipment, personnel, work practices, or control methods
that may result in new or additional exposures to chromium (VI), or
when the employer has any reason to believe that new or additional
exposures have occurred.
(5) Employee notification of monitoring results. (i) Within 15
working days after the receipt of the results of any monitoring
performed under this section, the employer shall either notify each
affected employee individually in writing of the results or shall post
the results of the exposure monitoring in an appropriate location that
is accessible to all affected employees.
(ii) Whenever monitoring results indicate that employee exposure is
above the PEL, the employer shall describe in the written notification
the corrective action being taken to reduce employee exposure to or
below the PEL.
(6) Accuracy of measurement. The employer shall use a method of
monitoring and analysis that can measure chromium (VI) to within an
accuracy of plus or minus 25 percent (+/- 25%) and can produce accurate
measurements to within a statistical confidence level of 95 percent for
airborne concentrations at or above the action level.
(7) Observation of monitoring. (i) The employer shall provide
affected employees or their designated representatives an opportunity
to observe any monitoring of employee exposure to chromium (VI).
(ii) When observation of monitoring requires entry into an area
where the use of protective clothing or equipment is required, the
employer shall provide the observer with clothing and equipment and
shall assure that the observer uses such clothing and equipment and
complies with all other applicable safety and health procedures.
(e) Regulated areas. (1) Establishment. The employer shall
establish a regulated area wherever an employee's exposure to airborne
concentrations of chromium (VI) is, or can reasonably be expected to
be, in excess of the PEL.
(2) Demarcation. The employer shall ensure that regulated areas are
demarcated from the rest of the workplace in a manner that adequately
establishes and alerts employees of the boundaries of the regulated
area, and shall include the warning signs required under paragraph
(l)(2) of this section.
(3) Access. The employer shall limit access to regulated areas to:
(i) Persons authorized by the employer and required by work duties
to be present in the regulated area;
(ii) Any person entering such an area as a designated
representative of employees for the purpose of exercising the right to
observe monitoring procedures under paragraph (d) of this section; or
(iii) Any person authorized by the Occupational Safety and Health
Act or regulations issued under it to be in a regulated area.
(f) Methods of compliance. (1) Engineering and work practice
controls. (i) Except as permitted in paragraph (f)(1)(ii) of this
section, the employer shall use engineering and work practice controls
to reduce and maintain employee exposure to chromium (VI) to or below
the PEL unless the employer can demonstrate that such controls are not
feasible. Wherever feasible engineering and work practice controls are
not sufficient to reduce employee exposure to or below the PEL, the
employer shall use them to reduce employee exposure to the lowest
levels achievable, and shall supplement them by the use of respiratory
protection that complies with the requirements of paragraph (g) of this
section.
(ii) Where the employer has a reasonable basis for believing that
no employee in a process or task will be exposed above the PEL for 30
or more days per year (12 consecutive months), the requirement to
implement engineering and work practice controls to achieve the PEL
does not apply to that process or task.
(2) Prohibition of rotation. The employer shall not rotate
employees to different jobs to achieve compliance with the PEL.
(g) Respiratory protection. (1) General. The employer shall provide
respiratory protection for employees during:
(i) Periods necessary to install or implement feasible engineering
and work practice controls;
(ii) Work operations, such as maintenance and repair activities,
for which engineering and work practice controls are not feasible;
(iii) Work operations for which an employer has implemented all
feasible engineering and work practice controls and such controls are
not sufficient to reduce exposures to or below the PEL;
(iv) Work operations where employees are exposed above the PEL for
fewer than 30 days per year, and the employer has elected not to
implement engineering and work practice controls to achieve the PEL; or
(v) Emergencies.
(2) Respiratory protection program. Where respirator use is
required by this section, the employer shall institute a respiratory
protection program in accordance with 29 CFR 1910.134.
(h) Protective work clothing and equipment. (1) Provision and use.
Where a hazard is present or is likely to be present from skin or eye
contact with chromium (VI), the employer shall provide appropriate
personal protective
[[Page 59466]]
clothing and equipment at no cost to employees, and shall ensure that
employees use such clothing and equipment.
(2) Removal and storage. (i) The employer shall ensure that
employees remove all protective clothing and equipment contaminated
with chromium (VI) at the end of the work shift or at the completion of
their tasks involving chromium (VI) exposure, whichever comes first.
(ii) The employer shall ensure that no employee removes chromium
(VI)-contaminated protective clothing or equipment from the workplace,
except for those employees whose job it is to launder, clean, maintain,
or dispose of such clothing or equipment.
(iii) When contaminated protective clothing or equipment is removed
for laundering, cleaning, maintenance, or disposal, the employer shall
ensure that it is stored and transported in sealed, impermeable bags or
other closed, impermeable containers.
(iv) Bags or containers of contaminated protective clothing or
equipment that are removed from change rooms for laundering, cleaning,
maintenance, or disposal shall be labeled in accordance with paragraph
(l) of this section.
(3) Cleaning and replacement. (i) The employer shall clean,
launder, repair and replace all protective clothing and equipment
required by this section as needed to maintain its effectiveness.
(ii) The employer shall prohibit the removal of chromium (VI) from
protective clothing and equipment by blowing, shaking, or any other
means that disperses chromium (VI) into the air or onto an employee's
body.
(iii) The employer shall inform any person who launders or cleans
protective clothing or equipment contaminated with chromium (VI) of the
potentially harmful effects of exposure to chromium (VI) and that the
clothing and equipment should be laundered or cleaned in a manner that
minimizes skin or eye contact with chromium (VI) and effectively
prevents the release of airborne chromium (VI) in excess of the PEL.
(i) Hygiene areas and practices. (1) General. Where protective
clothing and equipment is required, the employer shall provide change
rooms in conformance with 29 CFR 1910.141. Where skin contact with
chromium (VI) occurs, the employer shall provide washing facilities in
conformance with 29 CFR 1910.141. Eating and drinking areas provided by
the employer shall also be in conformance with Sec. 1910.141.
(2) Change rooms. The employer shall assure that change rooms are
equipped with separate storage facilities for protective clothing and
equipment and for street clothes, and that these facilities prevent
cross-contamination.
(3) Washing facilities. (i) The employer shall provide readily
accessible washing facilities capable of removing chromium (VI) from
the skin, and shall ensure that affected employees use these facilities
when necessary.
(ii) The employer shall ensure that employees who have skin contact
with chromium (VI) wash their hands and faces at the end of the work
shift and prior to eating, drinking, smoking, chewing tobacco or gum,
applying cosmetics, or using the toilet.
(4) Eating and drinking areas. (i) Whenever the employer allows
employees to consume food or beverages at a worksite where chromium
(VI) is present, the employer shall ensure that eating and drinking
areas and surfaces are maintained as free as practicable of chromium
(VI).
(ii) The employer shall ensure that employees do not enter eating
and drinking areas with protective work clothing or equipment unless
surface chromium (VI) has been removed from the clothing and equipment
by methods that do not disperse chromium (VI) into the air or onto an
employee's body.
(5) Prohibited activities. The employer shall ensure that employees
do not eat, drink, smoke, chew tobacco or gum, or apply cosmetics in
regulated areas, or in areas where skin or eye contact with chromium
(VI) occurs; or carry the products associated with these activities, or
store such products in these areas.
(j) Housekeeping. (1) General. The employer shall ensure that:
(i) All surfaces are maintained as free as practicable of
accumulations of chromium (VI).
(ii) All spills and releases of chromium (VI) containing material
are cleaned up promptly.
(2) Cleaning methods. (i) The employer shall ensure that surfaces
contaminated with chromium (VI) are cleaned by HEPA-filter vacuuming or
other methods that minimize the likelihood of exposure to chromium
(VI).
(ii) Shoveling, sweeping, and brushing may be used only where HEPA-
filtered vacuuming or other methods that minimize the likelihood of
exposure to chromium (VI) have been tried and found not to be
effective.
(iii) The employer shall not allow compressed air to be used to
remove chromium (VI) from any surface unless the compressed air is used
in conjunction with a ventilation system designed to capture the dust
cloud created by the compressed air.
(iv) The employer shall ensure that cleaning equipment is handled
in a manner that minimizes the reentry of chromium (VI) into the
workplace.
(3) Disposal. The employer shall ensure that:
(i) Waste, scrap, debris, and any other materials contaminated with
chromium (VI) and consigned for disposal are collected and disposed of
in sealed, impermeable bags or other closed, impermeable containers.
(ii) Bags or containers of waste, scrap, debris, and any other
materials contaminated with chromium (VI) that are consigned for
disposal are labeled in accordance with paragraph (l) of this section.
(k) Medical surveillance. (1) General. (i) The employer shall make
medical surveillance available at no cost to the employee, and at a
reasonable time and place, for all employees:
(A) Who are or may be occupationally exposed to chromium (VI) above
the PEL for 30 or more days a year;
(B) Experiencing signs or symptoms of the adverse health effects
associated with chromium (VI) exposure; or
(C) Exposed in an emergency.
(ii) The employer shall assure that all medical examinations and
procedures required by this section are performed by or under the
supervision of a PLHCP.
(2) Frequency. The employer shall provide a medical examination:
(i) Within 30 days after initial assignment, unless the employee
has received a chromium (VI) related medical examination, provided in
accordance with this standard, within the last twelve months;
(ii) Annually;
(iii) Within 30 days after a PLHCP's written medical opinion
recommends an additional examination;
(iv) Whenever an employee shows signs or symptoms of the adverse
health effects associated with chromium (VI) exposure;
(v) Within 30 days after exposure during an emergency which results
in an uncontrolled release of chromium (VI); or
(vi) At the termination of employment, unless the last examination
that satisfied the requirements of paragraph (k) of this section was
less than six months prior to the date of termination.
(3) Contents of examination. A medical examination consists of:
(i) A medical and work history, with emphasis on: past, present,
and anticipated future exposure to chromium (VI); any history of
respiratory system dysfunction; any
[[Page 59467]]
history of asthma, dermatitis, skin ulceration, or nasal septum
perforation; and smoking status and history;
(ii) A physical examination of the skin and respiratory tract; and
(iii) Any additional tests deemed appropriate by the examining
PLHCP.
(4) Information provided to the PLHCP. The employer shall ensure
that the examining PLHCP has a copy of this standard, and shall provide
the following information:
(i) A description of the affected employee's former, current, and
anticipated duties as they relate to the employee's occupational
exposure to chromium (VI);
(ii) The employee's former, current, and anticipated levels of
occupational exposure to chromium (VI);
(iii) A description of any personal protective equipment used or to
be used by the employee, including when and for how long the employee
has used that equipment; and
(iv) Information from records of employment-related medical
examinations previously provided to the affected employee, currently
within the control of the employer.
(5) PLHCP's written medical opinion. (i) The employer shall obtain
a written medical opinion from the PLHCP, within 30 days for each
medical examination performed on each employee, which contains:
(A) The PLHCP's opinion as to whether the employee has any detected
medical condition(s) that would place the employee at increased risk of
material impairment to health from further exposure to chromium (VI);
(B) Any recommended limitations upon the employee's exposure to
chromium (VI) or upon the use of personal protective equipment such as
respirators;
(C) A statement that the PLHCP has explained to the employee the
results of the medical examination, including any medical conditions
related to chromium (VI) exposure that require further evaluation or
treatment, and any special provisions for use of protective clothing or
equipment.
(ii) The PLHCP shall not reveal to the employer specific findings
or diagnoses unrelated to occupational exposure to chromium (VI).
(iii) The employer shall provide a copy of the PLHCP's written
medical opinion to the examined employee within two weeks after
receiving it.
(l) Communication of chromium (VI) hazards to employees.
(1) General. In addition to the requirements of the Hazard
Communication Standard, 29 CFR 1910.1200, for labels, material safety
data sheets, and training, employers shall comply with the following
requirements.
(2) Warning signs. (i) The employer shall ensure that legible and
readily visible warning signs are displayed at all approaches to
regulated areas so that an employee may read the signs and take
necessary protective steps before entering the area.
(ii) Warning signs required by paragraph (l)(2)(i) of this section
shall include at least the following information:
DANGER
CHROMIUM (VI)
CANCER HAZARD
CAN DAMAGE SKIN, EYES, NASAL PASSAGES, AND LUNGS
AUTHORIZED PERSONNEL ONLY
RESPIRATORS REQUIRED IN THIS AREA
(3) Warning labels. The employer shall ensure that bags or
containers of contaminated clothing and equipment to be removed for
laundering, cleaning, or maintenance, and containers of waste, scrap,
debris, and any other materials contaminated with chromium (VI) that
are consigned for disposal, bear appropriate warning labels that
include at least the following information:
DANGER
CONTAINS CHROMIUM (VI)
CANCER HAZARD
CAN DAMAGE SKIN, EYES, NASAL PASSAGES, AND LUNGS
(4) Employee information and training. (i) For all employees who
are exposed to airborne chromium (VI), or who have skin or eye contact
with chromium (VI), the employer shall provide training, ensure
employee participation in training, and maintain a record of training
provided.
(ii) The employer shall provide initial training prior to or at the
time of initial assignment to a job involving potential exposure to
chromium (VI). An employer who is able to demonstrate that a new
employee has received training within the last 12 months that addresses
the elements specified in paragraph (l)(4)(iii) of this section is not
required to repeat such training provided that the employee can
demonstrate knowledge of those elements.
(iii) The employer shall provide training that is understandable to
the employee and shall ensure that each employee can demonstrate
knowledge of at least the following:
(A) The health hazards associated with chromium (VI) exposure;
(B) The location, manner of use, and release of chromium (VI) in
the workplace and the specific nature of operations that could result
in exposure to chromium (VI), especially exposure above the PEL;
(C) The engineering controls and work practices associated with the
employee's job assignment;
(D) The purpose, proper selection, fitting, proper use, and
limitations of respirators and protective clothing;
(E) Emergency procedures;
(F) Measures employees can take to protect themselves from exposure
to chromium (VI), including modification of personal hygiene and habits
such as smoking;
(G) The purpose and a description of the medical surveillance
program required by paragraph (k) of this section;
(H) The contents of this section; and
(I) The employee's rights of access to records under 29 CFR
1910.1020(g).
(iv) The employer shall provide additional training when:
(A) Training is necessary to ensure that each employee maintains an
understanding of the safe use and handling of chromium (VI) in the
workplace.
(B) Workplace changes (such as modification of equipment, tasks, or
procedures) result in an increase in employee exposures to chromium
(VI), and those exposures exceed or can reasonably be expected to
exceed the action level or result in a hazard from skin or eye contact
with chromium (VI).
(v) The employer shall make a copy of this section and its
appendices readily available without cost to all affected employees.
(m) Recordkeeping. (1) Exposure measurements. (i) The employer
shall maintain an accurate record of all measurements taken to monitor
employee exposure to chromium (VI) as prescribed in paragraph (d) of
this section.
(ii) This record shall include at least the following information:
(A) The date of measurement for each sample taken;
(B) The operation involving exposure to chromium (VI) that is being
monitored;
(C) Sampling and analytical methods used and evidence of their
accuracy;
(D) Number, duration, and the results of samples taken;
(E) Type of personal protective equipment, such as respirators
worn; and
(F) Name, social security number, and job classification of all
employees represented by the monitoring, indicating which employees
were actually monitored.
(iii) The employer shall ensure that exposure records are
maintained and made available in accordance with 29 CFR 1910.1020.
[[Page 59468]]
(2) Historical monitoring data. (i) Where the employer has
monitored for chromium (VI) in the past 12 months, and has relied on
this historical monitoring data to demonstrate that exposures on a
particular job will be below the action level, the employer shall
establish and maintain an accurate record of the historical monitoring
data relied upon.
(ii) The record shall include information that reflects the
following conditions:
(A) The data were collected using methods that meet the accuracy
requirements of paragraph (d)(6) of this section;
(B) The processes and work practices that were in use when the
historical monitoring data were obtained are essentially the same as
those to be used during the job for which initial monitoring will not
be performed;
(C) The characteristics of the chromium (VI) containing material
being handled when the historical monitoring data were obtained are the
same as those on the job for which initial monitoring will not be
performed;
(D) Environmental conditions prevailing when the historical
monitoring data were obtained are the same as those on the job for
which initial monitoring will not be performed; and
(E) Other data relevant to the operations, materials, processing,
or employee exposures covered by the exception.
(iii) The employer shall ensure that historical exposure records
are maintained and made available in accordance with 29 CFR 1910.1020.
(3) Objective data. (i) Where an employer uses objective data to
satisfy initial monitoring requirements, the employer shall establish
and maintain an accurate record of the objective data relied upon.
(ii) This record shall include at least the following information:
(A) The chromium (VI)-containing material in question;
(B) The source of the objective data;
(C) The testing protocol and results of testing, or analysis of the
material for the release of chromium (VI);
(D) A description of the operation exempted from initial monitoring
and how the data support the exemption; and
(E) Other data relevant to the operations, materials, processing or
employee exposures covered by the exemption.
(iii) The employer shall maintain this record for the duration of
the employer's reliance upon such objective data and shall make such
records available in accordance with 29 CFR 1910.1020.
(4) Medical surveillance. (i) The employer shall establish and
maintain an accurate record for each employee covered by medical
surveillance under paragraph (k) of this section.
(ii) The record shall include the following information about the
employee:
(A) Name and social security number;
(B) A copy of the PLHCP's written opinions;
(C) A copy of the information provided to the PLHCP as required by
paragraph (k)(4) of this section.
(iii) The employer shall ensure that medical records are maintained
and made available in accordance with 29 CFR 1910.1020.
(5) Training. (i) At the completion of training, the employer shall
prepare a record that indicates the identity of the individuals trained
and the date the training was completed. This record shall be
maintained for three years after the completion of training.
(ii) The employer shall provide to the Assistant Secretary or the
Director, upon request, all materials relating to employee information
and training.
(n) Dates. (1) Effective date. This section shall become effective
[60 days after publication of the final rule in the Federal Register].
(2) Start-up dates. All obligations of this section commence 90
days after the effective date except as follows:
(i) Change rooms required by paragraph (i) of this section shall be
provided no later than one year after the effective date.
(ii) Engineering controls required by paragraph (f) of this section
shall be implemented no later than two years after the effective date.
PART 1915--[AMENDED]
4. The authority citation for 29 CFR part 1915 is revised to read
as follows:
Authority: Sec. 41, Longshore and Harbor Workers' Compensation
Act (33 U.S.C. 941); secs. 4, 6, 8, Occupational Safety and Health
Act of 1970 (29 U.S.C. 653, 655, 657); Secretary of Labor's Order
No. 12-71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), 1-90
(55 FR 9033), 6-96 (62 FR 111), 3-2000 (65 FR 50017) or 5-2002 (67
FR 65008), as applicable.
Sections 1915.120, 1915.152 and 1915.1026 also issued under 29
CFR part 1911.
5. In Sec. 1915.1000, Table Z, the entry for ``Chromic acid and
chromates (as CrO(3)) 0.1'' is removed and the following entry added in
its place:
Sec. 1915.1000 Air contaminants.
* * * * *
TABLE Z--SHIPYARDS
----------------------------------------------------------------------------------------------------------------
Substance CAS No.d ppm a * mg/m 3 b * Skin designation
----------------------------------------------------------------------------------------------------------------
* * * * * * *
Chromium (VI) compounds (as Cr);
see 1915.1026.
* * * * * * *
----------------------------------------------------------------------------------------------------------------
* * * * * * *
3 Use Asbestos Limit Sec. 1915.1001.
* * * * * * *
* The PELS are 8-hour TWAs unless otherwise noted; a (C) designation denotes a ceiling limit. They are to be
determined from breathing-zone air samples.
a Parts of vapor or gas per million parts of contaminated air by volume at 25[deg] C and 760 torr.
b Milligrams of substance per cubic meter of air. When entry is in this column only, the value is exact; when
listed with a ppm entry, it is approximate.
* * * * * * *
d The CAS number is for information only. Enforcement is based on the substance name. For an entry covering more
than one metal compound, measured as the metal, the CAS number for the metal is given--not CAS numbers for the
individual compounds.
[[Page 59469]]
* * * * *
6. A new Sec. 1915.1026 is added, to read as follows:
Sec. 1915.1026 Chromium (VI).
(a) Scope. This standard applies to occupational exposures to
chromium (VI) in all forms and compounds in shipyards, marine
terminals, and longshoring.
(b) Definitions. For the purposes of this section the following
definitions apply:
Assistant Secretary means the Assistant Secretary of Labor for
Occupational Safety and Health, U.S. Department of Labor, or designee.
Chromium (VI) [hexavalent chromium or Cr(VI)] means chromium with a
valence of positive six, in any form and in any compound.
Director means the Director of the National Institute for
Occupational Safety and Health (NIOSH), U.S. Department of Health and
Human Services, or designee.
Emergency means any occurrence that results, or is likely to
result, in an uncontrolled release of chromium (VI). 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.
Employee exposure means the exposure to airborne chromium (VI) that
would occur if the employee were not using a respirator.
High-efficiency particulate air [HEPA] filter means a filter that
is at least 99.97 percent efficient in removing mono-dispersed
particles of 0.3 micrometers in diameter or larger.
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 paragraph (h) of this
section.
This section means this chromium (VI) standard.
(c) Permissible exposure limit (PEL). The employer shall ensure
that no employee is exposed to an airborne concentration of chromium
(VI) in excess of 1 microgram per cubic meter of air (1 [mu]g/m\3\),
calculated as an 8-hour time-weighted average (TWA).
(d) Methods of compliance. (1) Engineering and work practice
controls. (i) Except as permitted in paragraph (d)(1)(ii) of this
section, the employer shall use engineering and work practice controls
to reduce and maintain employee exposure to chromium (VI) to or below
the PEL unless the employer can demonstrate that such controls are not
feasible. Wherever feasible engineering and work practice controls are
not sufficient to reduce employee exposure to or below the PEL, the
employer shall use them to reduce employee exposure to the lowest
levels achievable, and shall supplement them by the use of respiratory
protection that complies with the requirements of paragraph (e) of this
section.
(ii) Where the employer has a reasonable basis for believing that
no employee in a process or task will be exposed above the PEL for 30
or more days per year (12 consecutive months), the requirement to
implement engineering and work practice controls to achieve the PEL
does not apply to that process or task.
(2) Prohibition of rotation. The employer shall not rotate
employees to different jobs to achieve compliance with the PEL.
(e) Respiratory protection. (1) General. The employer shall provide
respiratory protection for employees during:
(i) Periods necessary to install or implement feasible engineering
and work practice controls;
(ii) Work operations, such as maintenance and repair activities,
for which engineering and work practice controls are not feasible;
(iii) Work operations for which an employer has implemented all
feasible engineering and work practice controls and such controls are
not sufficient to reduce exposures to or below the PEL;
(iv) Work operations where employees are exposed above the PEL for
fewer than 30 days per year, and the employer has elected not to
implement engineering and work practice controls to achieve the PEL; or
(v) Emergencies.
(2) Respiratory protection program. Where respirator use is
required by this section, the employer shall institute a respiratory
protection program in accordance with 29 CFR 1910.134.
(f) Protective work clothing and equipment. (1) Provision and use.
Where a hazard is present or is likely to be present from skin or eye
contact with chromium (VI), the employer shall provide appropriate
personal protective clothing and equipment at no cost to employees, and
shall ensure that employees use such clothing and equipment.
(2) Removal and storage. (i) The employer shall ensure that
employees remove all protective clothing and equipment contaminated
with chromium (VI) at the end of the work shift or at the completion of
their tasks involving chromium (VI) exposure, whichever comes first.
(ii) The employer shall ensure that no employee removes chromium
(VI)-contaminated protective clothing or equipment from the workplace,
except for those employees whose job it is to launder, clean, maintain,
or dispose of such clothing or equipment.
(iii) When contaminated protective clothing or equipment is removed
for laundering, cleaning, maintenance, or disposal, the employer shall
ensure that it is stored and transported in sealed, impermeable bags or
other closed, impermeable containers.
(iv) Bags or containers of contaminated protective clothing or
equipment that are removed from change rooms for laundering, cleaning,
maintenance, or disposal shall be labeled in accordance with paragraph
(i) of this section.
(3) Cleaning and replacement. (i) The employer shall clean,
launder, repair and replace all protective clothing and equipment
required by this section as needed to maintain its effectiveness.
(ii) The employer shall prohibit the removal of chromium (VI) from
protective clothing and equipment by blowing, shaking, or any other
means that disperses chromium (VI) into the air or onto an employee's
body.
(iii) The employer shall inform any person who launders or cleans
protective clothing or equipment contaminated with chromium (VI) of the
potentially harmful effects of exposure to chromium (VI) and that the
clothing and equipment should be laundered or cleaned in a manner that
minimizes skin or eye contact with chromium (VI) and effectively
prevents the release of airborne chromium (VI) in excess of the PEL.
(g) Hygiene areas and practices. (1) General. Where protective
clothing and equipment is required, the employer shall provide change
rooms in conformance with 29 CFR 1910.141. Where skin contact with
chromium (VI) occurs, the employer shall provide washing facilities in
conformance with 29 CFR 1915.97. Eating and drinking areas provided by
the employer shall also be in conformance with Sec. 1915.97.
(2) Change rooms. The employer shall assure that change rooms are
equipped with separate storage facilities for protective clothing and
equipment and for street clothes, and that these facilities prevent
cross-contamination.
(3) Washing facilities. (i) The employer shall provide readily
accessible washing facilities capable of removing chromium (VI) from
the skin, and shall ensure that affected employees use these facilities
when necessary.
[[Page 59470]]
(ii) The employer shall ensure that employees who have skin contact
with chromium (VI) wash their hands and faces at the end of the work
shift and prior to eating, drinking, smoking, chewing tobacco or gum,
applying cosmetics, or using the toilet.
(4) Eating and drinking areas. (i) Whenever the employer allows
employees to consume food or beverages at a worksite where chromium
(VI) is present, the employer shall ensure that eating and drinking
areas and surfaces are maintained as free as practicable of chromium
(VI).
(ii) The employer shall ensure that employees do not enter eating
and drinking areas with protective work clothing or equipment unless
surface chromium (VI) has been removed from the clothing and equipment
by methods that do not disperse chromium (VI) into the air or onto an
employee's body.
(5) Prohibited activities. The employer shall ensure that employees
do not eat, drink, smoke, chew tobacco or gum, or apply cosmetics in
areas where skin or eye contact with chromium (VI) occurs; or carry the
products associated with these activities, or store such products in
these areas.
(h) Medical surveillance. (1) General. (i) The employer shall make
medical surveillance available at no cost to the employee, and at a
reasonable time and place, for all employees:
(A) Experiencing signs or symptoms of the adverse health effects
associated with chromium (VI) exposure; or
(B) Exposed in an emergency.
(ii) The employer shall assure that all medical examinations and
procedures required by this section are performed by or under the
supervision of a PLHCP.
(2) Frequency. The employer shall provide a medical examination:
(i) Whenever an employee shows signs or symptoms of the adverse
health effects associated with chromium (VI) exposure;
(ii) Within 30 days after exposure during an emergency which
results in an uncontrolled release of chromium (VI); or
(iii) Within 30 days after a PLHCP's written medical opinion
recommends an additional examination.
(3) Contents of examination. A medical examination consists of:
(i) A medical and work history, with emphasis on: Past, present,
and anticipated future exposure to chromium (VI); any history of
respiratory system dysfunction; any history of asthma, dermatitis, skin
ulceration, or nasal septum perforation; and smoking status and
history;
(ii) A physical examination of the skin and respiratory tract; and
(iii) Any additional tests deemed appropriate by the examining
PLHCP.
(4) Information provided to the PLHCP. The employer shall ensure
that the examining PLHCP has a copy of this standard, and shall provide
the following information:
(i) A description of the affected employee's former, current, and
anticipated duties as they relate to the employee's occupational
exposure to chromium (VI);
(ii) The employee's former, current, and anticipated levels of
occupational exposure to chromium (VI);
(iii) A description of any personal protective equipment used or to
be used by the employee, including when and for how long the employee
has used that equipment; and
(iv) Information from records of employment-related medical
examinations previously provided to the affected employee, currently
within the control of the employer.
(5) PLHCP's written medical opinion. (i) The employer shall obtain
a written medical opinion from the PLHCP, within 30 days for each
medical examination performed on each employee, which contains:
(A) The PLHCP's opinion as to whether the employee has any detected
medical condition(s) that would place the employee at increased risk of
material impairment to health from further exposure to chromium (VI);
(B) Any recommended limitations upon the employee's exposure to
chromium (VI) or upon the use of personal protective equipment such as
respirators;
(C) A statement that the PLHCP has explained to the employee the
results of the medical examination, including any medical conditions
related to chromium (VI) exposure that require further evaluation or
treatment, and any special provisions for use of protective clothing or
equipment.
(ii) The PLHCP shall not reveal to the employer specific findings
or diagnoses unrelated to occupational exposure to chromium (VI).
(iii) The employer shall provide a copy of the PLHCP's written
medical opinion to the examined employee within two weeks after
receiving it.
(i) Communication of chromium (VI) hazards to employees.
(1) General. In addition to the requirements of the Hazard
Communication Standard, 29 CFR 1910.1200, for labels, material safety
data sheets, and training, employers shall comply with the following
requirements.
(2) Warning labels. The employer shall ensure that bags or
containers of contaminated clothing and equipment to be removed for
laundering, cleaning, or maintenance, bear appropriate warning labels
that include at least the following information:
DANGER
CONTAINS CHROMIUM (VI)
CANCER HAZARD
CAN DAMAGE SKIN, EYES, NASAL PASSAGES, AND LUNGS
(3) Employee information and training. (i) The employer shall
provide training for all employees who are potentially exposed to
chromium (VI), ensure employee participation in training, and maintain
a record of training provided.
(ii) The employer shall provide initial training prior to or at the
time of initial assignment to a job involving potential exposure to
chromium (VI). An employer who is able to demonstrate that a new
employee has received training within the last 12 months that addresses
the elements specified in paragraph (l)(4)(iii) of this section is not
required to repeat such training provided that the employee can
demonstrate knowledge of those elements.
(iii) The employer shall provide training that is understandable to
the employee and shall ensure that each employee can demonstrate
knowledge of at least the following:
(A) The health hazards associated with chromium (VI) exposure;
(B) The location, manner of use, and release of chromium (VI) in
the workplace and the specific nature of operations that could result
in exposure to chromium (VI), especially exposure above the PEL;
(C) The engineering controls and work practices associated with the
employee's job assignment;
(D) The purpose, proper selection, fitting, proper use, and
limitations of respirators and protective clothing;
(E) Emergency procedures;
(F) Measures employees can take to protect themselves from exposure
to chromium (VI), including modification of personal hygiene and habits
such as smoking;
(G) The purpose and a description of the medical surveillance
program required by paragraph (h) of this section;
(H) The contents of this section; and
(I) The employee's rights of access to records under 29 CFR
1910.1020(g).
(iv) The employer shall provide additional training when:
(A) Training is necessary to ensure that each employee maintains an
understanding of the safe use and handling of chromium (VI) in the
workplace.
[[Page 59471]]
(B) Workplace changes (such as modification of equipment, tasks, or
procedures) result in an increase in employee exposures to chromium
(VI), and those exposures exceed or can reasonably be expected to
exceed the PEL or result in a hazard from skin or eye contact with
chromium (VI).
(v) The employer shall make a copy of this section and its
appendices readily available without cost to all affected employees.
(j) Recordkeeping. (1) Medical surveillance. (i) The employer shall
establish and maintain an accurate record for each employee covered by
medical surveillance under paragraph (h) of this section.
(ii) The record shall include the following information about the
employee:
(A) Name and social security number;
(B) A copy of the PLHCP's written opinions;
(C) A copy of the information provided to the PLHCP as required by
paragraph (h)(4) of this section.
(iii) The employer shall ensure that medical records are maintained
and made available in accordance with Sec. 1910.1020.
(2) Training. (i) At the completion of training, the employer shall
prepare a record that indicates the identity of the individuals trained
and the date the training was completed. This record shall be
maintained for three years after the completion of training.
(ii) The employer shall provide to the Assistant Secretary or the
Director, upon request, all materials relating to employee information
and training.
(k) Dates. (1) Effective date. This section shall become effective
[60 days after publication of the final rule in the Federal Register].
(2) Start-up dates. All obligations of this section commence 90
days after the effective date except as follows:
(i) Change rooms required by paragraph (g) of this section shall be
provided no later than one year after the effective date.
(ii) Engineering controls required by paragraph (d) of this section
shall be implemented no later than two years after the effective date.
PART 1917--[AMENDED]
7. The authority citation for 29 CFR Part 1917 is revised to read
as follows:
Authority: Sec. 41, Longshore and Harbor Workers' Compensation
Act (33 U.S.C. 941); secs. 4, 6, 8, Occupational Safety and Health
Act of 1970 (29 U.S.C. 653, 655, 657); Secretary of Labor's Order
Nos. 12-71 (36 FR 8754), 8-76 (41 FR 25059), 9-83 (48 FR 35736), 6-
96 (62 FR 111), or 5-2002 (67 FR 65008), as applicable; 29 CFR part
1911.
Section 1917.28 also issued under 5 U.S.C. 553.
8. New paragraphs (a)(2)(xiii)(E) and (b) are added to Sec.
1917.1, to read as follows:
Sec. 1917.1 Scope and applicability.
* * * * *
(a) * * *
(2) * * *
(xiii) * * *
(E) Hexavalent chromium Sec. 1910.1026 (See Sec. 1915.1026)
* * * * *
(b) Section 1915.1026 applies to any occupational exposures to
hexavalent chromium in workplaces covered by this part.
PART 1918--[AMENDED]
9. The authority citation for 29 CFR Part 1918 is revised to read
as follows:
Authority: Secs. 4, 6, 8, Occupational Safety and Health Act of
1970, 29 U.S.C. 653, 655, 657; Walsh-Healey Act, 41 U.S.C. 35 et
seq.; Service Contract Act of 1965, 41 U.S.C. 351 et seq,; Sec. 107,
Contract Work Hours and Safety Standards Act (Construction Safety
Act), 40 U.S.C. 333; Sec. 41, Longshore and Harbor Workers'
Compensation Act, 33 U.S.C. 941; National Foundation of Arts and
Humanities Act, 20 U.S.C. 951 et seq.; Secretary of Labor's Order
Nos. 6-96 (62 FR 111) or 5-2002 (67 FR 65008), as applicable; and 29
CFR part 1911.
10. New paragraphs (b)(9)(v) and (c) are added to Sec. 1918.1 to
read as follows:
Sec. 1918.1 Scope and application.
* * * * *
(b) * * *
(9) * * *
(v) Hexavalent chromium Sec. 1910.1026 (See Sec. 1915.1026)
* * * * *
(c) Section 1915.1026 applies to any occupational exposures to
hexavalent chromium in workplaces covered by this part.
PART 1926--[AMENDED]
Subpart D--[Amended]
11. The authority citation for subpart D of 29 CFR Part 1926 is
revised to
