[Federal Register Volume 81, Number 58 (Friday, March 25, 2016)][Rules and Regulations]
[Pages 16285-16890]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2016-04800]
Vol. 81
Friday,
No. 58
March 25, 2016
Part II
Book 2 of 3 Books
Pages 16285-16890
Department of Labor
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Occupational Safety and Health Administration
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29 CFR Parts 1910, 1915, and 1926
Occupational Exposure to Respirable Crystalline Silica; Final Rule
Federal Register / Vol. 81 , No. 58 / Friday, March 25, 2016 / Rules
and Regulations
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DEPARTMENT OF LABOR
Occupational Safety and Health Administration
29 CFR Parts 1910, 1915, and 1926
[Docket No. OSHA-2010-0034]
RIN 1218-AB70
Occupational Exposure to Respirable Crystalline Silica
AGENCY: Occupational Safety and Health Administration (OSHA),
Department of Labor.
ACTION: Final rule.
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SUMMARY: The Occupational Safety and Health Administration (OSHA) is
amending its existing standards for occupational exposure to respirable
crystalline silica. OSHA has determined that employees exposed to
respirable crystalline silica at the previous permissible exposure
limits face a significant risk of material impairment to their health.
The evidence in the record for this rulemaking indicates that workers
exposed to respirable crystalline silica are at increased risk of
developing silicosis and other non-malignant respiratory diseases, lung
cancer, and kidney disease. This final rule establishes a new
permissible exposure limit of 50 micrograms of respirable crystalline
silica per cubic meter of air (50 [mu]g/m\3\) as an 8-hour time-
weighted average in all industries covered by the rule. It also
includes other provisions to protect employees, such as requirements
for exposure assessment, methods for controlling exposure, respiratory
protection, medical surveillance, hazard communication, and
recordkeeping.
OSHA is issuing two separate standards--one for general industry
and maritime, and the other for construction--in order to tailor
requirements to the circumstances found in these sectors.
DATES: The final rule is effective on June 23, 2016. Start-up dates for
specific provisions are set in Sec. 1910.1053(l) for general industry
and maritime and in Sec. 1926.1153(k) for construction.
Collections of Information
There are a number of collections of information contained in this
final rule (see Section VIII, Paperwork Reduction Act). Notwithstanding
the general date of applicability that applies to all other
requirements contained in the final rule, affected parties do not have
to comply with the collections of information until the Department of
Labor publishes a separate notice in the Federal Register announcing
the Office of Management and Budget has approved them under the
Paperwork Reduction Act.
ADDRESSES: In accordance with 28 U.S.C. 2112(a), the Agency designates
Ann Rosenthal, Associate Solicitor of Labor for Occupational Safety and
Health, Office of the Solicitor of Labor, Room S-4004, U.S. Department
of Labor, 200 Constitution Avenue NW., Washington, DC 20210, to receive
petitions for review of the final rule.
FOR FURTHER INFORMATION CONTACT: For general information and press
inquiries, contact Frank Meilinger, Director, Office of Communications,
Room N-3647, OSHA, U.S. Department of Labor, 200 Constitution Avenue
NW., Washington, DC 20210; telephone (202) 693-1999; email
meilinger.francis2@dol.gov.
For technical inquiries, contact William Perry or David O'Connor,
Directorate of Standards and Guidance, Room N-3718, OSHA, U.S.
Department of Labor, 200 Constitution Avenue NW., Washington, DC 20210;
telephone (202) 693-1950.
SUPPLEMENTARY INFORMATION: The preamble to the rule on occupational
exposure to respirable crystalline silica follows this outline:
I. Executive Summary
II. Pertinent Legal Authority
III. Events Leading to the Final Standards
IV. Chemical Properties and Industrial Uses
V. Health Effects
VI. Final Quantitative Risk Assessment and Significance of Risk
VII. Summary of the Final Economic Analysis and Final Regulatory
Flexibility Analysis
VIII. Paperwork Reduction Act
IX. Federalism
X. State-Plan States
XI. Unfunded Mandates
XII. Protecting Children From Environmental Health and Safety Risks
XIII. Consultation and Coordination With Indian Tribal Governments
XIV. Environmental Impacts
XV. Summary and Explanation of the Standards
Scope
Definitions
Specified Exposure Control Methods
Alternative Exposure Control Methods
Permissible Exposure Limit
Exposure Assessment
Regulated Areas
Methods of Compliance
Respiratory Protection
Housekeeping
Written Exposure Control Plan
Medical Surveillance
Communication of Respirable Crystalline Silica Hazards to
Employees
Recordkeeping
Dates
Authority and Signature
Citation Method
In the docket for the respirable crystalline silica rulemaking,
found at http://www.regulations.gov, every submission was assigned a
document identification (ID) number that consists of the docket number
(OSHA-2010-0034) followed by an additional four-digit number. For
example, the document ID number for OSHA's Preliminary Economic
Analysis and Initial Regulatory Flexibility Analysis is OSHA-2010-0034-
1720. Some document ID numbers include one or more attachments, such as
the National Institute for Occupational Safety and Health (NIOSH)
prehearing submission (see Document ID OSHA 2010-0034-2177).
When citing exhibits in the docket, OSHA includes the term
"Document ID" followed by the last four digits of the document ID
number, the attachment number or other attachment identifier, if
applicable, page numbers (designated "p." or "Tr." for pages from a
hearing transcript), and in a limited number of cases a footnote number
(designated "Fn"). In a citation that contains two or more document
ID numbers, the document ID numbers are separated by semi-colons. For
example, a citation referring to the NIOSH prehearing comments and
NIOSH testimony obtained from the hearing transcript would be indicated
as follows: (Document ID 2177, Attachment B, pp. 2-3; 3579, Tr. 132).
In some sections, such as Section V, Health Effects, author names and
year of study publication are included before the document ID number in
a citation, for example: (Hughes et al., 2001, Document ID 1060;
McDonald et al., 2001, 1091; McDonald et al., 2005, 1092; Rando et al.,
2001, 0415).
I. Executive Summary
This final rule establishes a permissible exposure limit (PEL) for
respirable crystalline silica of 50 [mu]g/m\3\ as an 8-hour time-
weighted average (TWA) in all industries covered by the rule. In
addition to the PEL, the rule includes provisions to protect employees
such as requirements for exposure assessment, methods for controlling
exposure, respiratory protection, medical surveillance, hazard
communication, and recordkeeping. OSHA is issuing two separate
standards--one for general industry and maritime, and the other for
construction--in order to tailor requirements to the circumstances
found in these sectors. There are, however, numerous common elements in
the two standards.
The final rule is based on the requirements of the Occupational
Safety and Health Act (OSH Act) and court interpretations of the Act.
For health standards issued under section 6(b)(5) of the OSH Act, OSHA
is required to promulgate a standard that reduces significant risk to
the extent that it is technologically and economically feasible to do
so. See Section II, Pertinent Legal Authority, for a full discussion of
OSH Act legal requirements.
OSHA has conducted an extensive review of the literature on adverse
health effects associated with exposure to respirable crystalline
silica. OSHA has also developed estimates of the risk of silica-related
diseases, assuming exposure over a working lifetime, at the preceding
PELs as well as at the revised PEL and action level. Comments received
on OSHA's preliminary analysis, and the Agency's final findings, are
discussed in Section V, Health Effects, and Section VI, Final
Quantitative Risk Assessment and Significance of Risk. OSHA finds that
employees exposed to respirable crystalline silica at the preceding
PELs are at an increased risk of lung cancer mortality and silicosis
mortality and morbidity. Occupational exposures to respirable
crystalline silica also result in increased risk of death from other
nonmalignant respiratory diseases including chronic obstructive
pulmonary disease (COPD), and from kidney disease. OSHA further
concludes that exposure to respirable crystalline silica constitutes a
significant risk of material impairment to health and that the final
rule will substantially lower that risk. The Agency considers the level
of risk remaining at the new PEL to be significant. However, based on
the evidence evaluated during the rulemaking process, OSHA has
determined a PEL of 50 [mu]g/m\3\ is appropriate because it is the
lowest level feasible for all affected industries.
OSHA's examination of the technological and economic feasibility of
the rule is presented in the Final Economic Analysis and Final
Regulatory Flexibility Analysis (FEA), and is summarized in Section VII
of this preamble. OSHA concludes that the PEL of 50 [mu]g/m\3\ is
technologically feasible for most operations in all affected
industries, although it will be a technological challenge for several
affected sectors and will require the use of respirators for a limited
number of job categories and tasks.
OSHA developed quantitative estimates of the compliance costs of
the rule for each of the affected industry sectors. The estimated
compliance costs were compared with industry revenues and profits to
provide a screening analysis of the economic feasibility of complying
with the rule and an evaluation of the economic impacts. Industries
with unusually high costs as a percentage of revenues or profits were
further analyzed for possible economic feasibility issues. After
performing these analyses, OSHA finds that compliance with the
requirements of the rule is economically feasible in every affected
industry sector.
The final rule includes several major changes from the proposed
rule as a result of OSHA's analysis of comments and evidence received
during the comment periods and public hearings. The major changes are
summarized below and are fully discussed in Section XV, Summary and
Explanation of the Standards.
Scope. As proposed, the standards covered all occupational
exposures to respirable crystalline silica with the exception of
agricultural operations covered under 29 CFR part 1928. OSHA has made a
final determination to exclude exposures in general industry and
maritime where the employer has objective data demonstrating that
employee exposure to respirable crystalline silica will remain below 25
[mu]g/m\3\ as an 8-hour TWA under any foreseeable conditions. OSHA is
also excluding exposures in construction where employee exposure to
respirable crystalline silica will remain below 25 [mu]g/m\3\ as an 8-
hour TWA under any foreseeable conditions. In addition, OSHA is
excluding exposures that result from the processing of sorptive clays
from the scope of the rule. The standard for general industry and
maritime also allows employers to comply with the standard for
construction in certain circumstances.
Specified Exposure Control Methods. OSHA has revised the structure
of the standard for construction to emphasize the specified exposure
control methods for construction tasks that are presented in Table 1 of
the standard. Unlike in the proposed rule, employers who fully and
properly implement the controls listed on Table 1 are not separately
required to comply with the PEL, and are not subject to provisions for
exposure assessment and methods of compliance. The entries on Table 1
have also been revised extensively.
Protective Clothing. The proposed rule would have required use of
protective clothing in certain limited situations. The final rule does
not include requirements for use of protective clothing to address
exposure to respirable crystalline silica.
Housekeeping. The proposed rule would have prohibited use of
compressed air, dry sweeping, and dry brushing to clean clothing or
surfaces contaminated with crystalline silica where such activities
could contribute to employee exposure to respirable crystalline silica
that exceeds the PEL. The final rule allows for use of compressed air,
dry sweeping, and dry brushing in certain limited situations.
Written Exposure Control Plan. OSHA did not propose a requirement
for employers to develop a written exposure control plan. The final
rule includes a requirement for employers covered by the rule to
develop a written exposure control plan, and the standard for
construction includes a provision for a competent person (i.e., a
designated individual who is capable of identifying crystalline silica
hazards in the workplace and who possesses the authority to take
corrective measures to address them) to implement the written exposure
control plan.
Regulated Areas. OSHA proposed to provide employers covered by the
rule with the alternative of either establishing a regulated area or an
access control plan to limit access to areas where exposure to
respirable crystalline silica exceeds the PEL. The final standard for
general industry and maritime requires employers to establish a
regulated area in such circumstances. The final standard for
construction does not include a provision for regulated areas, but
includes a requirement that the written exposure control plan include
procedures used to restrict access to work areas, when necessary, to
minimize the numbers of employees exposed to respirable crystalline
silica and their level of exposure. The access control plan alternative
is not included in the final rule.
Medical Surveillance. The proposed rule would have required
employers to make medical surveillance available to employees exposed
to respirable crystalline silica above the PEL for 30 or more days per
year. The final standard for general industry and maritime requires
that medical surveillance be made available to employees exposed to
respirable crystalline silica at or above the action level of 25 [mu]g/
m\3\ as an 8-hour TWA for 30 or more days per year. The final standard
for construction requires that medical surveillance be made available
to employees who are required by the standard to use respirators for 30
or more days per year.
The rule requires the employer to obtain a written medical opinion
from physicians or other licensed health care professionals (PLHCPs)
for medical examinations provided under the rule but limits the information
provided to the employer to the date of the examination, a statement
that the examination has met the requirements of the standard, and any
recommended limitations on the employee's use of respirators. The
proposed rule would have required that such opinions contain additional
information, without requiring employee authorization, such as any
recommended limitations upon the employee's exposure to respirable
crystalline silica, and any referral to a specialist. In the final
rule, the written opinion provided to the employer will only include
recommended limitations on the employee's exposure to respirable
crystalline silica and referral to a specialist if the employee
provides written authorization. The final rule requires a separate
written medical report provided to the employee to include this
additional information, as well as detailed information related to the
employee's health.
Dates. OSHA proposed identical requirements for both standards: an
effective date 60 days after publication of the rule; a date for
compliance with all provisions except engineering controls and
laboratory requirements of 180 days after the effective date; a date
for compliance with engineering controls requirements, which was one
year after the effective date; and a date for compliance with
laboratory requirements of two years after the effective date.
OSHA has revised the proposed compliance dates in both standards.
The final rule is effective 90 days after publication. For general
industry and maritime, all obligations for compliance commence two
years after the effective date, with two exceptions: The obligation for
engineering controls commences five years after the effective date for
hydraulic fracturing operations in the oil and gas industry; and the
obligation for employers in general industry and maritime to offer
medical surveillance commences two years after the effective date for
employees exposed above the PEL, and four years after the effective
date for employees exposed at or above the action level. For
construction, all obligations for compliance commence one year after
the effective date, with the exception that certain requirements for
laboratory analysis commence two years after the effective date.
Under the OSH Act's legal standard directing OSHA to set health
standards based on findings of significant risk of material impairment
and technological and economic feasibility, OSHA does not use cost-
benefit analysis to determine the PEL or other aspects of the rule. It
does, however, determine and analyze costs and benefits for its own
informational purposes and to meet certain Executive Order
requirements, as discussed in Section VII. Summary of the Final
Economic Analysis and Final Regulatory Flexibility Analysis and in the
FEA. Table I-1--which is derived from material presented in Section VII
of this preamble--provides a summary of OSHA's best estimate of the
costs and benefits of the rule using a discount rate of 3 percent. As
shown, the rule is estimated to prevent 642 fatalities and 918
moderate-to-severe silicosis cases annually once it is fully effective,
and the estimated cost of the rule is $1,030 million annually. Also as
shown in Table I-1, the discounted monetized benefits of the rule are
estimated to be $8.7 billion annually, and the rule is estimated to
generate net benefits of approximately $7.7 billion annually.
II. Pertinent Legal Authority
The purpose of the Occupational Safety and Health Act (29 U.S.C.
651 et seq.) ("the Act" or "the OSH Act"), is "to assure so far as
possible every working man and woman in the Nation safe and healthful
working conditions and to preserve our human resources" (29 U.S.C.
651(b)). To achieve this goal Congress authorized the Secretary of
Labor ("the Secretary") "to set mandatory occupational safety and
health standards applicable to businesses affecting interstate
commerce" (29 U.S.C. 651(b)(3); see 29 U.S.C. 654(a) (requiring
employers to comply with OSHA standards), 655(a) (authorizing summary
adoption of existing consensus and federal standards within two years
of the Act's enactment), and 655(b) (authorizing promulgation,
modification or revocation of standards pursuant to notice and
comment)). The primary statutory provision relied upon by the Agency in
promulgating health standards is section 6(b)(5) of the Act; other
sections of the OSH Act, however, authorize the Occupational Safety and
Health Administration (OSHA) to require labeling and other appropriate
forms of warning, exposure assessment, medical examinations, and
recordkeeping in its standards (29 U.S.C. 655(b)(5), 655(b)(7),
657(c)).
The Act provides that in promulgating standards dealing with toxic
materials or harmful physical agents, such as respirable crystalline
silica, the Secretary shall set the standard which "most adequately
assures, to the extent feasible, on the basis of the best available
evidence, that no employee will suffer material impairment of health .
. . 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.
655(b)(5)). Thus, "[w]hen Congress passed the Occupational Safety and
Health Act in 1970, it chose to place pre-eminent value on assuring
employees a safe and healthful working environment, limited only by the
feasibility of achieving such an environment" (American Textile Mfrs.
Institute, Inc. v. Donovan, 452 US 490, 541 (1981) ("Cotton Dust")).
OSHA proposed this new standard for respirable crystalline silica
and conducted its rulemaking pursuant to section 6(b)(5) of the Act
((29 U.S.C. 655(b)(5)). The preceding silica standard, however,
was adopted under the Secretary's authority in section 6(a) of the
OSH Act (29 U.S.C. 655(a)), to adopt national consensus
and established Federal standards within two years of the
Act's enactment (see 29 CFR 1910.1000 Table Z-1). Any rule that
"differs substantially from an existing national consensus standard"
must "better effectuate the purposes of this Act than the national
consensus standard" (29 U.S.C. 655(b)(8)). Several additional legal
requirements arise from the statutory language in sections 3(8) and
6(b)(5) of the Act (29 U.S.C. 652(8), 655(b)(5)). The remainder of this
section discusses these requirements, which OSHA must consider and meet
before it may promulgate this occupational health standard regulating
exposure to respirable crystalline silica.
Material Impairment of Health
Subject to the limitations discussed below, when setting standards
regulating exposure to toxic materials or harmful physical agents, the
Secretary is required to set health standards that ensure that "no
employee will suffer material impairment of health or functional
capacity..." (29 U.S.C. 655(b)(5)). OSHA has, under this section,
considered medical conditions such as irritation of the skin, eyes, and
respiratory system, asthma, and cancer to be material impairments of
health. What constitutes material impairment in any given case is a
policy determination on which OSHA is given substantial leeway. "OSHA
is not required to state with scientific certainty or precision the
exact point at which each type of [harm] becomes a material
impairment" (AFL-CIO v. OSHA, 965 F.2d 962, 975 (11th Cir. 1992)).
Courts have also noted that OSHA should consider all forms and degrees
of material impairment--not just death or serious physical harm (AFL-
CIO, 965 F.2d at 975). Thus the Agency has taken the position that
"subclinical" health effects, which may be precursors to more serious
disease, can be material impairments of health that OSHA should address
when feasible (43 FR 52952, 52954 (11/14/78) (Preamble to the Lead
Standard)).
Significant Risk
Section 3(8) of the Act requires that workplace safety and health
standards be "reasonably necessary or appropriate to provide safe or
healthful employment" (29 U.S.C. 652(8)). The Supreme Court, in its
decision on OSHA's benzene standard, interpreted section 3(8) to mean
that "before promulgating any standard, the Secretary must make a
finding that the workplaces in question are not safe" (Indus. Union
Dep't, AFL-CIO v. Am. Petroleum Inst., 448 U.S. 607, 642 (1980)
(plurality opinion) ("Benzene")). The Court further described OSHA's
obligation as requiring it to evaluate "whether significant risks are
present and can be eliminated or lessened by a change in practices"
(Benzene, 448 U.S. at 642). The Court's holding is consistent with
evidence in the legislative record, with regard to section 6(b)(5) of
the Act (29 U.S.C. 655(b)(5)), that Congress intended the Agency to
regulate unacceptably severe occupational hazards, and not "to
establish a utopia free from any hazards" or to address risks
comparable to those that exist in virtually any occupation or workplace
(116 Cong. Rec. 37614 (1970), Leg. Hist. 480-82). It is also consistent
with Section 6(g) of the OSH Act, which states that, in determining
regulatory priorities, "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" (29 U.S.C. 655(g)).
The Supreme Court in Benzene clarified that OSHA has considerable
latitude in defining significant risk and in determining the
significance of any particular risk. The Court did not specify a means
to distinguish significant from insignificant risks, but rather
instructed OSHA to develop a reasonable approach to making its
significant risk determination. The Court stated that "[i]t is the
Agency's responsibility to determine, in the first instance, what it
considers to be a `significant' risk" (Benzene, 448 U.S. at 655), and
it did not "express any opinion on the... difficult question of
what factual determinations would warrant a conclusion that significant
risks are present which make promulgation of a new standard reasonably
necessary or appropriate" (Benzene, 448 U.S. at 659). The Court
stated, however, that the section 6(f) (29 U.S.C. 655(b)(f))
substantial evidence standard applicable to OSHA's significant risk
determination does not require the Agency "to support its finding that
a significant risk exists with anything approaching scientific
certainty" (Benzene, 448 U.S. at 656). Rather, OSHA may rely on "a
body of reputable scientific thought" to which "conservative
assumptions in interpreting the data..." may be applied, "risking
error on the side of overprotection" (Benzene, 448 U.S. at 656; see
also United Steelworkers of Am., AFL-CIO-CLC v. Marshall, 647 F.2d
1189, 1248 (D.C. Cir. 1980) ("Lead I") (noting the Benzene Court's
application of this principle to carcinogens and applying it to the
lead standard, which was not based on carcinogenic effects)). OSHA may
thus act with a "pronounced bias towards worker safety" in making its
risk determinations (Bldg & Constr. Trades Dep't v. Brock, 838 F.2d
1258, 1266 (D.C. Cir. 1988) ("Asbestos II").
The Supreme Court further recognized that what constitutes
"significant risk" is "not a mathematical straitjacket" (Benzene,
448 U.S. at 655) and will be "based largely on policy considerations"
(Benzene, 448 U.S. at 655 n.62). The Court gave the following example:
If...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% benzene will be fatal, a reasonable person might well
consider the risk significant...(Benzene, 448 U.S. at 655).
Following Benzene, OSHA has, in many of its health standards,
considered the one-in-a-thousand metric when determining whether a
significant risk exists. Moreover, as "a prerequisite to more
stringent regulation" in all subsequent health standards, OSHA has,
consistent with the Benzene plurality decision, based each standard on
a finding of significant risk at the "then prevailing standard" of
exposure to the relevant hazardous substance (Asbestos II, 838 F.2d at
1263). Once a significant risk of material impairment of health is
demonstrated, it is of no import that the incidence of the illness may
be declining (see Nat'l Min. Assoc. v. Sec'y, U.S. Dep't of Labor, Nos.
14-11942, 14-12163, slip op. at 80 (11th Cir. Jan. 25, 2016)
(interpreting the Mine Act, 30 U.S.C. 811(a)(6)(A), which contains the
same language as section 6(b)(5) of the OSH Act requiring the Secretary
to set standards that assure no employee will suffer material
impairment of health)).
The Agency's final risk assessment is derived from existing
scientific and enforcement data and its final conclusions are made only
after considering all evidence in the rulemaking record. Courts
reviewing the validity of these standards have uniformly held the
Secretary to the significant risk standard first articulated by the
Benzene plurality and have generally upheld the Secretary's significant
risk determinations as supported by substantial evidence and "a
reasoned explanation for his policy assumptions and conclusions"
(Asbestos II, 838 F.2d at 1266).
Once OSHA makes its significant risk finding, the "more stringent
regulation" (Asbestos II, 838 F.2d at 1263) it promulgates must be
"reasonably necessary or appropriate" to reduce or eliminate that
risk, within the meaning of section 3(8) of the Act (29 U.S.C. 652(8))
and Benzene (448 U.S. at 642) (see Asbestos II, 838 F.2d at 1269). The
courts have interpreted section 6(b)(5) of the OSH Act as requiring
OSHA to set the standard that eliminates or reduces risk to the lowest
feasible level; as discussed below, the limits of technological and
economic feasibility usually determine where the new standard is set
(see UAW v. Pendergrass, 878 F.2d 389, 390 (D.C. Cir. 1989)). In
choosing among regulatory alternatives, however, "[t]he determination
that [one standard] is appropriate, as opposed to a marginally [more or
less protective] standard, is a technical decision entrusted to the
expertise of the agency..." (Nat'l Mining Ass'n v. Mine Safety and
Health Admin., 116 F.3d 520, 528 (D.C. Cir. 1997)) (analyzing a Mine
Safety and Health Administration ("MSHA") standard under the Benzene
significant risk standard). In making its choice, OSHA may incorporate
a margin of safety even if it theoretically regulates below the lower
limit of significant risk (Nat'l Mining Ass'n, 116 F.3d at 528 (citing
American Petroleum Inst. v. Costle, 665 F.2d 1176, 1186 (D.C. Cir.
1982))).
Working Life Assumption
The OSH Act requires OSHA to set the standard that most adequately
protects employees against harmful workplace exposures for the period
of their "working life" (29 U.S.C. 655(b)(5)). OSHA's longstanding
policy is to define "working life" as constituting 45 years; thus, it
assumes 45 years of exposure when evaluating the risk of material
impairment to health caused by a toxic or hazardous substance. This
policy is not based on empirical data that most employees are exposed
to a particular hazard for 45 years. Instead, OSHA has adopted the
practice to be consistent with the statutory directive that "no
employee" suffer material impairment of health "even if" such
employee is exposed to the hazard for the period of his or her working
life (see 74 FR 44796 (8/31/09)). OSHA's policy was given judicial
approval in a challenge to an OSHA standard that lowered the
permissible exposure limit (PEL) for asbestos (Asbestos II, 838 F.2d at
1264-1265). In that case, the petitioners claimed that the median
duration of employment in the affected industry sectors was only five
years. Therefore, according to petitioners, OSHA erred in assuming a
45-year working life in calculating the risk of health effects caused
by asbestos exposure. The D.C. Circuit disagreed, stating,
Even if it is only the rare worker who stays with asbestos-
related tasks for 45 years, that worker would face a 64/1000 excess
risk of contracting cancer; Congress clearly authorized OSHA to
protect such a worker (Asbestos II, 838 F.2d at 1264-1265).
OSHA might calculate the health risks of exposure, and the related
benefits of lowering the exposure limit, based on an assumption of a
shorter working life, such as 25 years, but such estimates are for
informational purposes only.
Best Available Evidence
Section 6(b)(5) of the Act requires OSHA to set standards "on the
basis of the best available evidence" and to consider the "latest
available scientific data in the field" (29 U.S.C. 655(b)(5)). As
noted above, the Supreme Court, in its Benzene decision, explained that
OSHA must look to "a body of reputable scientific thought" in making
its material harm and significant risk determinations, while noting
that a reviewing court must "give OSHA some leeway where its findings
must be made on the frontiers of scientific knowledge" (Benzene, 448
U.S. at 656). The courts of appeals have afforded OSHA similar latitude
to issue health standards in the face of scientific uncertainty. The
Second Circuit, in upholding the vinyl chloride standard, stated:
...the ultimate facts here in dispute are `on the frontiers
of scientific knowledge', and, though the factual finger points, it
does not conclude. Under the command of OSHA, it remains the duty of
the Secretary to act to protect the workingman, and to act even in
circumstances where existing methodology or research is deficient
(Society of the Plastics Industry, Inc. v. OSHA, 509 F.2d 1301, 1308
(2d Cir. 1975) (quoting Indus. Union Dep't, AFL-CIO v. Hodgson, 499
F.2d 467, 474 (D.C. Cir. 1974) ("Asbestos I"))).
The D.C. Circuit, in upholding the cotton dust standard, stated:
"OSHA's mandate necessarily requires it to act even if information is
incomplete when the best available evidence indicates a serious threat
to the health of workers" (Am. Fed'n of Labor & Cong. of Indus. Orgs.
v. Marshall, 617 F.2d 636, 651 (D.C. Cir. 1979), aff'd in part and
vacated in part on other grounds, American Textile Mfrs. Inst., Inc. v.
Donovan, 452 U.S. 490 (1981)).
When there is disputed scientific evidence, OSHA must review the
evidence on both sides and "reasonably resolve" the dispute (Pub.
Citizen Health Research Grp. v. Tyson, 796 F.2d 1479, 1500 (D.C. Cir.
1986)). In Public Citizen, there was disputed scientific evidence
regarding whether there was a threshold exposure level for the health
effects of ethylene oxide. The Court noted that, where "OSHA has the
expertise we lack and it has exercised that expertise by carefully
reviewing the scientific data," a dispute within the scientific
community is not occasion for it to take sides about which view is
correct (Pub. Citizen Health Research Grp., 796 F.2d at 1500).
"Indeed, Congress did `not [intend] that the Secretary be paralyzed by
debate surrounding diverse medical opinions' " (Pub. Citizen Health
Research Grp., 796 F.2d at 1497 (quoting H.R.Rep. No. 91-1291, 91st
Cong., 2d Sess. 18 (1970), reprinted in Legislative History of the
Occupational Safety and Health Act of 1970 at 848 (1971))).
A recent decision by the Eleventh Circuit Court of Appeals
upholding a coal dust standard promulgated by MSHA emphasized that
courts should give "an extreme degree of deference to the agency when
it is evaluating scientific data within its technical expertise"
(Nat'l Min. Assoc. v. Sec'y, U.S. Dep't of Labor, Nos. 14-11942, 14-
12163, slip op. at 43 (11th Cir. Jan. 25, 2016) (quoting Kennecott
Greens Creek Min. Co. v. MSHA, 476 F.3d 946, 954-955 (D.C. Cir. 2007)
(internal quotation marks omitted)). The Court emphasized that because
the Mine Act, like the OSH Act, "evinces a clear bias in favor of [ ]
health and safety," the agency's responsibility to use the best
evidence and consider feasibility should not be used as a counterweight
to the agency's duty to protect the lives and health of workers (Nat'l
Min. Assoc., Nos. 14-11942, 14-12163, slip op. at 43 (11th Cir. Jan.
25, 2016)).
Feasibility
The OSH Act requires that, in setting a standard, OSHA must
eliminate the risk of material health impairment "to the extent
feasible" (29 U.S.C. 655(b)(5)). The statutory mandate to consider the
feasibility of the standard encompasses both technological and economic
feasibility; these analyses have been done primarily on an industry-by-
industry basis (Lead I, 647 F.2d at 1264, 1301) in general industry.
The Agency has also used application groups, defined by common tasks,
as the structure for its feasibility analyses in construction (Pub.
Citizen Health Research Grp. v. OSHA, 557 F.3d 165, 177-179 (3d Cir.
2009) ("Chromium (VI)"). The Supreme Court has broadly defined
feasible as "capable of being done" (Cotton Dust, 452 U.S. at 509-510).
Although OSHA must set the most protective PEL that the Agency
finds to be technologically and economically feasible, it retains
discretion to set a uniform PEL even when the evidence demonstrates
that certain industries or operations could reasonably be expected to
meet a lower PEL. OSHA health standards generally set a single PEL for
all affected employers; OSHA exercised this discretion most recently in
its final rule on occupational exposure to chromium (VI) (71 FR 10100,
10337-10338 (2/28/2006); see also 62 FR 1494, 1575 (1/10/97) (methylene
chloride)). In its decision upholding the chromium (VI) standard,
including the uniform PEL, the Court of Appeals for the Third Circuit
addressed this issue as one of deference, stating "OSHA's decision to
select a uniform exposure limit is a legislative policy decision that
we will uphold as long as it was reasonably drawn from the record"
(Chromium (VI), 557 F.3d at 183 (3d Cir. 2009)); see also Am. Iron &
Steel Inst. v. OSHA, 577 F.2d 825, 833 (3d Cir. 1978)). OSHA's reasons
for choosing one chromium (VI) PEL, rather than imposing different PELs
on different application groups or industries, included: Multiple PELs
would create enforcement and compliance problems because many
workplaces, and even workers, were affected by multiple categories of
chromium (VI) exposure; discerning individual PELs for different groups
of establishments would impose a huge evidentiary burden on the Agency
and unnecessarily delay implementation of the standard; and a uniform
PEL would, by eliminating confusion and simplifying compliance, enhance
worker protection (Chromium (VI), 557 F.3d at 173, 183-184). The Court
held that OSHA's rationale for choosing a uniform PEL, despite evidence
that some application groups or industries could meet a lower PEL, was
reasonably drawn from the record and that the Agency's decision was
within its discretion and supported by past practice (Chromium (VI),
557 F.3d at 183-184).
Technological Feasibility
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 (Lead I, 647 F.2d at 1272; Amer. Iron & Steel
Inst. v. OSHA, 939 F.2d 975, 980 (D.C. Cir. 1991) ("Lead II")). While
the test for technological feasibility is normally articulated in terms
of the ability of employers to decrease exposures to the PEL,
provisions such as exposure measurement requirements must also be
technologically feasible (Forging Indus. Ass'n v. Sec'y of Labor, 773
F.2d 1436, 1453 (4th Cir. 1985)).
OSHA's standards may be "technology forcing," i.e., where the
Agency gives an industry a reasonable amount of time to develop new
technologies, OSHA is not bound by the "technological status quo"
(Lead I, 647 F.2d at 1264); see also Kennecott Greens Creek Min. Co. v.
MSHA, 476 F.3d 946, 957 (D.C. Cir. 2007) (MSHA standards, like OSHA
standards, may be technology-forcing); Nat'l Petrochemical & Refiners
Ass'n v. EPA, 287 F.3d 1130, 1136 (D.C. Cir. 2002) (agency is "not
obliged to provide detailed solutions to every engineering problem,"
but only to "identify the major steps for improvement and give
plausible reasons for its belief that the industry will be able to
solve those problems in the time remaining.").
In its Lead decisions, the D.C. Circuit described OSHA's obligation
to demonstrate the technological feasibility of reducing occupational
exposure to a hazardous substance.
[W]ithin the limits of the best available evidence...OSHA
must prove a reasonable possibility that the typical firm will be
able to develop and install engineering and work practice controls
that can meet the PEL in most of its operations...The effect of
such proof is to establish a presumption that industry can meet the
PEL without relying on respirators...Insufficient proof of
technological feasibility for a few isolated operations within an
industry, or even OSHA's concession that respirators will be
necessary in a few such operations, will not undermine this general
presumption in favor of feasibility. Rather, in such operations
firms will remain responsible for installing engineering and work
practice controls to the extent feasible, and for using them to
reduce...exposure as far as these controls can do so (Lead I,
647 F.2d at 1272).
Additionally, the D.C. Circuit explained that "[f]easibility of
compliance turns on whether exposure levels at or below [the PEL] can
be met in most operations most of the time..." (Lead II, 939 F.2d
at 990).
Courts have given OSHA significant deference in reviewing its
technological feasibility findings.
So long as we require OSHA to show that any required means of
compliance, even if it carries no guarantee of meeting the PEL, will
substantially lower...exposure, we can uphold OSHA's
determination that every firm must exploit all possible means to
meet the standard (Lead I, 647 F.2d at 1273).
Even in the face of significant uncertainty about technological
feasibility in a given industry, OSHA has been granted broad discretion
in making its findings (Lead I, 647 F.2d at 1285).
OSHA cannot let workers suffer while it awaits...scientific
certainty. It can and must make reasonable [technological
feasibility] predictions on the basis of `credible sources of
information,' whether data from existing plants or expert testimony
(Lead I, 647 F.2d at 1266 (quoting Am. Fed'n of Labor & Cong. of
Indus. Orgs., 617 F.2d at 658)).
For example, in Lead I, the D.C. Circuit allowed OSHA to use, as
best available evidence, information about new and expensive industrial
smelting processes that had not yet been adopted in the U.S. and would
require the rebuilding of plants (Lead I, 647 F.2d at 1283-1284). Even
under circumstances where OSHA's feasibility findings were less certain
and the Agency was relying on its "legitimate policy of technology
forcing," the D.C. Circuit approved of OSHA's feasibility findings
when the Agency granted lengthy phase-in periods to allow particular
industries time to comply (Lead I, 647 F.2d at 1279-1281, 1285).
OSHA is permitted to adopt a standard that some employers will not
be able to meet some of the time, with employers limited to challenging
feasibility at the enforcement stage (Lead I, 647 F.2d at 1273 & n.
125; Asbestos II, 838 F.2d at 1268). Even when the Agency recognized
that it might have to balance its general feasibility findings with
flexible enforcement of the standard in individual cases, the courts of
appeals have generally upheld OSHA's technological feasibility findings
(Lead II, 939 F.2d at 980; see Lead I, 647 F.2d at 1266-1273; Asbestos
II, 838 F.2d at 1268). Flexible enforcement policies have been approved
where there is variability in measurement of the regulated hazardous
substance or where exposures can fluctuate uncontrollably (Asbestos II,
838 F.2d at 1267-1268; Lead II, 939 F.2d at 991). A common means of
dealing with the measurement variability inherent in sampling and
analysis is for the Agency to add the standard sampling error to its
exposure measurements before determining whether to issue a citation
(e.g., 51 FR 22612, 22654 (06/20/86) (Preamble to the Asbestos
Standard)).
Economic Feasibility
In addition to technological feasibility, OSHA is required to
demonstrate that its standards are economically feasible. A reviewing
court will examine the cost of compliance with an OSHA standard "in
relation to the financial health and profitability of the industry
and the likely effect of such costs on unit consumer prices..."
(Lead I, 647 F.2d at 1265 (omitting citation)). As articulated by
the D.C. Circuit in Lead I,
OSHA must construct a reasonable estimate of compliance costs
and demonstrate a reasonable likelihood that these costs will not
threaten the existence or competitive structure of an industry, even
if it does portend disaster for some marginal firms (Lead I, 647
F.2d at 1272).
A reasonable estimate entails assessing "the likely range of costs
and the likely effects of those costs on the industry" (Lead I, 647
F.2d at 1266). As with OSHA's consideration of scientific data and
control technology, however, the estimates need not be precise (Cotton
Dust, 452 U.S. at 528-29 & n.54) as long as they are adequately
explained. Thus, as the D.C. Circuit further explained:
Standards may be economically feasible even though, from the
standpoint of employers, they are financially burdensome and affect
profit margins adversely. Nor does the concept of economic
feasibility necessarily guarantee the continued existence of
individual employers. It would appear to be consistent with the
purposes of the Act to envisage the economic demise of an employer
who has lagged behind the rest of the industry in protecting the
health and safety of employees and is consequently financially
unable to comply with new standards as quickly as other employers.
As the effect becomes more widespread within an industry, the
problem of economic feasibility becomes more pressing (Asbestos I,
499 F.2d. at 478).
OSHA standards therefore satisfy the economic feasibility criterion
even if they impose significant costs on regulated industries so long
as they do not cause massive economic dislocations within a particular
industry or imperil the very existence of the industry (Lead II, 939
F.2d at 980; Lead I, 647 F.2d at 1272; Asbestos I, 499 F.2d. at 478).
As with its other legal findings, OSHA "is not required to prove
economic feasibility with certainty, but is required to use the best
available evidence and to support its conclusions with substantial
evidence" (Lead II, 939 F.2d at 980-981) (citing Lead I, 647 F.2d at
1267)). Granting industries additional time to comply with new PELs may
enhance the economic, as well as technological, feasibility of a
standard (Lead I, 647 F.2d at 1265).
Because section 6(b)(5) of the Act explicitly imposes the "to the
extent feasible" limitation on the setting of health standards, OSHA
is not permitted to use cost-benefit analysis to make its standards-
setting decisions (29 U.S.C. 655(b)(5)).
Congress itself defined the basic relationship between costs and
benefits, by placing the "benefit" of worker health above all
other considerations save those making attainment of this
"benefit" unachievable. Any standard based on a balancing of costs
and benefits by the Secretary that strikes a different balance than
that struck by Congress would be inconsistent with the command set
forth in Sec. 6(b)(5) (Cotton Dust, 452 U.S. at 509).
Thus, while OSHA estimates the costs and benefits of its proposed
and final rules, these calculations do not form the basis for the
Agency's regulatory decisions; rather, they are performed in
acknowledgement of requirements such as those in Executive Orders 12866
and 13563.
Structure of OSHA Health Standards
OSHA's health standards traditionally incorporate a comprehensive
approach to reducing occupational disease. OSHA substance-specific
health standards generally include the "hierarchy of controls,"
which, as a matter of OSHA's preferred policy, mandates that employers
install and implement all feasible engineering and work practice
controls before respirators may be used. The Agency's adherence to the
hierarchy of controls has been upheld by the courts (ASARCO, Inc. v.
OSHA, 746 F.2d 483, 496-498 (9th Cir. 1984); Am. Iron & Steel Inst. v.
OSHA, 182 F.3d 1261, 1271 (11th Cir. 1999)). In fact, courts view the
legal standard for proving technological feasibility as incorporating
the hierarchy:
OSHA must prove a reasonable possibility that the typical firm
will be able to develop and install engineering and work practice
controls that can meet the PEL in most of its operations....The
effect of such proof is to establish a presumption that industry can
meet the PEL without relying on respirators (Lead I, 647 F.2d at
1272).
The hierarchy of controls focuses on removing harmful materials at
their source. OSHA allows employers to rely on respiratory protection
to protect their employees only when engineering and work practice
controls are insufficient or infeasible. In fact, in the control of
"those occupational diseases caused by breathing air contaminated with
harmful dusts, fogs, fumes, mists, gases, smokes, sprays, or vapors,"
the employers' primary objective "shall be to prevent atmospheric
contamination. This shall be accomplished as far as feasible by
accepted engineering control measures (for example, enclosure or
confinement of the operation, general and local ventilation, and
substitution of less toxic materials). When effective engineering
controls are not feasible, or while they are being instituted,
appropriate respirators shall be used pursuant to this section" (29
CFR 1910.134).
The reasons supporting OSHA's continued reliance on the hierarchy
of controls, as well as its reasons for limiting the use of
respirators, are numerous and grounded in good industrial hygiene
principles (see Section XV, Summary and Explanation of the Standards,
Methods of Compliance). Courts have upheld OSHA's emphasis on
engineering and work practice controls over personal protective
equipment in challenges to previous health standards, such as chromium
(VI): "Nothing in...any case reviewing an airborne toxin standard,
can be read to support a technological feasibility rule that would
effectively encourage the routine and widespread use of respirators to
comply with a PEL" (Chromium (VI), 557 F.3d at 179; see Am. Fed'n of
Labor & Cong. of Indus. Orgs. v. Marshall, 617 F.2d 636, 653 (D.C. Cir.
1979) cert. granted, judgment vacated sub nom. Cotton Warehouse Ass'n
v. Marshall, 449 U.S. 809 (1980) and aff'd in part, vacated in part sub
nom. Am. Textile Mfrs. Inst., Inc. v. Donovan, 452 U.S. 490 (1981)
(finding "uncontradicted testimony in the record that respirators can
cause severe physical discomfort and create safety problems of their
own")).
In health standards such as this one, the hierarchy of controls is
augmented by ancillary provisions. These provisions work with the
hierarchy of controls and personal protective equipment requirements to
provide comprehensive protection to employees in affected workplaces.
Such provisions typically include exposure assessment, medical
surveillance, hazard communication, and recordkeeping. This approach is
recognized as effective in dealing with air contaminants such as
respirable crystalline silica; for example, the industry standards for
respirable crystalline silica, ASTM E 1132-06, Standard Practice for
Health Requirements Relating to Occupational Exposure to Respirable
Crystalline Silica, and ASTM E 2626-09, Standard Practice for
Controlling Occupational Exposure to Respirable Crystalline Silica for
Construction and Demolition Activities, take a similar comprehensive
approach (Document ID 1466; 1504).
The OSH Act compels OSHA to require all feasible measures for
reducing significant health risks (29 U.S.C. 655(b)(5); Pub. Citizen
Health Research Grp., 796 F.2d at 1505 ("if in fact a STEL [short-term
exposure limit] would further reduce a significant health risk and is
feasible to implement, then the OSH Act compels the agency to adopt it
(barring alternative avenues to the same result)"). When there is
significant risk below the PEL, as is the case with respirable
crystalline silica, the DC Circuit indicated that OSHA should
use its regulatory authority to impose additional requirements
on employers when those requirements will result in a greater than de
minimis incremental benefit to workers' health (Asbestos II, 838 F.2d
at 1274). The Supreme Court alluded to a similar issue in Benzene,
pointing out that "in setting a permissible exposure level in reliance
on less-than-perfect methods, OSHA would have the benefit of a backstop
in the form of monitoring and medical testing" (Benzene, 448 U.S. at
657). OSHA believes that the ancillary provisions in this final
standard provide significant benefits to worker health by providing
additional layers and types of protection to employees exposed to
respirable crystalline silica.
Finally, while OSHA is bound by evidence in the rulemaking record,
and generally looks to its prior standards for guidance on how to
structure and specify requirements in a new standard, it is not limited
to past approaches to regulation. In promulgating health standards,
"[w]henever practicable, the standard promulgated shall be expressed
in terms of objective criteria and of the performance desired" (29
U.S.C. 655(b)(5)). In cases of industries or tasks presenting unique
challenges in terms of assessing and controlling exposures, it may be
more practicable and provide greater certainty to require specific
controls with a demonstrated track record of efficacy in reducing
exposures and, therefore, risk (especially when supplemented by
appropriate respirator usage). Such an approach could more effectively
protect workers than the traditional exposure assessment-and-control
approach when exposures may vary because of factors such as changing
environmental conditions or materials, and an assessment may not
reflect typical exposures associated with a task or operation. As
discussed at length in Section XV, Summary and Explanation of the
Standards, the specified exposure control measures option in the
construction standard (i.e., Table 1, in paragraph (c)(1)) for
respirable crystalline silica represents the type of innovative,
objective approach available to the Secretary when fashioning a rule
under these circumstances.
III. Events Leading to the Final Standards
The Occupational Safety and Health Administration's (OSHA's)
previous standards for workplace exposure to respirable crystalline
silica were adopted in 1971, pursuant to section 6(a) of the
Occupational Safety and Health Act (29 U.S.C. 651 et seq.) ("the Act"
or "the OSH Act") (36 FR 10466 (5/29/71)). Section 6(a) (29 U.S.C.
655(a)) authorized OSHA, in the first two years after the effective
date of the Act, to promulgate "start-up" standards, on an expedited
basis and without public hearing or comment, based on national
consensus or established Federal standards that improved employee
safety or health. Pursuant to that authority, OSHA in 1971 promulgated
approximately 425 permissible exposure limits (PELs) for air
contaminants, including crystalline silica, which were derived
principally from Federal standards applicable to government contractors
under the Walsh-Healey Public Contracts Act, 41 U.S.C. 35, and the
Contract Work Hours and Safety Standards Act (commonly known as the
Construction Safety Act), 40 U.S.C. 333. The Walsh-Healey Act and
Construction Safety Act standards had been adopted primarily from
recommendations of the American Conference of Governmental Industrial
Hygienists (ACGIH).
For general industry (see 29 CFR 1910.1000, Table Z-3), the PEL for
crystalline silica in the form of respirable quartz was based on two
alternative formulas: (1) A particle-count formula,
PELmppcf=250/(% quartz + 5) as respirable dust; and (2) a
mass formula proposed by ACGIH in 1968, PEL=(10 mg/m3)/(%
quartz + 2) as respirable dust. The general industry PELs for
crystalline silica in the form of cristobalite and tridymite were one-
half of the value calculated from either of the above two formulas for
quartz. For construction (see 29 CFR 1926.55, Appendix A) and shipyards
(see 29 CFR 1915.1000, Table Z), the formula for the PEL for
crystalline silica in the form of quartz (PELmppcf=250/(%
quartz + 5) as respirable dust), which requires particle counting, was
derived from the 1970 ACGIH threshold limit value (TLV).\1\ Based on
the formulas, the PELs for quartz, expressed as time-weighted averages
(TWAs), were approximately equivalent to 100 [mu]g/m3 for
general industry and 250 [mu]g/m3 for construction and
shipyards. The PELs were not supplemented by additional protective
provisions--such as medical surveillance requirements--as are included
in other OSHA standards. OSHA believes that the formula based on
particle-counting technology used in the general industry,
construction, and shipyard PELs has been rendered obsolete by
respirable mass (gravimetric) sampling.
---------------------------------------------------------------------------
\1\ The Mineral Dusts tables that contain the silica PELs for
construction and shipyards do not clearly express PELs for
cristobalite and tridymite. 29 CFR 1926.55; 29 CFR 1915.1000. This
lack of textual clarity likely results from a transcription error in
the Code of Federal Regulations. OSHA's final rule provides the same
PEL for quartz, cristobalite, and tridymite in general industry,
maritime, and construction.
---------------------------------------------------------------------------
In 1974, the National Institute for Occupational Safety and Health
(NIOSH), an agency within the Department of Health and Human Services
created by the OSH Act and designed to carry out research and recommend
standards for occupational safety and health hazards, evaluated
crystalline silica as a workplace hazard and issued criteria for a
recommended standard (29 U.S.C. 669, 671; Document ID 0388). NIOSH
recommended that occupational exposure to crystalline silica be
controlled so that no worker is exposed to a TWA of free (respirable
crystalline) silica greater than 50 [mu]g/m3 as determined
by a full-shift sample for up to a 10-hour workday over a 40-hour
workweek. The document also recommended a number of ancillary
provisions for a standard, such as exposure monitoring and medical
surveillance.
In December 1974, OSHA published an Advance Notice of Proposed
Rulemaking (ANPRM) based on the recommendations in the NIOSH criteria
document (39 FR 44771 (12/27/74)). In the ANPRM, OSHA solicited
"public participation on the issues of whether a new standard for
crystalline silica should be issued on the basis of the [NIOSH]
criteria or any other information, and, if so, what should be the
contents of a proposed standard for crystalline silica" (39 FR at
44771). OSHA also set forth the particular issues of concern on which
comments were requested. The Agency did not issue a proposed rule or
pursue a final rule for crystalline silica at that time.
As information on the health effects of silica exposure developed
during the 1980s and 1990s, national and international classification
organizations came to recognize crystalline silica as a human
carcinogen. In June 1986, the International Agency for Research on
Cancer (IARC), which is the specialized cancer agency within the World
Health Organization, evaluated the available evidence regarding
crystalline silica carcinogenicity and concluded, in 1987, that
crystalline silica is probably carcinogenic to humans
(http://monographs.iarc.fr/ENG/Monographs/suppl7/Suppl7.pdf). An
IARC working group met again in October 1996 to evaluate the complete
body of research, including research that had been conducted since the
initial 1986 evaluation. IARC concluded, more decisively this time,
that "crystalline silica inhaled in the form of quartz or cristobalite
from occupational sources is carcinogenic to humans" (Document ID
2258, Attachment 8, p. 211). In 2012, IARC reaffirmed that
"Crystalline silica in the form of quartz or cristobalite dust is
carcinogenic to humans" (Document ID 1473, p. 396).
In 1991, in the Sixth Annual Report on Carcinogens, the U.S.
National Toxicology Program (NTP), within the U.S. Department of Health
and Human Services, concluded that respirable crystalline silica was
"reasonably anticipated to be a human carcinogen" (as referenced in
Document ID 1417, p. 1). NTP reevaluated the available evidence and
concluded, in the Ninth Report on Carcinogens, that "respirable
crystalline silica (RCS), primarily quartz dust occurring in industrial
and occupational settings, is known to be a human carcinogen, based on
sufficient evidence of carcinogenicity from studies in humans
indicating a causal relationship between exposure to RCS and increased
lung cancer rates in workers exposed to crystalline silica dust"
(Document ID 1417, p. 1). ACGIH listed respirable crystalline silica
(in the form of quartz) as a suspected human carcinogen in 2000, while
lowering the TLV to 0.05 mg/m3 (50 [mu]g/m3)
(Document ID 1503, p. 15). ACGIH subsequently lowered the TLV for
crystalline silica to 0.025 mg/m3 (25 [mu]g/m3)
in 2006, which is ACGIH's current recommended exposure limit (Document
ID 1503, pp. 1, 15).
In 1989, OSHA established 8-hour TWA PELs of 0.1 mg/m3
(100 [mu]g/m3) for quartz and 0.05 mg/m3 (50
[mu]g/m3) for cristobalite and tridymite, as part of the Air
Contaminants final rule for general industry (54 FR 2332 (1/19/89)).
OSHA stated that these limits presented no substantial change from the
Agency's former formula limits, but would simplify sampling procedures.
In providing comments on the proposed rule, NIOSH recommended that
crystalline silica be considered a potential carcinogen.
In 1992, OSHA, as part of the Air Contaminants proposed rule for
maritime, construction, and agriculture, proposed the same PELs as for
general industry, to make the PELs consistent across all the OSHA-
regulated sectors (57 FR 26002 (6/12/92)). However, the U.S. Court of
Appeals for the Eleventh Circuit vacated the 1989 Air Contaminants
final rule for general industry (Am. Fed'n of Labor and Cong. of Indus.
Orgs. v. OSHA, 965 F.2d 962 (1992)), and also mooted the proposed rule
for maritime, construction, and agriculture. The Court's decision to
vacate the rule forced the Agency to return to the original 1971 PELs
for all compounds, including silica, adopted as section 6(a) standards.
In 1994, OSHA initiated a process to determine which safety and
health hazards in the U.S. needed the most attention. A priority
planning committee included safety and health experts from OSHA, NIOSH,
and the Mine Safety and Health Administration (MSHA). The committee
reviewed available information on occupational deaths, injuries, and
illnesses and communicated extensively with representatives of labor,
industry, professional and academic organizations, the States,
voluntary standards organizations, and the public. The OSHA National
Advisory Committee on Occupational Safety and Health and the Advisory
Committee on Construction Safety and Health (ACCSH) also made
recommendations. Rulemaking for crystalline silica exposure was one of
the priorities designated by this process. OSHA indicated that
crystalline silica would be added to the Agency's regulatory agenda as
other standards were completed and resources became available.
In 1996, OSHA instituted a Special Emphasis Program (SEP) to step
up enforcement of the crystalline silica standards. The SEP was
intended to reduce worker silica dust exposures that can cause
silicosis and lung cancer. It included extensive outreach designed to
educate and train employers and employees about the hazards of silica
and how to control them, as well as inspections to enforce the
standards. Among the outreach materials available were slides
presenting information on hazard recognition and crystalline silica
control technology, a video on crystalline silica and silicosis, and
informational cards for workers explaining crystalline silica, health
effects related to exposure, and methods of control. The SEP provided
guidance for targeting inspections of worksites that had employees at
risk of developing silicosis. The inspections resulted in the
collection of exposure data from the various worksites visited by
OSHA's compliance officers.
As a follow-up to the SEP, OSHA undertook numerous non-regulatory
actions to address silica exposures. For example, in October of 1996,
OSHA launched a joint silicosis prevention effort with MSHA, NIOSH, and
the American Lung Association (see https://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=NEWS_RELEASES&p_id=14110). This public
education campaign involved distribution of materials on how to prevent
silicosis, including a guide for working safely with silica and
stickers for hard hats to remind workers of crystalline silica hazards.
Spanish language versions of these materials were also made available.
OSHA and MSHA inspectors distributed materials at mines, construction
sites, and other affected workplaces. The joint silicosis prevention
effort included a National Conference to Eliminate Silicosis in
Washington, DC, in March of 1997, which brought together approximately
650 participants from labor, business, government, and the health and
safety professions to exchange ideas and share solutions regarding the
goal of eliminating silicosis (see https://industrydocuments.library.ucsf.edu/documentstore/s/h/d/p//shdp0052/shdp0052.pdf).
In 1997, OSHA announced in its Unified Agenda under Long-Term
Actions that it planned to publish a proposed rule on crystalline
silica
...because the agency has concluded that there will be no
significant progress in the prevention of silica-related diseases
without the adoption of a full and comprehensive silica standard,
including provisions for product substitution, engineering controls,
training and education, respiratory protection and medical screening
and surveillance. A full standard will improve worker protection,
ensure adequate prevention programs, and further reduce silica-
related diseases (62 FR 57755, 57758 (10/29/97)).
In November 1998, OSHA moved "Occupational Exposure to Crystalline
Silica" to the pre-rule stage in the Regulatory Plan (63 FR 61284,
61303-61304 (11/9/98)). OSHA held a series of stakeholder meetings in
1999 and 2000 to get input on the rulemaking. Stakeholder meetings for
all industry sectors were held in Washington, Chicago, and San
Francisco. A separate stakeholder meeting for the construction sector
was held in Atlanta.
OSHA initiated Small Business Regulatory Enforcement Fairness Act
(SBREFA) proceedings in 2003, seeking the advice of small business
representatives on the proposed rule (68 FR 30583, 30584 (5/27/03)).
The SBREFA panel, including representatives from OSHA, the Small
Business Administration's Office of Advocacy, and the Office of
Management and Budget (OMB), was convened on October 20, 2003.
The panel conferred with small entity representatives (SERs)
from general industry, maritime, and construction on
November 10 and 12, 2003, and delivered its final report,
which included comments from the SERs and recommendations to
OSHA for the proposed rule, to OSHA's Assistant Secretary on December
19, 2003 (Document ID 0937).
In 2003, OSHA examined enforcement data for the years 1997 to 2002
and identified high rates of noncompliance with the OSHA respirable
crystalline silica PELs, particularly in construction. This period
covers the first five years of the SEP. These enforcement data,
presented in Table III-1, indicate that 24 percent of silica samples
from the construction industry and 13 percent from general industry
were at least three times the then-existing OSHA PELs. The data
indicate that 66 percent of the silica samples obtained during
inspections in general industry were in compliance with the PEL, while
only 58 percent of the samples collected in construction were in
compliance.
In an effort to expand the 1996 SEP, on January 24, 2008, OSHA
implemented a National Emphasis Program (NEP) to identify and reduce or
eliminate the health hazards associated with occupational exposure to
crystalline silica (CPL-03-007 (1/24/08)). The NEP targeted worksites
with elevated exposures to crystalline silica and included new program
evaluation procedures designed to ensure that the goals of the NEP were
measured as accurately as possible, detailed procedures for conducting
inspections, updated information for selecting sites for inspection,
development of outreach programs by each Regional and Area Office
emphasizing the formation of voluntary partnerships to share
information, and guidance on calculating PELs in construction and
shipyards. In each OSHA Region, at least two percent of inspections
every year are silica-related inspections. Additionally, the silica-
related inspections are conducted at a range of facilities reasonably
representing the distribution of general industry and construction work
sites in that region.
A more recent analysis of OSHA enforcement data from January 2003
to December 2009 (covering the period of continued implementation of
the SEP and the first two years of the NEP) shows that considerable
noncompliance with the then-existing PELs continued to occur. These
enforcement data, presented in Table III-2, indicate that 14 percent of
silica samples from the construction industry and 19 percent for
general industry were at least three times the OSHA PEL during this
period. The data indicate that 70 percent of the silica samples
obtained during inspections in general industry were in compliance with
the PEL, and 75 percent of the samples collected in construction were
in compliance.
Both industry and worker groups have recognized that a
comprehensive standard is needed to protect workers exposed to
respirable crystalline silica. For example, ASTM International
(originally known as the American Society for Testing and Materials)
has published voluntary consensus standards for addressing the hazards
of crystalline silica, and the Building and Construction Trades
Department, AFL-CIO also has recommended a comprehensive program
standard. These recommended standards include provisions for methods of
compliance, exposure monitoring, training, and medical surveillance.
The National Industrial Sand Association has also developed an
occupational exposure program for crystalline silica that addresses
exposure assessment and medical surveillance.
Throughout the crystalline silica rulemaking process, OSHA has
presented information to, and consulted with, ACCSH and the Maritime
Advisory Committee on Occupational Safety and Health. In December of
2009, OSHA representatives met with ACCSH to discuss the rulemaking and
receive their comments and recommendations. On December 11, 2009, ACCSH
passed motions supporting the concept of Table 1 in the draft proposed
construction rule, recognizing that the controls listed in Table 1 are
effective. As discussed with regard to paragraph (f) of the proposed
standard for construction (paragraph (c) of the final standard for
construction), Table 1 presents specified control measures for selected
construction tasks. ACCSH also recommended that OSHA maintain the
protective clothing provision found in the SBREFA panel draft
regulatory text and restore the "competent person" requirement and
responsibilities to the proposed rule. Additionally, the group
recommended that OSHA move forward expeditiously with the rulemaking
process.
In January 2010, OSHA completed a peer review of the draft Health
Effects Analysis and Preliminary Quantitative Risk Assessment following
procedures set forth by OMB in the Final Information Quality Bulletin
for Peer Review, published on the OMB Web site on December 16, 2004
(see 70 FR 2664 (1/14/05)). Each peer reviewer submitted a written
report to OSHA. The Agency revised its draft documents as appropriate
and made the revised documents available to the public as part of its
Notice of Proposed Rulemaking (NPRM). OSHA also made the written charge
to the peer reviewers, the peer reviewers' names, the peer reviewers'
reports, and the Agency's response to the peer reviewers' reports
publicly available with publication of the proposed rule (Document ID
1711; 1716). Five of the seven original peer reviewers submitted post-
hearing reports, commenting on OSHA's disposition of their original
peer review comments in the proposed rule, as well as commenting on
written and oral testimony presented at the silica hearing (Document ID
3574).
On August 23, 2013, OSHA posted its NPRM for respirable crystalline
silica on its Web site and requested comments on the proposed rule. On
September 12, 2013, OSHA published the NPRM in the Federal Register (78
FR 56273 (9/12/13)). In the NPRM, the Agency made a preliminary
determination that employees exposed to respirable crystalline silica
at the current PELs face a significant risk to their health and that
promulgating the proposed standards would substantially reduce that
risk. The NPRM required commenters to submit their comments by December
11, 2013. In response to stakeholder requests, OSHA extended the
comment period until January 27, 2014 (78 FR 65242 (10/31/13)). On
January 14, 2014, OSHA held a web chat to provide small businesses and
other stakeholders an additional opportunity to obtain information from
the Agency about the proposed rule. Subsequently, OSHA further extended
the comment period to February 11, 2014 (79 FR 4641 (1/29/14)).
As part of the instructions for submitting comments, OSHA requested
(but did not require) that parties submitting technical or scientific
studies or research results and those submitting comments or testimony
on the Agency's analyses disclose the nature of financial relationships
with (e.g., consulting agreement), and extent of review by, parties
interested in or affected by the rulemaking (78 FR 56274).
Parties submitting studies or research results were also asked
to disclose sources of funding and sponsorship for their research.
OSHA intended for the disclosure of such information to promote
the transparency and scientific integrity of evidence submitted
to the record and stated that the request was consistent with
Executive Order 13563.
The Agency received several comments related to this request. For
example, an industrial hygiene engineer supported the disclosure of
potential conflict of interest information (Document ID 2278, p. 5).
Other commenters, such as congressional representatives and industry
associations, opposed the request, asserting that it could lead to
prejudgment or questioning of integrity, in addition to dissuading
participation in the rulemaking; some also questioned the legality of
such a request or OSHA's interpretation of Executive Order 13563 (e.g.,
Document ID 1811, p. 2; 2101, pp. 2-3). A number of stakeholders from
academia and industry submitted information related to the request for
funding, sponsorships, and review by interested parties (e.g., Document
ID 1766, p. 1; 2004, p. 2; 2211, p. 2; 2195, p. 17). OSHA emphasizes
that it reviewed and considered all evidence submitted to the record.
An informal public hearing on the proposed standards was held in
Washington, DC from March 18 through April 4, 2014. Administrative Law
Judges Daniel F. Solomon and Stephen L. Purcell presided over the
hearing. The Agency heard testimony from over 200 stakeholders
representing more than 70 organizations, such as public health groups,
trade associations, and labor unions. Chief Administrative Law Judge
Stephen L. Purcell closed the public hearing on April 4, 2014, allowing
45 days--until May 19, 2014--for participants who filed a notice of
intention to appear at the hearings to submit additional evidence and
data, and an additional 45 days--until July 3, 2014--to submit final
briefs, arguments, and summations (Document ID 3589, Tr. 4415-4416).
After the hearing concluded, OSHA extended the deadline to give those
participants who filed a notice of intention to appear at the hearings
until June 3, 2014 to submit additional information and data to the
record, and until July 18, 2014 to submit final briefs and arguments
(Document ID 3569). Based upon requests from stakeholders, the second
deadline was extended, and parties who filed a notice of intention to
appear at the hearing were given until August 18, 2014, to submit their
final briefs and arguments (Document ID 4192).
OSHA provided the public with multiple opportunities to participate
in the rulemaking process, including stakeholder meetings, the SBREFA
panel, two comment periods (pre- and post-hearing), and a 14-day public
hearing. Commenters were provided more than five months to comment on
the rule before the hearing, and nearly as long to submit additional
information, final briefs, and arguments after the hearing. OSHA
received more than 2,000 comments on the silica NPRM during the entire
pre-and post-hearing public participation period. In OSHA's view,
therefore, the public was given sufficient opportunities and ample time
to fully participate in this rulemaking.
The final rule on occupational exposure to respirable crystalline
silica is based on consideration of the entire record of this
rulemaking proceeding, including materials discussed or relied upon in
the proposal, the record of the hearing, and all written comments and
exhibits timely received. Thus, in promulgating this final rule, OSHA
considered all comments in the record, including those that suggested
that OSHA withdraw its proposal and merely enforce the existing silica
standards, as well as those that argued the proposed rule was not
protective enough. Based on this comprehensive record, OSHA concludes
that employees exposed to respirable crystalline silica are at
significant risk of developing silicosis and other non-malignant
respiratory disease, lung cancer, kidney effects, and immune system
effects. The Agency concludes that the PEL of 50 [mu]g/m\3\ reduces the
significant risks of material impairments of health posed to workers by
occupational exposure to respirable crystalline silica to the maximum
extent that is technologically and economically feasible. OSHA's
substantive determinations with regard to the comments, testimony, and
other information in the record, the legal standards governing the
decision-making process, and the Agency's analysis of the data
resulting in its assessments of risks, benefits, technological and
economic feasibility, and compliance costs are discussed elsewhere in
this preamble.
IV. Chemical Properties and Industrial Uses
Silica is a compound composed of the elements silicon and oxygen
(chemical formula SiO2). Silica has a molecular weight of
60.08, and exists in crystalline and amorphous states, both in the
natural environment and as produced during manufacturing or other
processes. These substances are odorless solids, have no vapor
pressure, and create non-explosive dusts when particles are suspended
in air (Document ID 3637, pp. 1-3).
Silica is classified as part of the "silicate" class of minerals,
which includes compounds that are composed of silicon and oxygen and
which may also be bonded to metal ions or their oxides. The basic
structural units of silicates are silicon tetrahedrons
(SiO4), pyramidal structures with four triangular sides
where a silicon atom is located in the center of the structure and an
oxygen atom is located at each of the four corners. When silica
tetrahedrons bond exclusively with other silica tetrahedrons, each
oxygen atom is bonded to the silicon atom of its original ion, as well
as to the silicon atom from another silica ion. This results in a ratio
of one atom of silicon to two atoms of oxygen, expressed as
SiO2. The silicon-oxygen bonds within the tetrahedrons use
only one-half of each oxygen's total bonding energy. This leaves
negatively charged oxygen ions available to bond with available
positively charged ions. When they bond with metal and metal oxides,
commonly of iron, magnesium, aluminum, sodium, potassium, and calcium,
they form the silicate minerals commonly found in nature (Document ID
1334, p. 7).
In crystalline silica, the silicon and oxygen atoms are arranged in
a three-dimensional repeating pattern. Silica is said to be
polymorphic, as different forms are created when the silica
tetrahedrons combine in different crystalline structures. The primary
forms of crystalline silica are quartz, cristobalite, and tridymite. In
an amorphous state, silicon and oxygen atoms are present in the same
proportions but are not organized in a repeating pattern. Amorphous
silica includes natural and manufactured glasses (vitreous and fused
silica, quartz glass), biogenic silica, and opals, which are amorphous
silica hydrates (Document ID 2258, Attachment 8, pp. 45-50).
Quartz is the most common form of crystalline silica and accounts
for almost 12% by volume of the earth's crust. Alpha quartz, the quartz
form that is stable below 573 [deg]C, is the most prevalent form of
crystalline silica found in the workplace. It accounts for the
overwhelming majority of naturally found silica and is present in
varying amounts in almost every type of mineral. Alpha quartz is found
in igneous, sedimentary, and metamorphic rock, and all soils contain at
least a trace amount of quartz (Document ID 1334, p. 9).
Alpha quartz is used in many products throughout various industries
and is a common component of building materials (Document ID 1334, pp.
11-15). Common trade names for commercially available quartz include:
CSQZ, DQ 12, Min-U-Sil, Sil-Co-Sil, Snowit, Sykron F300, and Sykron
F600 (Document ID 2258, Attachment 8, p. 43).
Cristobalite is a form of crystalline silica that is formed at high
temperatures (>1470 [deg]C). Although naturally occurring cristobalite
is relatively rare, volcanic eruptions, such as Mount St. Helens, can
release cristobalite dust into the air. Cristobalite can also be
created during some processes conducted in the workplace. For example,
flux-calcined diatomaceous earth is a material used as a filtering aid
and as a filler in other products (Document ID 2258, Attachment 8, p.
44). It is produced when diatomaceous earth (diatomite), a geological
product of decayed unicellular organisms called diatoms, is heated with
flux. The finished product can contain between 40 and 60 percent
cristobalite. Also, high temperature furnaces are often lined with
bricks that contain quartz. When subjected to prolonged high
temperatures, this quartz can convert to cristobalite.
Tridymite is another material formed at high temperatures (>870
[deg]C) that is associated with volcanic activity. The creation of
tridymite requires the presence of a flux such as sodium oxide.
Tridymite is rarely found in nature and rarely reported in the
workplace (Document ID 1424 pp. 5, 14).
When heated or cooled sufficiently, crystalline silica can
transition between the polymorphic forms, with specific transitions
occurring at different temperatures. At higher temperatures the
linkages between the silica tetrahedrons break and reform, resulting in
new crystalline structures. Quartz converts to cristobalite at 1470
[deg]C, and at 1723 [deg]C cristobalite loses its crystalline structure
and becomes amorphous fused silica. These high temperature transitions
reverse themselves at extremely slow rates, with different forms co-
existing for a long time after the crystal cools (Document ID 2258,
Attachment 8, p. 47).
Other types of transitions occur at lower temperatures when the
silica-oxygen bonds in the silica tetrahedron rotate or stretch,
resulting in a new crystalline structure. These low-temperature, or
alpha to beta, transitions are readily and rapidly reversed as the
crystal cools. At temperatures encountered by workers, only the alpha
form of crystalline silica exists (Document ID 2258, Attachment 8, pp.
46-48).
Crystalline silica minerals produce distinct X-ray diffraction
patterns, specific to their crystalline structure. The patterns can be
used to distinguish the crystalline polymorphs from each other and from
amorphous silica (Document ID 2258, Attachment 8, p. 45).
The specific gravity and melting point of silica vary between
polymorphs. Silica is insoluble in water at 20 [deg]C and in most
acids, but its solubility increases with higher temperatures and pH,
and it dissolves readily in hydrofluoric acid. Solubility is also
affected by the presence of trace metals and by particle size. Under
humid conditions water vapor in the air reacts with the surface of
silica particles to form an external layer of silinols (SiOH). When
these silinols are present the crystalline silica becomes more
hydrophilic. Heating or acid washing reduces the amount of silinols on
the surface area of crystalline silica particles. There is an external
amorphous layer found in aged quartz, called the Beilby layer, which is
not found on freshly cut quartz. This amorphous layer is more water
soluble than the underlying crystalline core. Etching with hydrofluoric
acid removes the Beilby layer as well as the principal metal impurities
on quartz (Document ID 2258, Attachment 8, pp. 44-49).
Crystalline silica has limited chemical reactivity. It reacts with
alkaline aqueous solutions, but does not readily react with most acids,
with the exception of hydrofluoric acid. In contrast, amorphous silica
and most silicates react with most mineral acids and alkaline
solutions. Analytical chemists relied on this difference in acid
reactivity to develop the silica point count analytical method that was
widely used prior to the current X-ray diffraction and infrared methods
(Document ID 2258, Attachment 8, pp. 48-51; 1355, p. 994).
Crystalline silica is used in industry in a wide variety of
applications. Sand and gravel are used in road building and concrete
construction. Sand with greater than 98% silica is used in the
manufacture of glass and ceramics. Silica sand is used to form molds
for metal castings in foundries, and in abrasive blasting operations.
Silica is also used as a filler in plastics, rubber, and paint, and as
an abrasive in soaps and scouring cleansers. Silica sand is used to
filter impurities from municipal water and sewage treatment plants, and
in hydraulic fracturing for oil and gas recovery (Document ID 1334, p.
11). Silica is also used to manufacture artificial stone products used
as bathroom and kitchen countertops, and the silica content in those
products can exceed 85 percent (Document ID 1477, pp. 3 and 11; 2178,
Attachment 5, p. 420).
There are over 30 major industries and operations where exposures
to crystalline silica can occur. They include such diverse workplaces
as foundries, dental laboratories, concrete products and paint and
coating manufacture, as well as construction activities including
masonry cutting, drilling, grinding and tuckpointing, and use of heavy
equipment during demolition activities involving silica-containing
materials. A more detailed discussion of the industries affected by the
proposed standard is presented in Section VII, Summary of the Final
Economic Analysis and Final Regulatory Flexibility Analysis.
Crystalline silica exposures can also occur in mining (which is under
the jurisdiction of the Mine Safety and Health Administration), and in
agriculture during plowing and harvesting.
V. Health Effects
A. Introduction
As discussed more thoroughly in Section II of this preamble,
Pertinent Legal Authority, section 6(b)(5) of the Occupational Safety
and Health Act (OSH Act or Act) requires the Secretary of Labor, in
promulgating standards dealing with toxic materials or harmful physical
agents, 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 dealt
with by such standard for the period of his working life" (29 U.S.C.
655). Thus, in order to set a new health standard, the Secretary must
determine 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 Secretary's significant risk and material impairment
determinations must be made "on the basis of the best available
evidence" (29 U.S.C. 655(b)(5)). Although the Supreme Court, in its
decision on OSHA's Benzene standard, explained that OSHA must look to
"a body of reputable scientific thought" in making its material harm
and significant risk determinations, the Court added that a reviewing
court must "give OSHA some leeway where its findings must be made on
the frontiers of scientific knowledge" (Indus. Union Dep't,
AFL-CIO v. Am. Petroleum Inst., 448 U.S. 607, 656 (1980) (plurality opinion)
("Benzene")). Thus, while OSHA's significant risk determination must be
supported by substantial evidence, the Agency "is not required to support
the finding that a significant risk exists with anything approaching
scientific certainty" (Benzene, 448 U.S. at 656).
This section provides an overview of OSHA's material harm and
significant risk determinations: (1) Summarizing OSHA's preliminary
methods and findings from the proposal; (2) addressing public comments
dealing with OSHA's evaluation of the scientific literature and methods
used to estimate quantitative risk; and (3) presenting OSHA's final
conclusions, with consideration of the rulemaking record, on the health
effects and quantitative risk estimates associated with worker exposure
to respirable crystalline silica. The quantitative risk estimates and
significance of those risks are then discussed in detail in Section VI,
Final Quantitative Risk Assessment and Significance of Risk.
B. Summary of Health and Risk Findings
As discussed in detail throughout this section and in Section VI,
Final Quantitative Risk Assessment and Significance of Risk, OSHA
finds, based upon the best available evidence in the published, peer-
reviewed scientific literature, that exposure to respirable crystalline
silica increases the risk of silicosis, lung cancer, other non-
malignant respiratory disease (NMRD), and renal and autoimmune effects.
In its Preliminary Quantitative Risk Assessment (QRA), OSHA used the
best available exposure-response data from epidemiological studies to
estimate quantitative risks. After carefully reviewing stakeholder
comments on the Preliminary QRA and new information provided to the
rulemaking record, OSHA finds there to be a clearly significant risk at
the previous PELs for respirable crystalline silica (equivalent to
approximately 100 [mu]g/m\3\ for general industry and between 250 and
500 [mu]g/m\3\ for construction/shipyards), with excess lifetime risk
estimates for lung cancer mortality, silicosis mortality, and NMRD
mortality each being much greater than 1 death per 1,000 workers
exposed for a working life of 45 years. Cumulative risk estimates for
silicosis morbidity are also well above 1 case per 1,000 workers
exposed at the previous PELs. At the revised PEL of 50 [mu]g/m\3\
respirable crystalline silica, these estimated risks are substantially
reduced. Thus, OSHA concludes that the new PEL of 50 [mu]g/m\3\
provides a large reduction in the lifetime and cumulative risk posed to
workers exposed to respirable crystalline silica.
These findings and conclusions are consistent with those of the
World Health Organization's International Agency for Research on Cancer
(IARC), the U.S. Department of Health and Human Services' (HHS)
National Toxicology Program (NTP), the National Institute for
Occupational Safety and Health (NIOSH), and many other organizations
and individuals, as evidenced in the rulemaking record and further
discussed below. Many other scientific organizations and governments
have recognized the strong body of scientific evidence pointing to the
health risks of respirable crystalline silica and have deemed it
necessary to take action to reduce those risks. As far back as 1974,
NIOSH recommended that the exposure limit for crystalline silica be
reduced to 50 [mu]g/m\3\ (Document ID 2177b, p. 2). In 2000, the
American Conference of Governmental Industrial Hygienists (ACGIH), a
professional society that has recommended workplace exposure limits for
six decades, revised their Threshold Limit Value (TLV) for respirable
crystalline silica to 50 [mu]g/m\3\ and has since further lowered its
TLV for respirable crystalline silica to 25 [mu]g/m\3\. OSHA is setting
its revised PEL at 50 [mu]g/m\3\ based on consideration of the body of
evidence describing the health risks of crystalline silica as well as
on technological feasibility considerations, as discussed in Section
VII of this preamble and Chapter IV of the Final Economic Analysis and
Final Regulatory Flexibility Analysis (FEA).
To reach these conclusions, OSHA performed an extensive search and
review of the peer-reviewed scientific literature on the health effects
of inhalation exposure to crystalline silica, particularly silicosis,
lung cancer, other NMRD, and renal and autoimmune effects (Document ID
1711, pp. 7-265). Based upon this review, OSHA preliminarily determined
that there was substantial evidence that exposure to respirable
crystalline silica increases the risk of silicosis, lung cancer, NMRD,
and renal and autoimmune effects (Document ID 1711, pp. 164, 181-208,
229). OSHA also found there to be suitable exposure-response data from
many well-conducted epidemiological studies that permitted the Agency
to estimate quantitative risks for lung cancer mortality, silicosis and
NMRD mortality, renal disease mortality, and silicosis morbidity
(Document ID 1711, p. 266).
As part of the preliminary quantitative risk assessment, OSHA
calculated estimates of the risk of silica-related diseases assuming
exposure over a working life (45 years) to 25, 50, 100, 250, and 500
[mu]g/m\3\ respirable crystalline silica (corresponding to cumulative
exposures over 45 years to 1.125, 2.25, 4.5, 11.25, and 22.5 mg/m\3\-
yrs) (see Bldg & Constr. Trades Dep't v. Brock, 838 F.2d 1258, 1264-65
(D.C. Cir. 1988) approving OSHA's policy of using 45 years for the
working life of an employee in setting a toxic substance standard). To
estimate lifetime excess mortality risks at these exposure levels, OSHA
used, for each key study, the exposure-response risk model(s) and
regression coefficient from the model(s) in a life table analysis that
accounted for competing causes of death due to background causes and
cumulated risk through age 85 (Document ID 1711, pp. 360-378). For
these analyses, OSHA used lung cancer, NMRD, or renal disease mortality
and all-cause mortality rates to account for background risks and
competing risks (U.S. 2006 data for lung cancer and NMRD mortality in
all males, 1998 data for renal disease mortality, obtained from cause-
specific death rate tables published by the National Center for Health
Statistics (2009, Document ID 1104)). The mortality risk estimates were
presented in terms of lifetime excess risk per 1,000 workers for
exposure over an 8-hour working day, 250 days per year, and a 45-year
working lifetime. For silicosis morbidity, OSHA based its risk
estimates on the cumulative risk model(s) used in each study to develop
quantitative exposure-response relationships. These models
characterized the risk of developing silicosis, as detected by chest
radiography, up to the time that cohort members, including both active
and retired workers, were last examined (78 FR 56273, 56312 (9/12/13)).
OSHA then combined its review of the health effects literature and
preliminary quantitative risk assessment into a draft document,
entitled "Occupational Exposure to Respirable Crystalline Silica--
Review of Health Effects Literature and Preliminary Quantitative Risk
Assessment," and submitted it to a panel of scientific experts \2\ for
independent peer review, in accordance with the Office of Management and
Budget's (OMB) "Final Information Quality Bulletin for Peer Review"
(Document ID 1336). The peer reviewers reviewed OSHA's draft Review of
Health Effects Literature and Preliminary QRA. The peer-review panel
responded to nearly 20 charge questions from OSHA and commented on
various aspects of OSHA's analysis (Document ID 1716).
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\2\ OSHA's contractor, Eastern Research Group, Inc. (ERG),
conducted a search for nationally recognized experts in occupational
epidemiology, biostatistics and risk assessment, animal and cellular
toxicology, and occupational medicine who had no actual or apparent
conflict of interest. ERG chose seven of the applicants to be peer
reviewers based on their qualifications and the necessity of
ensuring a broad and diverse panel in terms of scientific and
technical expertise (see Document ID 1711, pp. 379-381). The seven
peer reviewers were: Bruce Allen, Bruce Allen Consulting; Kenneth
Crump, Ph.D., Louisiana Tech University Foundation; Murray
Finkelstein, MD, Ph.D., McMaster University, Ontario; Gary Ginsberg,
Ph.D., Connecticut Department of Public Health; Brian Miller, Ph.D.,
Institute of Occupational Medicine (IOM) Consulting Ltd., Scotland;
Andrew Salmon, Ph.D., private consultant; and Noah Seixas, Ph.D.,
University of Washington, Seattle (Document ID 1711, p. 380).
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Overall, the peer reviewers found that OSHA was very thorough in
its review of the literature and was reasonable in its interpretation
of the studies with regards to the various endpoints examined, such
that the Agency's conclusions on health effects were generally well
founded (Document ID 1711, p. 381). The reviewers had various comments
on OSHA's draft Preliminary QRA (Document ID 1716, pp. 107-218). OSHA
provided a response to each comment in the Review of Health Effects
Literature and Preliminary QRA and, where appropriate, made revisions
(Document ID 1711, pp. 381-399). The Agency then placed the Review of
Health Effects Literature and Preliminary QRA into the rulemaking
docket as a background document (Document ID 1711). With the
publication of the Notice of Proposed Rulemaking (78 FR 56723 on 9/12/
13), all aspects of the Review of Health Effects Literature and
Preliminary QRA were open for public comment.
Following the publication of the proposed rule (78 FR 56273 (9/12/
13)) and accompanying revised Review of Health Effects Literature and
Preliminary QRA (Document ID 1711), the peer reviewers were invited to
review the revised analysis, examine the written comments in the
docket, and attend the public hearing to listen to oral testimony as it
applied to the health effects and quantitative risk assessment. Five
peer reviewers were available and attended. In their final comments,
provided to OSHA following the hearings, all five peer reviewers
indicated that OSHA had adequately addressed their original comments
(Document ID 3574). The peer reviewers also offered additional comments
on concerns raised during the hearing. Many of the reviewers commented
on the difficulty of evaluating exposure-response thresholds, and
responded to public comments regarding causation and other specific
issues (Document ID 3574). OSHA has incorporated many of the peer
reviewers' additional comments into its risk assessment discussion in
the preamble. Thus, OSHA believes that the external, independent peer-
review process supports and lends legitimacy to its risk assessment
methods and findings.
OSHA also received substantial public comment and testimony from a
wide variety of stakeholders supporting its Review of Health Effects
Literature and Preliminary QRA. In general, supportive comments and
testimony were received from NIOSH (Document ID 2177; 3998; 4233), the
public health and medical community, labor unions, affected workers,
private citizens, and others.
Regarding health effects, NIOSH commented that the adverse health
effects of exposure to respirable crystalline silica are "well-known,
long lasting, and preventable" (Document ID 2177b, p. 2). Darius
Sivin, Ph.D., of the UAW, commented, "[o]ccupational exposure to
silica has been recognized for centuries as a serious workplace
hazard" (Document ID 2282, Attachment 3, p. 4). Similarly, David
Goldsmith, Ph.D., testified:
There have been literally thousands of research studies on
exposure to crystalline silica in the past 30 years. Almost every
study tells the occupational research community that workers need
better protection to prevent severe chronic respiratory diseases,
including lung cancer and other diseases in the future. What OSHA is
proposing to do in revising the workplace standard for silica seems
to be a rational response to the accumulation of published evidence
(Document ID 3577, Tr. 865-866).
Franklin Mirer, Ph.D., CIH, Professor of Environmental and
Occupational Health at CUNY School of Public Health, on behalf of the
American Federation of Labor and Congress of Industrial Organizations
(AFL-CIO), reiterated that silica "is a clear and present danger to
workers health at exposure levels prevailing now in a large number of
industries. Workers are at significant risk for mortality and illnesses
including lung cancer and non-malignant respiratory disease including
COPD, and silicosis" (Document ID 2256, Attachment 3, p. 3). The AFL-
CIO also noted that there is "overwhelming evidence in the record that
exposure to respirable crystalline silica poses a significant health
risk to workers" (Document ID 4204, p. 11). The Building and
Construction Trades Department, AFL-CIO, further commented that the
rulemaking record "clearly supports OSHA's risk determination"
(Document ID 4223, p. 2). Likewise, the Sorptive Minerals Institute, a
national trade association, commented, "It is beyond dispute that OSHA
has correctly determined that industrial exposure to certain types of
silica can cause extremely serious, sometimes even fatal disease. In
the massive rulemaking docket being compiled by the Agency, credible
claims to the contrary are sparse to non-existent" (Document ID 4230,
p. 8). OSHA also received numerous comments supportive of the revised
standard from affected workers and citizens (e.g., Document ID 1724,
1726, 1731, 1752, 1756, 1759, 1762, 1764, 1787, 1798, 1800, 1802).
Regarding OSHA's literature review for its quantitative risk
assessment, the American Public Health Association (APHA) and the
National Consumers League (NCL) commented, "OSHA has thoroughly
reviewed and evaluated the peer-reviewed literature on the health
effects associated with exposure to respirable crystalline silica.
OSHA's quantitative risk assessment is sound. The agency has relied on
the best available evidence and acted appropriately in giving greater
weight to those studies with the most robust designs and statistical
analyses" (Document ID 2178, Attachment 1, p. 1; 2373, p. 1).
Dr. Mirer, who has served on several National Academy of Sciences
committees setting risk assessment guidelines, further commented that
OSHA's risk analysis is "scientifically correct, and consistent with
the latest thinking on risk assessment," (Document ID 2256, Attachment
3, p. 3), citing the National Academies' National Research Council's
Science and Decisions: Advancing Risk Assessment (Document ID 4052),
which makes technical recommendations on risk assessment and risk-based
decision making (Document ID 3578, Tr. 935-936). In post-hearing
comments expanding on this testimony, the AFL-CIO also noted that
OSHA's risk assessment methodologies are transparent and consistent
with practices recommended by the National Research Council in its
publication, Risk Assessment in the Federal Government: Managing the
Process, and with the Environmental Protection Agency's Guidelines for
Carcinogenic Risk Assessment (Document ID 4204, p. 20). Similarly, Kyle
Steenland, Ph.D., Professor in the Department of Environmental Health
at Rollins School of Public Health, Emory University, one of the
researchers on whose studies OSHA relied, testified that "OSHA has
done a very capable job in conducting the summary of the literature and
doing its own risk assessment" (Document ID 3580, Tr. 1235).
Collectively, these comments and testimony support OSHA's use of the
best available evidence and methods to estimate quantitative risks of
lung cancer mortality, silicosis and NMRD mortality, renal disease
mortality, and silicosis morbidity from exposure to respirable
crystalline silica.
Based on OSHA's Preliminary QRA, many commenters recognized that
reducing the permissible exposure limit is necessary to reduce
significant risks presented by exposure to respirable crystalline
silica (Document ID 4204, pp. 11-12; 2080, p. 1; 2339, p. 2). For
example, the AFL-CIO stated that "OSHA based its proposal on more than
adequate evidence, but more recent publications have described further
the risk posed by silica exposure, and further justify the need for new
silica standards" (Document ID 4204, pp. 11-12). Similarly, the
American Society of Safety Engineers (ASSE) remarked that "[w]hile
some may debate the science underlying the findings set forth in the
proposed rule, overexposure to crystalline silica has been linked to
occupational illness since the time of the ancient Greeks, and
reduction of the current permissible exposure limit (PEL) to that
recommended for years by the National Institute for Occupational Safety
and Health (NIOSH) is long overdue" (Document ID 2339, p. 2).
Not every commenter agreed, however, as OSHA also received critical
comments and testimony from various employers and their
representatives, as well as some organizations representing affected
industries. In general, these comments were critical of the underlying
studies on which OSHA relied for its quantitative risk assessment, or
with the methods used by OSHA to estimate quantitative risks. Some
commenters also presented additional studies for OSHA to consider. OSHA
thoroughly reviewed these and did not find them adequate to alter
OSHA's overall conclusions of health risk, as discussed in great detail
in the sections that follow.
After considering the evidence and testimony in the record, as
discussed below, OSHA affirms its approach to quantify health risks
related to exposure to respirable crystalline silica and the Agency's
preliminary conclusions. In the final risk assessment that is now
presented as part of this final rule in Section VI, Final Quantitative
Risk Assessment and Significance of Risk, OSHA concludes that there is
a clearly significant risk at the previous PELs for respirable
crystalline silica, with excess lifetime risk estimates for lung cancer
mortality, silicosis mortality, and NMRD mortality each being much
greater than 1 death per 1,000 workers as a result of exposure for 45
working years (see Section VI, Final Quantitative Risk Assessment and
Significance of Risk). At the revised PEL of 50 [micro]g/m\3\
respirable crystalline silica, OSHA finds the estimated risks to be
substantially reduced. Cumulative risk estimates for silicosis
morbidity are also well above 1 case per 1,000 workers at the previous
PELs, with a substantial reduction at the revised PEL (see Section VI,
Final Quantitative Risk Assessment and Significance of Risk, Table VI-
1).
The health effects associated with silica exposure are well-
established and supported by the record. Based on the record evidence,
OSHA concludes that exposure to respirable crystalline silica causes
silicosis and is the only known cause of silicosis. This causal
relationship has long been accepted in the scientific and medical
communities. In fact, the Department of Labor produced a video in 1938
featuring then Secretary of Labor Frances Perkins discussing the
occurrence of silicosis among workers exposed to silica
(see https://www.osha.gov/silica/index.html). Silicosis is a progressive disease
induced by the inflammatory effects of respirable crystalline silica in
the lung, which leads to lung damage and scarring and, in some cases,
progresses to complications resulting in disability and death (see
Section VI, Final Quantitative Risk Assessment and Significance of
Risk). OSHA used a weight-of-evidence approach to evaluate the
scientific studies in the literature to determine their overall quality
and whether there is substantial evidence that exposure to respirable
crystalline silica increases the risk of a particular health effect.
For lung cancer, OSHA reviewed the published, peer-reviewed
scientific literature, including 60 epidemiological studies covering
more than 30 occupational groups in over a dozen industrial sectors
(see Document ID 1711, pp. 77-170). Based on this comprehensive review,
and after considering the rulemaking record as a whole, OSHA concludes
that the data provide ample evidence that exposure to respirable
crystalline silica increases the risk of lung cancer among workers (see
Document ID 1711, p. 164). OSHA's conclusion is consistent with that of
IARC, which is the specialized cancer agency that is part of the World
Health Organization and utilizes interdisciplinary (e.g.,
biostatistics, epidemiology, and laboratory sciences) experts to
comprehensively identify the causes of cancer. In 1997, IARC classified
respirable crystalline silica dust, in the form of quartz or
cristobalite, as Group 1, i.e., "carcinogenic to humans," following a
thorough expert committee review of the peer-reviewed scientific
literature (Document ID 2258, Attachment 8, p. 211). OSHA notes that
IARC classifications and accompanying monographs are well recognized in
the scientific community, having been described as "the most
comprehensive and respected collection of systematically evaluated
agents in the field of cancer epidemiology" (Demetriou et al., 2012,
Document ID 4131, p. 1273). For silica, IARC's overall finding was
based on studies of nine occupational cohorts that it considered to be
the least influenced by confounding factors (see Document ID 1711, p.
76). OSHA included these studies in its review, in addition to several
other studies (Document ID 1711, pp. 77-170).
Since IARC's 1997 determination that respirable crystalline silica
is a Group 1 carcinogen, the scientific community has reaffirmed the
soundness of this finding. In March of 2009, 27 scientists from eight
countries participated in an additional IARC review of the scientific
literature and reaffirmed that respirable crystalline silica dust is a
Group 1 human carcinogen (Document ID 1473, p. 396). Additionally, in
2000, the NTP, which is a widely-respected interagency program under
HHS that evaluates chemicals for possible toxic effects on public
health, also concluded that respirable crystalline silica is a known
human carcinogen (Document ID 1164, p. 1).
For NMRD other than silicosis, based on its review of several
studies and all subsequent record evidence, OSHA concludes that
exposure to respirable crystalline silica increases the risk of
emphysema, chronic bronchitis, and pulmonary function impairment (see
Section VI, Final Quantitative Risk Assessment and Significance of
Risk; Document ID 1711, pp. 181-208). For renal disease, OSHA reviewed
the epidemiological literature and finds that a number of
epidemiological studies reported statistically significant associations
between occupational exposure to silica dust and chronic renal disease,
subclinical renal changes, end-stage renal disease morbidity, chronic
renal disease mortality, and granulomatosis with polyangitis (see
Section VI, Final Quantitative Risk Assessment and Significance of
Risk; Document ID 1711, p. 228). For autoimmune effects, OSHA reviewed
epidemiological information in the record suggesting an association
between respirable crystalline silica exposure and increased risk of
systemic autoimmune diseases, including scleroderma, rheumatoid
arthritis, and systemic lupus erythematosus (see Section VI, Final
Quantitative Risk Assessment and Significance of Risk; Document ID
1711, p. 229). Therefore, OSHA concludes that there is substantial
evidence that silica exposure increases the risks of renal and of
autoimmune disease (see Section VI, Final Quantitative Risk Assessment
and Significance of Risk; Document ID 1711, p. 229).
OSHA also finds there to be suitable exposure-response data from
many well-conducted studies that permit the Agency to estimate
quantitative risks for lung cancer mortality, silicosis and NMRD
mortality, renal disease mortality, and silicosis morbidity (see
Section VI, Final Quantitative Risk Assessment and Significance of
Risk; Document ID 1711, p. 266). OSHA believes the exposure-response
data in these studies collectively represent the best available
evidence for use in estimating the quantitative risks related to silica
exposure. For lung cancer mortality, OSHA relies upon a number of
published studies that analyzed exposure-response relationships between
respirable crystalline silica and lung cancer. These included studies
of cohorts from several industry sectors: Diatomaceous earth workers
(Rice et al., 2001, Document ID 1118), Vermont granite workers
(Attfield and Costello, 2004, Document ID 0285), North American
industrial sand workers (Hughes et al., 2001, Document ID 1060), and
British coal miners (Miller and MacCalman, 2009, Document ID 1306).
These studies are scientifically sound due to their sufficient size and
adequate years of follow-up, sufficient quantitative exposure data,
lack of serious confounding by exposure to other occupational
carcinogens, consideration (for the most part) of potential confounding
by smoking, and absence of any apparent selection bias (see Section VI,
Final Quantitative Risk Assessment and Significance of Risk; Document
ID 1711, p. 165). They all demonstrated positive, statistically
significant exposure-response relationships between exposure to
crystalline silica and lung cancer mortality. Also compelling was a
pooled analysis (Steenland et al., 2001a, Document ID 0452) of 10
occupational cohorts (with a total of 65,980 workers and 1,072 lung
cancer deaths), which was also used as a basis for IARC's 2009
reaffirmation of respirable crystalline silica as a human carcinogen.
This analysis by Steenland et al. found an overall positive exposure-
response relationship between cumulative exposure to crystalline silica
and lung cancer mortality (see Section VI, Final Quantitative Risk
Assessment and Significance of Risk; Document ID 1711, pp. 269-292).
Based on these studies, OSHA estimates that the lifetime lung cancer
mortality excess risk associated with 45 years of exposure to
respirable crystalline silica ranges from 11 to 54 deaths per 1,000
workers at the previous general industry PEL of 100 [micro]g/m\3\
respirable crystalline silica, and 5 to 23 deaths per 1,000 workers at
the revised PEL of 50 [micro]g/m\3\ respirable crystalline silica (see
Section VI, Final Quantitative Risk Assessment and Significance of
Risk, Table VI-1). These estimates exceed by a substantial margin the
one in a thousand benchmark that OSHA has generally applied to its
health standards following the Supreme Court's Benzene decision (448
U.S. 607, 655 (1980)).
For silicosis and NMRD mortality, OSHA relies upon two published,
peer-reviewed studies: A pooled analysis of silicosis mortality data
from six epidemiological studies (Mannetje et al., 2002b, Document ID
1089), and an exposure-response analysis of NMRD mortality among
diatomaceous earth workers (Park et al, 2002, Document ID 0405) (see
Section VI, Final Quantitative Risk Assessment and Significance of
Risk; Document ID 1711, p. 292). The pooled analysis had a total of
18,634 subjects, 150 silicosis deaths, and 20 deaths from unspecified
pneumoconiosis, and demonstrated an increasing mortality rate with
silica exposure (Mannetje et al., 2002b, Document ID 1089; see also
1711, pp. 292-295). To estimate the risks of silicosis mortality, OSHA
used the model described by Mannetje et al. but used rate ratios that
were estimated from a sensitivity analysis conducted by ToxaChemica,
Inc. that was expected to better control for age and exposure
measurement uncertainty (2004, Document ID 0469; 1711, p. 295). OSHA's
estimate of lifetime silicosis mortality risk is 11 deaths per 1,000
workers at the previous general industry PEL, and 7 deaths per 1,000
workers at the revised PEL (see Section VI, Final Quantitative Risk
Assessment and Significance of Risk, Table VI-1).
The NMRD analysis by Park et al. (2002, Document 0405) included
pneumoconiosis (including silicosis), chronic bronchitis, and
emphysema, since silicosis is a cause of death that is often
misclassified as emphysema or chronic bronchitis (see Document ID 1711,
p. 295). Positive exposure-response relationships were found between
exposure to crystalline silica and excess risk for NMRD mortality (see
Section VI, Final Quantitative Risk Assessment and Significance of
Risk; Document ID 1711, pp. 204-206, 295-297). OSHA's estimate of
excess lifetime NMRD mortality risk, calculated using the results from
Park et al., is 85 deaths per 1,000 workers at the previous general
industry PEL of 100 [micro]g/m\3\ respirable crystalline silica, and 44
deaths per 1,000 workers at the revised PEL (see Section VI, Final
Quantitative Risk Assessment and Significance of Risk, Table VI-1).\3\
---------------------------------------------------------------------------
\3\ The risk estimates for silicosis and NMRD are not directly
comparable, as the endpoint for the NMRD analysis (Park et al.,
2002, Document ID 0405) was death from all non-cancer lung diseases,
including silicosis, pneumoconiosis, emphysema, and chronic
bronchitis, whereas the endpoint for the silicosis analysis
(Mannetje et al., 2002b, Document ID 1089) was deaths coded as
silicosis or other pneumoconiosis only (Document ID 1711, pp. 297-
298).
---------------------------------------------------------------------------
For renal disease mortality, Steenland et al. (2002a, Document ID
0448) conducted a pooled analysis of three cohorts (with a total of
13,382 workers) that found a positive exposure-response relationship
for both multiple-cause mortality (i.e., any mention of renal disease
on the death certificate) and underlying cause mortality. OSHA used the
Steenland et al. (2002a, Document ID 0448) pooled analysis to estimate
risks, given its large number of workers from cohorts with sufficient
exposure data (see Section VI, Final Quantitative Risk Assessment and
Significance of Risk; Document ID 1711, pp. 314-315). OSHA's analysis
for renal disease mortality shows estimated lifetime excess risk of 39
deaths per 1,000 workers at the previous general industry PEL of 100
[micro]g/m\3\ respirable crystalline silica, and 32 deaths per 1,000
workers exposed at the revised PEL of 50 [micro]g/m\3\ (see Section VI,
Final Quantitative Risk Assessment and Significance of Risk, Table VI-
1). OSHA acknowledges, however, that there are considerably less data
for renal disease mortality, and thus the findings based on them are
less robust than those for silicosis, lung cancer, and NMRD mortality
(see Section VI, Final Quantitative Risk Assessment and Significance of
Risk; Document ID 1711, p. 229). For autoimmune disease, there were no
quantitative exposure-response data available for a quantitative risk
assessment (see Section VI, Final Quantitative Risk Assessment and
Significance of Risk; Document ID 1711, p. 229).
For silicosis morbidity, OSHA reviewed the principal studies
available in the scientific literature that have characterized the risk
to exposed workers of acquiring silicosis, as detected by the
appearance of opacities on chest radiographs (see Section VI, Final
Quantitative Risk Assessment and Significance of Risk; Document ID
1711, p. 357). The most reliable estimates of silicosis morbidity came
from five studies that evaluated radiographs over time, including after
workers left employment: The U.S. gold miner cohort studied by
Steenland and Brown (1995b, Document ID 0451); the Scottish coal miner
cohort studied by Buchanan et al. (2003, Document ID 0306); the Chinese
tin mining cohort studied by Chen et al. (2001, Document ID 0332); the
Chinese tin, tungsten, and pottery worker cohorts studied by Chen et
al. (2005, Document ID 0985); and the South African gold miner cohort
studied by Hnizdo and Sluis-Cremer (1993, Document ID 1052) (see
Section VI, Final Quantitative Risk Assessment and Significance of
Risk; Document ID 1711, pp. 316-343). These studies demonstrated
positive exposure-response relationships between exposure to
crystalline silica and silicosis risk. Based on the results of these
studies, OSHA estimates a cumulative risk for silicosis morbidity of
between 60 and 773 cases per 1,000 workers for a 45-year exposure to
the previous general industry PEL of 100 [micro]g/m\3\ respirable
crystalline silica depending upon the study used, and between 20 and
170 cases per 1,000 workers exposed at the new PEL of 50 [micro]g/m\3\
depending upon the study used (see Section VI, Final Quantitative Risk
Assessment and Significance of Risk, Table VI-1). Thus, like OSHA's
risk estimates for other health endpoints, the risk is substantially
lower, though still significant, at the revised PEL.
In conclusion, OSHA finds, based on the best available evidence and
methods to estimate quantitative risks of disease resulting from
exposure to respirable crystalline silica, that there are significant
risks of material health impairment at the former PELs for respirable
crystalline silica, which would be substantially reduced (but not
entirely eliminated) at the new PEL of 50 [mu]g/m\3\. In meeting its
legal burden to estimate the health risks posed by respirable
crystalline silica, OSHA has used the best available evidence and
methods to estimate quantitative risks of disease resulting from
exposure to respirable crystalline silica. As a result, the Agency
finds that the lifetime excess mortality risks (for lung cancer, NMRD
and silicosis, and renal disease) and cumulative risk (silicosis
morbidity) posed to workers exposed to respirable crystalline silica
over a working life represent significant risks that warrant
mitigation, and that these risks will be substantially reduced at the
revised PEL of 50 [mu]g/m\3\ respirable crystalline silica.
C. Summary of the Review of Health Effects Literature and Preliminary
QRA
As noted above, a wide variety of stakeholders offered comments and
testimony in this rulemaking on issues related to health and risk. Many
of these comments were submitted in response to OSHA's preliminary risk
and material impairment determinations, which were presented in two
background documents, entitled "Occupational Exposure to Respirable
Crystalline Silica--Review of Health Effects Literature and Preliminary
Quantitative Risk Assessment" (Document ID 1711) and "Supplemental
Literature Review of Epidemiological Studies on Lung Cancer Associated
with Exposure to Respirable Crystalline Silica" (Document ID 1711,
Attachment 1), and summarized in the proposal in Section V, Health
Effects Summary, and Section VI, Summary of OSHA's Preliminary
Quantitative Risk Assessment.
In this subsection, OSHA summarizes the major findings of the two
background documents. The Agency intends for this subsection to provide
the detailed background necessary to fully understand stakeholders'
comments and OSHA's responses.
1. Background
As noted above, OSHA's Review and Supplemental Review of Health
Effects Literature and Preliminary Quantitative Risk Assessment
(Document ID 1711; 1711, Attachment 1) were the result of the Agency's
extensive search and review of the peer-reviewed scientific literature
on the health effects of inhalation exposure to crystalline silica,
particularly silicosis, lung cancer and cancer at other sites, non-
malignant respiratory diseases (NMRD) other than silicosis, and renal
and autoimmune effects. The purposes of this detailed search and
scientific review were to determine the nature of the hazards presented
by exposure to respirable crystalline silica, and to evaluate whether
there was an adequate basis, with suitable data availability, for
quantitative risk assessment.
Much of the scientific evidence that describes the health effects
and risks associated with exposure to crystalline silica consisted of
epidemiological studies of worker populations; OSHA also reviewed
animal and in vitro studies. OSHA used a weight-of-evidence approach in
evaluating this evidence. Under this approach, OSHA evaluated the
relevant studies to determine their overall quality. Factors considered
in assessing the quality of studies included: (1) The size of the
cohort studied and the power of the study to detect a sufficiently low
level of disease risk; (2) the duration of follow-up of the study
population; (3) the potential for study bias (e.g., selection bias in
case-control studies or survivor effects in cross-sectional studies);
and (4) the adequacy of underlying exposure information for examining
exposure-response relationships. Studies were deemed suitable for
inclusion in OSHA's Preliminary Quantitative Risk Assessment (QRA)
where there was adequate quantitative information on exposure and
disease risks and the study was judged to be sufficiently high quality
according to these criteria.
Based upon this weight-of-evidence approach, OSHA preliminarily
determined that there is substantial evidence in the peer-reviewed
scientific literature that exposure to respirable crystalline silica
increases the risk of silicosis, lung cancer, other NMRD, and renal and
autoimmune effects. The Preliminary QRA indicated that, for silicosis
and NMRD mortality, lung cancer mortality, and renal disease mortality,
there is a significant risk at the previous PELs for respirable
crystalline silica, with excess lifetime risk estimates substantially
greater than 1 death per 1,000 workers as a result of exposure over a
working life (45 years, from age 20 to age 65). At the revised PEL of
50 [mu]g/m\3\ respirable crystalline silica, OSHA estimated that these
risks would be substantially reduced. Cumulative risk estimates for
silicosis morbidity were also well above 1 case per 1,000 workers at
the previous PELs, with a substantial reduction at the revised PEL.
2. Summary of the Review of Health Effects Literature
In its Review of Health Effects Literature, OSHA identified the
adverse health effects associated with the inhalation of respirable
crystalline silica (Document ID 1711). OSHA covered the following
topics: Silicosis (including relevant data from U.S. disease
surveillance efforts), lung cancer and cancer at other sites, non-
malignant respiratory diseases (NMRD) other than silicosis, renal and
autoimmune effects, and physical factors affecting the toxicity of
crystalline silica. Most of the evidence that described the health
risks associated with exposure to silica consisted of epidemiological
studies of worker populations; animal and in vitro studies on mode of
action and molecular toxicology were also described. OSHA focused
solely on those studies associated with airborne exposure to respirable
crystalline silica due to the lack of evidence of health hazards from
dermal or oral exposure. The review was further confined to issues
related to the inhalation of respirable dust, which is generally
defined as particles that are capable of reaching the pulmonary region
of the lung (i.e., particles less than 10 microns ([mu]m) in aerodynamic
diameter), in the form of either quartz or cristobalite, the two forms
of crystalline silica most often encountered in the workplace.
a. Silicosis
i. Types
Silicosis is an irreversible, progressive disease induced by the
inflammatory effects of respirable crystalline silica in the lung,
leading to lung damage and scarring and, in some cases, progressing to
complications resulting in disability and death. Exposure to respirable
crystalline silica is the only known cause of silicosis. Three types of
silicosis have been described: An acute form following intense exposure
to respirable dust of high crystalline silica content for a relatively
short period (i.e., a few months or years); an accelerated form,
resulting from about 5 to 15 years of heavy exposure to respirable
dusts of high crystalline silica content; and, most commonly, a chronic
form that typically follows less intense exposure of more than 20 years
(Becklake, 1994, Document ID 0294; Balaan and Banks, 1992, 0289). In
both the accelerated and chronic forms of the disease, lung
inflammation leads to the formation of excess connective tissue, or
fibrosis, in the lung. The hallmark of the chronic form of silicosis is
the silicotic islet or nodule, one of the few agent-specific lesions in
pathology (Balaan and Banks, 1992, Document ID 0289). As the disease
progresses, these nodules, or fibrotic lesions, increase in density and
can develop into large fibrotic masses, resulting in progressive
massive fibrosis (PMF). Once established, the fibrotic process of
chronic silicosis is thought to be irreversible (Becklake, 1994,
Document ID 0294). There is no specific treatment for silicosis (Davis,
1996, Document ID 0998; Banks, 2005, 0291).
Chronic silicosis is the most frequently observed type of silicosis
in the U.S. today. Affected workers may have a dry chronic cough,
sputum production, shortness of breath, and reduced pulmonary function.
These symptoms result from airway restriction and/or obstruction caused
by the development of fibrotic scarring in the alveolar sacs and lower
region of the lung. Prospective studies that follow the exposed cohort
over a long period of time with periodic examinations can provide the
best information on factors affecting the development and progression
of silicosis, which has a latency period (the interval between
beginning of exposure to silica and the onset of disease) from 10 to 30
years after first exposure (Weissman and Wagner, 2005; Document ID
0481).
ii. Diagnosis
The scarring caused by silicosis can be detected by chest x-ray or
computerized tomography (CT) when the lesions become large enough to
appear as visible opacities. The clinical diagnosis of silicosis has
three requirements: Recognition by the physician that exposure to
crystalline silica has occurred; the presence of chest radiographic
abnormalities consistent with silicosis; the absence of other illnesses
that could resemble silicosis on a chest radiograph (e.g., pulmonary
fungal infection or tuberculosis) (Balaan and Banks, 1992, Document ID
0289; Banks, 2005, 0291). A standardized system to classify opacities
seen in chest radiographs was developed by the International Labour
Organization (ILO) to describe the presence and severity of silicosis
on the basis of size, shape, and density of opacities, which together
indicate the severity and extent of lung involvement (ILO, 1980,
Document ID 1063; ILO, 2002, 1064; ILO, 2011, 1475; Merchant and
Schwartz, 1998, 1096; NIOSH, 2011, 1513). The density of opacities seen
on chest radiographs is classified on a 4-point category scale (0, 1,
2, or 3), with each category divided into three, giving a 12-
subcategory scale between 0/0 and 3/+. For each subcategory, the top
number indicates the major category that the profusion most closely
resembles, and the bottom number indicates the major category that was
given secondary consideration. Category 0 indicates the absence of
visible opacities and categories 1 to 3 reflect increasing profusion of
opacities and a concomitant increase in severity of disease. The bottom
number can deviate from the top number by 1. At the extremes of the
scale, a designation of 0/- or 3/+ may be used. Subcategory 0/-
represents a radiograph that is obviously absent of small opacities.
Subcategory 3/+ represents a radiograph that shows much greater
profusion than depicted on a standard 3/3 radiograph.
To address the low sensitivity of chest x-rays for detecting
silicosis, Hnizdo et al. (1993, Document ID 1050) recommended that
radiographs consistent with an ILO category of 0/1 or greater be
considered indicative of silicosis among workers exposed to a high
concentration of silica-containing dust. In like manner, to maintain
high specificity, chest x-rays classified as category 1/0 or 1/1 should
be considered as a positive diagnosis of silicosis. A biopsy is not
necessary to make a diagnosis and a diagnosis does not require that
chest x-ray films or digital radiographic images be rated using the ILO
system (NIOSH, 2002, Document ID 1110).
iii. Review of Occupation-Based Epidemiological Studies
The causal relationship between exposure to crystalline silica and
silicosis has long been accepted in the scientific and medical
communities. OSHA reviewed a large number of cross-sectional and
retrospective studies conducted to estimate the quantitative
relationship between exposure to crystalline silica and the development
of silicosis (e.g., Kreiss and Zhen, 1996, Document ID 1080; Love et
al., 1999, 0369; Ng and Chan, 1994, 0382; Rosenman et al., 1996, 0423;
Churchyard et al., 2003, 1295; Churchyard et al., 2004, 0986; Hughes et
al., 1998, 1059; Muir et al., 1989a, 1102; Muir et al., 1989b, 1101;
Park et al., 2002, 0405; Chen et al., 2001, 0332; Chen et al., 2005,
0985; Hnizdo and Sluis-Cremer, 1993, 1052; Miller et al., 1998, 0374;
Buchanan et al., 2003, 0306; Steenland and Brown, 1995b, 0451). In
general, these studies, particularly those that included retirees,
found a risk of radiological silicosis (usually defined as x-ray films
classified as ILO major category 1 or greater) among workers exposed
near the range of cumulative exposures permitted by current exposure
limits. The studies' methods and findings are presented in detail in
the Preliminary QRA (Document ID 1711, pp. 316-340); those studies on
which OSHA relied for its risk estimates are also discussed in the
Summary of the Preliminary QRA, below.
OSHA's review of the silicosis literature also focused on specific
issues associated with the factors that affect the progression of the
disease and the relationship between the appearance of radiological
abnormalities indicative of silicosis and pulmonary function decline.
From its review of the health literature, OSHA made a number of
preliminary findings. First, the size of opacities apparent on initial
x-ray films is a determinant of future disease progression, with subjects
exhibiting large opacities more likely to experience progression than
those having smaller opacities (Hughes et al., 1982, Document
ID 0362; Lee et al., 2001, 1086; Ogawa et al., 2003, 0398).
Second, continued exposure to respirable crystalline silica
following diagnosis of radiological silicosis increases the
probability of disease progression compared to those who are not
further exposed (Hessel et al., 1988, Document ID 1042), although there
remains a likelihood of progression even absent continued exposure
(Hessel et al., 1988, Document ID 1042; Miller et al., 1998, 0374;
Ogawa et al., 2003, 0398; Yang et al., 2006, 1134).
With respect to the relationship between radiological silicosis and
pulmonary function declines, literature findings are mixed. A number of
studies have reported pulmonary function declines among workers
exhibiting a degree of small-opacity profusion consistent with ILO
categories 2 and 3 (e.g., Ng and Chan, 1992, Document ID 1107).
However, although some studies have not found pulmonary function
declines associated with silicosis scored as ILO category 1, a number
of other studies have documented declines in pulmonary function in
persons exposed to silica and whose radiograph readings are in the
major ILO category 1 (i.e., 1/0, 1/1, 1/2), or even before changes were
seen on chest x-ray (Cowie, 1998, 0993; Cowie and Mabena, 1991, 0342;
Ng et al., 1987(a), 1108; Wang et al., 1997, 0478). Thus, OSHA
preliminarily concluded that at least some individuals will develop
pulmonary function declines absent radiological changes indicative of
silicosis. The Agency posited that this may reflect the relatively poor
sensitivity of x-ray films in detecting silicosis or may be due to
pulmonary function declines related to silica-induced chronic
obstructive pulmonary disease (see Document ID 1711, pp. 49-75).
iv. Surveillance
Unlike most occupational diseases, surveillance statistics are
available on silicosis mortality and morbidity in the U.S. The most
comprehensive and current source of surveillance data in the U.S.
related to occupational lung diseases, including silicosis, is the
National Institute for Occupational Safety and Health (NIOSH) Work-
Related Lung Disease (WoRLD) Surveillance System (NIOSH, 2008c,
Document ID 1308). Other sources are detailed in the Review of Health
Effects Literature (Document ID 1711). Mortality data are compiled from
death certificates reported to state vital statistics offices, which
are collected by the National Center for Health Statistics (NCHS), an
agency within the Centers for Disease Control and Prevention (e.g.,
CDC, 2005, Document ID 0319).
Silicosis-related mortality has declined in the U.S. over the time
period for which these data have been collected. From 1968 to 2005, the
annual number of silicosis deaths decreased from 1,157 to 161 (NIOSH,
2008c, Document ID 1308; http://wwwn.cdc.gov/eworld). The CDC cited two
main factors that were likely responsible for the declining trend in
silicosis mortality since 1968 (CDC, 2005, Document ID 0319). First,
many deaths during the early part of the study period were among
workers whose main exposure to respirable crystalline silica probably
occurred before introduction of national silica standards established
by OSHA and the Mine Safety and Health Administration (MSHA) (i.e.,
permissible exposure limits (PELs)); these standards likely led to
reduced silica dust exposure beginning in the 1970s. Second, employment
has declined in heavy industries (e.g., foundries) where silica
exposure was prevalent (CDC, 2005, Document ID 0319).
Despite this decline, silicosis deaths among workers of all ages
result in significant premature mortality; between 1996 and 2005, a
total of 1,746 deaths resulted in a total of 20,234 years of life lost
from life expectancy, with an average of 11.6 years of life lost. For
the same period, among 307 decedents who died before age 65 (the end of
a working life), there were 3,045 years of life lost up to age 65, with
an average of 9.9 years of life lost from a working life (NIOSH, 2008c,
Document ID 1308).
Surveillance data on silicosis morbidity, primarily from hospital
discharge records, are available only from the few states that have
administered disease surveillance programs for silicosis. For the
reporting period 1993-2002, these states recorded 879 cases of
silicosis (NIOSH 2008c, Document ID 1308). Nationwide hospital
discharge data compiled by NIOSH (2008c, Document ID 1308) and the
Council of State and Territorial Epidemiologists (CSTE, 2005, Document
ID 0996) indicate that, for the years 1970 to 2004, there were at least
1,000 hospitalizations that were coded for silicosis each year, except
one.
Relying exclusively on such passive case-based disease surveillance
systems that depend on the health care community to generate records is
likely to understate the prevalence of diseases associated with
respirable crystalline silica (Froines et al., 1989, Document ID 0385).
In order to diagnose occupational diseases, health care professionals
must have information about occupational histories and must be able to
recognize occupational diseases (Goldman and Peters, 1981, Document ID
1027; Rutstein et al., 1983, 0425). The first criterion to be met in
diagnosing silicosis is knowing a patient's history of exposure to
crystalline silica. In addition to the lack of information about
exposure histories, difficulty in recognizing occupational illnesses
like silicosis, that manifest themselves long after initial exposure,
contributes to under-recognition and underreporting by health care
providers. Based on an analysis of data from Michigan's silicosis
surveillance activities, Rosenman et al. (2003, Document ID 0420)
estimated that silicosis mortality and morbidity were understated by a
factor of between 2.5 and 5, and estimated that between 3,600 and 7,300
new cases of silicosis likely occurred in the U.S. annually between
1987 and 1996.
b. Lung Cancer
i. International Agency for Research on Cancer (IARC)
Classification
In 1997, the IARC determined that there was sufficient evidence to
regard crystalline silica as a human carcinogen (IARC, 1997, Document
ID 1062). This finding was based largely on nine studies of cohorts in
four industry sectors that IARC considered to be the least influenced
by confounding factors (sectors included quarries and granite works,
gold mining, ceramic/pottery/refractory brick industries, and the
diatomaceous earth industry). NIOSH also determined that crystalline
silica is a human carcinogen after evaluating updated literature (2002,
Document ID 1110).
ii. Review of Occupation-Based Epidemiological Studies
OSHA conducted an independent review of the epidemiological
literature on exposure to respirable crystalline silica and lung
cancer, covering more than 30 occupational groups in over a dozen
industrial sectors. OSHA's review included approximately 60 primary
epidemiological studies. Based on this review, OSHA preliminarily
concluded that the human data provides ample evidence that exposure to
respirable crystalline silica increases the risk of lung cancer among
workers.
The strongest evidence for carcinogenicity came from studies in
five industry sectors:
Diatomaceous Earth Workers (Checkoway et al., 1993,
Document ID 0324; Checkoway et al., 1996, 0325; Checkoway et al., 1997,
0326;
Checkoway et al., 1999, 0327; Seixas et al., 1997, 0431);
British Pottery Workers (Cherry et al., 1998, Document ID
0335; McDonald et al., 1995, 0371);
Vermont Granite Workers (Attfield and Costello, 2004,
Document ID 0285; Graham et al., 2004, 1031; Costello and Graham, 1988,
0991; Davis et al., 1983, 0999);
North American Industrial Sand Workers (Hughes et al.,
2001, Document ID 1060; McDonald et al., 2001, 1091; McDonald et al.,
2005, 1092; Rando et al., 2001, 0415; Sanderson et al., 2000, 0429;
Steenland and Sanderson, 2001, 0455); and
British Coal Miners (Miller et al., 2007, Document ID
1305; Miller and MacCalman, 2009, 1306).
OSHA considered these studies as providing the strongest evidence
for several reasons. They were all retrospective cohort or case-control
studies that demonstrated positive, statistically significant exposure-
response relationships between exposure to crystalline silica and lung
cancer mortality. Except for the British pottery studies, where
exposure-response trends were noted for average exposure only, lung
cancer risk was found to be related to cumulative exposure. In general,
these studies were of sufficient size and had adequate years of follow
up, and had sufficient quantitative exposure data to reliably estimate
exposures of cohort members. As part of their analyses, the authors of
these studies also found positive exposure-response relationships for
silicosis, indicating that underlying estimates of worker exposures
were not likely to be substantially misclassified. Furthermore, the
authors of these studies addressed potential confounding due to other
carcinogenic exposures through study design or data analysis.
In the diatomaceous earth industry, Checkoway et al. developed a
"semi-quantitative" cumulative exposure estimate that demonstrated a
statistically significant positive exposure-response trend between
duration of employment or cumulative exposure and lung cancer mortality
(1993, Document ID 0324). The quartile analysis with a 15-year lag
showed an increasing trend in relative risks (RR) of lung cancer
mortality, with the highest exposure quartile having a RR of 2.74 for
lung cancer mortality. Checkoway et al. conducted a re-analysis to
address criticisms of potential confounding due to asbestos and again
demonstrated a positive exposure-response risk gradient when
controlling for asbestos exposure and other variables (1996, Document
ID 0325). Rice et al. (2001, Document ID 1118) conducted a re-analysis
and quantitative risk assessment of the Checkoway et al. (1997,
Document ID 0326) study, finding that exposure to crystalline silica
was a significant predictor of lung cancer mortality. OSHA included
this re-analysis in its Preliminary QRA (Document ID 1711).
In the British pottery industry, excess lung cancer risk was found
to be associated with crystalline silica exposure among workers in a
proportionate mortality ratio (PMR) study \4\ (McDonald et al., 1995,
Document ID 0371) and in a cohort and nested case-control study \5\
(Cherry et al., 1998, Document ID 0335). In the former, elevated PMRs
for lung cancer were found after adjusting for potential confounding by
asbestos exposure. In the study by Cherry et al., odds ratios for lung
cancer mortality were statistically significantly elevated after
adjusting for smoking. Odds ratios were related to average, but not
cumulative, exposure to crystalline silica.
---------------------------------------------------------------------------
\4\ A PMR is the number of deaths within a population due to a
specific disease (e.g., lung cancer) divided by the total number of
deaths in the population during some time period.
\5\ A cohort study is a study in which the occurrence of disease
(e.g., lung cancer) is measured in a cohort of workers with
potential for a common exposure (e.g., silica). A nested case-
control study is a study in which workers with disease are
identified in an occupational cohort, and a control group consisting
of workers without disease is selected (independently of exposure
status) from the same cohort to determine whether there is a
difference in exposure between cases and controls. A number of
controls are matched to each case to control for potentially
confounding factors, such as age, gender, etc.
---------------------------------------------------------------------------
In the Vermont granite cohort, Costello and Graham (1988, Document
ID 0991) and Graham et al. (2004, Document ID 1031) in a follow-up
study found that workers employed prior to 1930 had an excess risk of
lung cancer. Lung cancer mortality among granite workers hired after
1940 (post-implementation of controls), however, was not elevated in
the Costello and Graham study and was only somewhat elevated (not
statistically significant) in the Graham et al. study. Graham et al.
(2004, Document ID 1031) concluded that their results did not support a
causal relationship between granite dust exposure and lung cancer
mortality.
Looking at the same population, Attfield and Costello (2004,
Document ID 0285) developed a quantitative estimate of cumulative
exposure (8 exposure categories) adapted from a job exposure matrix
developed by Davis et al. (1983, Document ID 0999). They found a
statistically significant trend between lung cancer mortality and log-
transformed cumulative exposure to crystalline silica. Lung cancer
mortality rose reasonably consistently through the first seven
increasing exposure groups, but fell in the highest cumulative exposure
group. With the highest exposure group omitted, a strong positive dose-
response trend was found for both untransformed and log-transformed
cumulative exposures. The authors explained that the highest exposure
group would have included the most unreliable exposure estimates being
reconstructed from exposures 20 years prior to study initiation when
exposure estimation was less precise. OSHA expressed its belief that
the study by Attfield and Costello (2004, Document ID 0285) was of
superior design in that it used quantitative estimates of exposure and
evaluated lung cancer mortality rates by exposure group. In contrast,
the findings by Graham et al. (2004, Document ID 1031) were based on a
dichotomous comparison of risk among high- versus low-exposure groups,
where date-of-hire before and after implementation of ventilation
controls was used as a surrogate for exposure. Consequently, OSHA used
the Attfield and Costello study in its Preliminary QRA (Document ID
1711). In its Supplemental Literature Review of Epidemiological Studies
on Lung Cancer Associated with Exposure to Respirable Crystalline
Silica, OSHA also discussed a more recent study of Vermont granite
workers by Vacek et al. (2011, Document ID 1486) that did not find an
association between silica exposure and lung cancer mortality (Document
ID 1711, Attachment 1, pp. 2-5). (OSHA examines this study in great
length in Section V.F, Comments and Responses Concerning Lung Cancer
Mortality.)
In the North American industrial sand industry, studies of two
overlapping cohorts found a statistically significant increased risk of
lung cancer mortality with increased cumulative exposure in both
categorical and continuous analyses (Hughes et al., 2001, Document ID
1060; McDonald et al., 2001, 1091; McDonald et al., 2005, 1092; Rando
et al., 2001, 0415; Sanderson et al., 2000, 0429; Steenland and
Sanderson, 2001, 0455). McDonald et al. (2001, Document ID 1091)
examined a cohort that entered the workforce, on average, a decade
earlier than the cohorts that Steenland and Sanderson (2001, Document
ID 0455) examined. The McDonald cohort, drawn from eight plants, had
more years of exposure in the industry (19 versus 8.8 years). The
Steenland and Sanderson (2001, Document ID 0455) cohort worked in 16
plants, 7 of which overlapped with the McDonald, et al.
(2001, Document ID 1091) cohort. McDonald et al. (2001, Document ID
1091), Hughes et al. (2001, Document ID 1060), and Rando et al. (2001,
Document ID 0415) had access to smoking histories, plant records, and
exposure measurements that allowed for historical reconstruction and
the development of a job exposure matrix. The McDonald et al. (2005,
Document ID 1092) study was a later update, with follow-up through
2000, of both the cohort and nested case-control studies. Steenland and
Sanderson (2001, Document ID 0455) had limited access to plant
facilities, less detailed historic exposure data, and used MSHA
enforcement records for estimates of recent exposure. These studies
(Hughes et al., 2001, Document ID 1060; McDonald et al., 2005, 1092;
Steenland and Sanderson, 2001, 0455) showed very similar exposure-
response patterns of increased lung cancer mortality with increased
exposure. OSHA included the quantitative exposure-response analysis
from the Hughes et al. (2001, Document ID 1060) study in its
Preliminary QRA, as it allowed for individual job, exposure, and
smoking histories to be taken into account.
OSHA noted that Brown and Rushton (2005a, Document ID 0303; 2005b,
0304) found no association between risk of lung cancer mortality and
exposure to respirable crystalline silica among British industrial sand
workers. However, a large portion of the cohort had relatively short
service times in the industry, with over one-half the cohort deaths and
almost three-fourths of the lung cancer mortalities having had less
than 10 years of service. Considering the apparent high turnover in
this industry and the absence of prior occupational histories,
exposures from work experience other than in the industrial sand
industry could be a significant confounder (Document ID 1711, p. 131).
Additionally, as Steenland noted in a letter review (2005a, Document ID
1313), the cumulative exposures of workers in the Brown and Ruston
(2005b, Document ID 0304) study were over 10 times lower than the
cumulative exposures experienced by the cohorts in the pooled analysis
that Steenland et al. (2001a, Document ID 0452) performed. The low
exposures experienced by this cohort would have made detecting a
positive association with lung cancer mortality even more difficult.
In British coal miners, excess lung cancer mortality was reported
in a large cohort study, which examined the mortality experience of
17,800 miners through the end of 2005 (Miller et al., 2007, Document ID
1305; Miller and MacCalman, 2009, 1306). By that time, the cohort had
accumulated 516,431 person years of observation (an average of 29 years
per miner), with 10,698 deaths from all causes. Overall lung cancer
mortality was elevated (SMR = 115.7, 95% C.I. 104.8-127.7), and a
positive exposure-response relationship with crystalline silica
exposure was determined from Cox regression after adjusting for smoking
history. Three of the strengths of this study were the detailed time-
exposure measurements of both quartz and total mine dust, detailed
individual work histories, and individual smoking histories. For lung
cancer, analyses based on Cox regression provided strong evidence that,
for these coal miners, although quartz exposures were associated with
increased lung cancer risk, simultaneous exposures to coal dust did not
cause increased lung cancer risk. Because of these strengths, OSHA
included this study in its Preliminary QRA (Document ID 1711).
In addition to the studies in these cohorts, OSHA also reviewed
studies of lung cancer mortality in metal ore mining populations. Many
of these mining studies, which showed mixed results, were subject to
confounding due to exposure to other potential carcinogens such as
radon and arsenic. IARC noted that only a few ore mining studies
accounted for confounding from other occupational carcinogens and that,
when confounding was absent or accounted for, an association between
silica exposure and lung cancer was absent (1997, Document ID 1062).
Many of the studies conducted since IARC's review, however, more
strongly implicate crystalline silica as a human carcinogen (1997,
Document ID 1062). Pelucchi et al. (2006, Document ID 0408), in a meta-
analysis of studies conducted since IARC's (1997, Document ID 1062)
review, reported statistically significantly elevated relative risks of
lung cancer mortality in underground and surface miners in three cohort
and four case-control studies. Cassidy et al., in a pooled case-control
analysis, showed a statistically significant increased risk of lung
cancer mortality among miners (OR = 1.48), and demonstrated a linear
trend of increasing odds ratios with increasing exposures (2007,
Document ID 0313).
OSHA also preliminarily determined that the results of the studies
conducted in three industry sectors (foundry, silicon carbide, and
construction sectors) were confounded by the presence of exposures to
other carcinogens. Exposure data from these studies were not sufficient
to distinguish between exposure to silica dust and exposure to other
occupational carcinogens. IARC previously made a similar determination
in reference to the foundry industry. However, with respect to the
construction industry, Cassidy et al. (2007, Document ID 0313), in a
large European community-based case-control study, reported finding a
clear linear trend of increasing odds ratios with increasing cumulative
exposure to crystalline silica (estimated semi-quantitatively) after
adjusting for smoking and exposure to insulation and wood dusts.
In addition, an analysis of 4.8 million death certificates from 27
states within the U.S. for the years 1982 to 1995 showed statistically
significant excesses in lung cancer mortality, silicosis mortality,
tuberculosis, and NMRD among persons with occupations involving medium
and high exposure to respirable crystalline silica (Calvert et al.,
2003, Document ID 0309). A national records and death certificate study
was also conducted in Finland by Pukkala et al., who found a
statistically significant excess of lung cancer incidence among men and
women with estimated medium and heavy exposures (2005, Document ID
0412).
One of the more compelling studies OSHA evaluated and used in the
Preliminary QRA (Document ID 1711) was Steenland et al.'s (2001a,
Document ID 0452) pooled analysis of 10 occupational cohorts (5 mines
and 5 industrial facilities), which demonstrated an overall positive
exposure-response relationship between cumulative exposure to
crystalline silica and lung cancer mortality. These 10 cohorts included
65,980 workers and 1,072 lung cancer deaths, and were selected because
of the availability of raw data on exposure to crystalline silica and
health outcomes. The investigators found lung cancer risk increased
with increasing cumulative exposure, log cumulative exposure, and
average exposure. Exposure-response trends were similar between mining
and non-mining cohorts.
iii. Confounding
Smoking is known to be a major risk factor for lung cancer.
However, OSHA maintained in the Preliminary QRA that it is unlikely
that smoking explained the observed exposure-response trends in the
studies described above (Document ID 1711). Studies by Hnizdo et al.
(1997, Document ID 1049), McLaughlin et al. (1992, Document ID 0372),
Hughes et al. (2001, Document ID 1060), McDonald et al. (2001, Document
ID 1091; 2005, 1092), Miller and MacCalman (2009, Document ID 1306),
and Cassidy et al. (2007, Document ID 0313) had detailed smoking
histories with sufficiently large populations and a sufficient
number of years of follow-up time to quantify the interaction
between crystalline silica exposure and cigarette smoking.
In a cohort of white South African gold miners (Hnizdo and
Sluis-Cremer, 1991, Document ID 1051) and in the follow-up nested
case-control study (Hnizdo et al., 1997, Document ID 1049), the
combined effect of exposure to respirable crystalline silica and
smoking was greater than additive, suggesting a multiplicative effect.
This effect appeared to be greatest for miners with greater than 35
pack-years of smoking and higher cumulative exposure to silica. In the
Chinese nested case-control studies (McLaughlin et al., 1992, Document
ID 0372), cigarette smoking was associated with lung cancer, but
control for smoking did not influence the association between silica
and lung cancer in the mining and pottery cohorts studied. The studies
of industrial sand workers (Hughes et al., 2001, Document ID 1060) and
British coal workers (Miller and MacCalman, 2009, Document ID 1306)
found positive exposure-response trends after adjusting for smoking
histories, as did Cassidy et al. (2007, Document ID 0313) in their
community-based case-control study of exposed European workers.
Given these findings of investigators who have accounted for the
impact of smoking, OSHA preliminarily determined that the weight of the
evidence reviewed identified respirable crystalline silica as an
independent risk factor for lung cancer mortality. OSHA also determined
that its finding was further supported by animal studies demonstrating
that exposure to silica alone can cause lung cancer (e.g., Muhle et
al., 1995, Document ID 0378).
iv. Lung Cancer and Silicosis
Animal and in vitro studies have demonstrated that the early steps
in the proposed mechanistic pathways that lead to silicosis and lung
cancer seem to share some common features (see Document ID 1711, pp.
171-172). This has led some researchers to suggest that silicosis is a
prerequisite to lung cancer. Some have suggested that any increased
lung cancer risk associated with silica may be a consequence of
inflammation (and concomitant oxidative stress) and increased
epithelial cell proliferation associated with the development of
silicosis. However, other researchers have noted additional genotoxic
and non-genotoxic mechanisms that may also be involved in
carcinogenesis induced by silica (see Section V.H, Mechanisms of
Silica-Induced Adverse Health Effects, and Document ID 1711, pp. 230-
239). IARC also noted that a direct genotoxic mechanism from silica to
induce a carcinogenic effect cannot be ruled out (2012, Document ID
1473). Thus, OSHA preliminarily concluded that available animal and in
vitro studies do not support the hypothesis that development of
silicosis is necessary for silica exposure to cause lung cancer.
In general, studies of workers with silicosis, as well as meta-
analyses that include these studies, have shown that workers with
radiologic evidence of silicosis have higher lung cancer risk than
those without radiologic abnormalities or mixed cohorts. Three meta-
analyses attempted to look at the association of increasing ILO
radiographic categories of silicosis with increasing lung cancer
mortality. Two of these analyses (Kurihara and Wada, 2004, Document ID
1084; Tsuda et al., 1997, 1127) showed no association with increasing
lung cancer mortality, while Lacasse et al. (2005, Document ID 0365)
demonstrated a positive dose-response for lung cancer with increasing
ILO radiographic category. A number of other studies found increased
lung cancer risk among exposed workers absent radiological evidence of
silicosis (Cassidy et al., 2007, Document ID 0313; Checkoway et al.,
1999, 0327; Cherry et al., 1998, 0335; Hnizdo et al., 1997, 1049;
McLaughlin et al., 1992, 0372). For example, the diatomaceous earth
study by Checkoway et al. showed a statistically significant exposure-
response relationship for lung cancer among persons without silicosis
(1999, Document ID 0327). Checkoway and Franzblau, reviewing the
international literature, found that all epidemiological studies
conducted to that date were insufficient to conclusively determine the
role of silicosis in the etiology of lung cancer (2000, Document ID
0323). OSHA preliminarily concluded that the more recent pooled and
meta-analyses do not provide compelling evidence that silicosis is a
necessary precursor to lung cancer.
c. Non-Malignant Respiratory Diseases (Other Than Silicosis)
In addition to causing silicosis, exposure to crystalline silica
has been associated with increased risks of other non-malignant
respiratory diseases (NMRD), primarily chronic obstructive pulmonary
disease (COPD), chronic bronchitis, and emphysema. COPD is a disease
state characterized by airflow limitation that is usually progressive
and not fully reversible. In patients with COPD, either chronic
bronchitis or emphysema may be present or both conditions may be
present together.
As detailed in the Review of Health Effects Literature, OSHA
reviewed several studies of NMRD morbidity and preliminarily concluded
that exposure to respirable crystalline silica may increase the risk of
emphysema, chronic bronchitis, and pulmonary function impairment,
regardless of whether signs of silicosis are present (Document ID
1711). Smokers may be at an increased risk relative to nonsmokers.
OSHA also reviewed studies of NMRD mortality that focused on causes
of death other than silicosis. Wyndham et al. found a significant
excess mortality for chronic respiratory diseases in a cohort of white
South African gold miners (1986, Document ID 0490). A case-referent
analysis found that, although the major risk factor for chronic
respiratory disease was smoking, there was a statistically significant
additional effect of cumulative exposure to silica-containing dust. A
multiplicative effect of smoking and cumulative dust exposure on
mortality from COPD was found in another study of white South African
gold miners (Hnizdo, 1990, Document ID 1045). Analysis of various
combinations of dust exposure and smoking found a trend in odds ratios
that indicated this synergism. There was a statistically significant
increasing trend for dust particle-years and for cigarette-years of
smoking.
Park et al. (2002, Document ID 0405) analyzed the California
diatomaceous earth cohort data originally studied by Checkoway et al.
(1997, Document ID 0326), consisting of 2,570 diatomaceous earth
workers employed for 12 months or more from 1942 to 1994, to quantify
the relationship between exposure to cristobalite and mortality from
chronic lung disease other than cancer (LDOC). Diseases in this
category included pneumoconiosis (which included silicosis), chronic
bronchitis, and emphysema, but excluded pneumonia and other infectious
diseases. Smoking information was available for about 50 percent of the
cohort and for 22 of the 67 LDOC deaths available for analysis,
permitting at least partial adjustment for smoking. Using the exposure
estimates developed for the cohort by Rice et al. (2001, Document ID
1118) in their exposure-response study of lung cancer risks, Park et
al. (2002, Document 0405) evaluated the quantitative exposure-response
relationship for LDOC mortality and found a strong positive
relationship with exposure to respirable crystalline silica. OSHA found
this study particularly compelling because of the strengths of the
study design and availability of smoking history data on part of the
cohort, as well as the high-quality exposure and job history data.
The study authors noted:
Data on smoking, collected since the 1960s in the company's
radiographic screening programme, were available for 1171 of the
subjects (50%). However, smoking habits were unknown for 45 of the
67 workers that died from LDOC (67%). Our Poisson regression
analyses for LDOC, stratified on smoking, have partially rectified
the confounding by smoking issue. Furthermore, analyses performed
without control for smoking produced slightly smaller and less
precise estimates of the effects of silica, suggesting that smoking
is a negative confounder. In their analysis of this cohort,
Checkoway et al. applied the method of Axelson concluding that it
was very unlikely that cigarette smoking could account for the
association found between mortality from LDOC and cumulative
exposure to silica (Document ID 0405, p. 41).
Consequently, OSHA used this study in its Preliminary QRA (Document
ID 1711, pp. 295-298).
Based on this evidence, and the other studies discussed in the
Review of Health Effects Literature, OSHA preliminarily concluded that
respirable crystalline silica increases the risk for mortality from
non-malignant respiratory disease (not including silicosis) in an
exposure-related manner. The Agency also preliminarily concluded that
the risk is strongly influenced by smoking, and opined that the effects
of smoking and silica exposure may be synergistic.
d. Renal Disease and Autoimmune Diseases
In its Review of Health Effects Literature, OSHA described the
available experimental and epidemiological data evaluating respirable
crystalline silica exposure and renal and/or autoimmune effects
(Document ID 1711). In addition to a number of case reports,
epidemiological studies have found statistically significant
associations between occupational exposure to silica dust and chronic
renal disease (Calvert et al., 1997, Document ID 0976), subclinical
renal changes (Ng et al., 1992c, Document ID 0386), end-stage renal
disease morbidity (Steenland et al., 1990, Document ID 1125), chronic
renal disease mortality (Steenland et al., 2001b, Document ID 0456;
2002a, 0448), and granulomatosis with polyangitis, a condition that can
affect the kidneys (Nuyts et al., 1995, Document ID 0397). In other
findings, silica-exposed individuals, both with and without silicosis,
had an increased prevalence of abnormal renal function (Hotz et al.,
1995, Document ID 0361), and renal effects have been reported to
persist after cessation of silica exposure (Ng et al., 1992c, Document
ID 0386). Possible mechanisms suggested for silica-induced renal
disease include a direct toxic effect on the kidney, deposition of
immune complexes (IgA) in the kidney following silica related pulmonary
inflammation, and an autoimmune mechanism (Calvert et al., 1997,
Document ID 0976; Gregorini et al., 1993, 1032).
In a pooled cohort analysis, Steenland et al. (2002a, Document ID
0448) combined the industrial sand cohort from Steenland et al. (2001b,
Document ID 0456), the gold mining cohort from Steenland and Brown
(1995a, Document ID 0450), and the Vermont granite cohort studies by
Costello and Graham (1988, Document ID 0991). In all, the combined
cohort consisted of 13,382 workers with exposure information available
for 12,783. The analysis demonstrated statistically significant
exposure-response trends for acute and chronic renal disease mortality
with quartiles of cumulative exposure to respirable crystalline silica.
In a nested case-control study design, a positive exposure-response
relationship was found across the three cohorts for both multiple-cause
mortality (i.e., any mention of renal disease on the death certificate)
and underlying cause mortality. Renal disease risk was most prevalent
among workers with cumulative exposures of 500 [micro]g/m\3\ or more
(Steenland et al., 2002a, Document ID 0448).
OSHA noted that other studies failed to find an excess renal
disease risk among silica-exposed workers. Davis et al. (1983, Document
ID 0999) found elevated, but not statistically significant, mortality
from diseases of the genitourinary system among Vermont granite shed
workers. There was no observed relationship between mortality from this
cause and cumulative exposure. A similar finding was reported by
Koskela et al. (1987, Document ID 0363) among Finnish granite workers,
where there were 4 deaths due to urinary tract disease compared to 1.8
expected. Both Carta et al. (1994, Document ID 0312) and Cocco et al.
(1994, Document ID 0988) reported finding no increased mortality from
urinary tract disease among workers in an Italian lead mine and zinc
mine. However, Cocco et al. (1994, Document ID 0988) commented that
exposures to respirable crystalline silica were low, averaging 7 and 90
[micro]g/m\3\ in the two mines, respectively, and that their study in
particular had low statistical power to detect excess mortality.
OSHA expressed its belief that there is substantial evidence,
particularly the 3-cohort pooled analysis conducted by Steenland et al.
(2002a, Document ID 0448), on which to base a finding that exposure to
respirable crystalline silica increases the risk of renal disease
mortality and morbidity. The pooled analysis by Steenland et al.
involved a large number of workers from three cohorts with well-
documented, validated job-exposure matrices; it found a positive,
monotonic increase in renal disease risk with increasing exposure for
both underlying and multiple cause data (2002a, Document ID 0448).
However, there are considerably less data available for renal disease
than there are for silicosis mortality and lung cancer mortality. The
findings based on these data are, therefore, less robust. Nevertheless,
OSHA preliminarily concluded that the underlying data are sufficient to
provide useful estimates of risk and included the Steenland et al.
(2002a, Document ID 0448) analysis in its Preliminary QRA.
For autoimmune effects, OSHA reviewed epidemiological information
suggesting an association between respirable silica exposure and
autoimmune diseases, including scleroderma (Sluis-Cremer et al., 1985,
Document ID 0439), rheumatoid arthritis (Klockars et al., 1987,
Document ID 1075; Rosenman and Zhu, 1995, 0424), and systemic lupus
erythematosus (Brown et al., 1997, Document ID 0974). However, there
were no quantitative exposure-response data available on which to base
a quantitative risk assessment for autoimmune diseases.
e. Physical Factors Affecting Toxicity of Crystalline Silica
OSHA also examined evidence on the comparative toxicity of the
silica polymorphs (quartz, cristobalite, and tridymite). A number of
animal studies appear to suggest that cristobalite and tridymite are
more toxic to the lung than quartz and more tumorigenic (e.g., King et
al., 1953, Document ID 1072; Wagner et al., 1980, 0476). However, in
contrast to these findings, several authors have reviewed the studies
done in this area and concluded that cristobalite and tridymite are not
more toxic than quartz (e.g., Bolsaitis and Wallace, 1996, Document ID
0298; Guthrie and Heaney, 1995, 1035). Furthermore, a difference in
toxicity between cristobalite and quartz has not been observed in
epidemiological studies (tridymite has not been studied) (NIOSH, 2002,
Document ID 1110). In an analysis of exposure-response for lung cancer,
Steenland et al. found similar exposure-response trends between
cristobalite-exposed workers and other cohorts exposed to quartz
(2001a, Document ID 0452).
OSHA also discussed other physical factors that may influence the
toxicologic potency of crystalline silica. A number of animal studies
compared the toxicity of freshly fractured silica to that of aged
silica (Porter et al., 2002, Document ID 1114; Shoemaker et al., 1995,
0437; Vallyathan et al., 1995, 1128). These studies have demonstrated
that although freshly fractured silica is more toxic than aged silica,
aged silica still retains significant toxicity. There have been no
studies comparing workers exposed to freshly fractured silica to those
exposed to aged silica. However, similarities between the results of
animal and human studies involving freshly fractured silica suggest
that the animal studies involving aged silica may also apply to humans.
For example, studies of workers exposed to freshly fractured silica
have demonstrated that these workers exhibit the same cellular effects
as seen in animals exposed to freshly fractured silica (Castranova et
al., 1998, Document ID 1294; Goodman et al., 1992, 1029). Animal
studies also suggest that pulmonary reactions of rats to short-duration
exposure to freshly fractured silica mimic those seen in acute
silicosis in humans (Vallyathan et al., 1995, Document ID 1128).
Surface impurities, particularly metals, have been shown to alter
silica toxicity. Iron, depending on its state and quantity, has been
shown to either increase or decrease toxicity (see Document ID 1711,
pp. 247-258). Aluminum has been shown to decrease toxicity (Castranova
et al., 1997, Document ID 0978; Donaldson and Borm, 1998, 1004; Fubini,
1998, 1016). Silica coated with aluminosilicate clay exhibits lower
toxicity, possibly as a result of reduced bioavailability of the silica
particle surface (Donaldson and Borm, 1998, Document ID 1004; Fubini,
1998, 1016). Aluminum as well as other metal ions are thought to modify
silanol groups on the silica surface, thus decreasing the membranolytic
and cytotoxic potency and resulting in enhanced particle clearance from
the lung before damage can take place (Fubini, 1998, Document ID 1016).
An epidemiological study found that the risk of silicosis was less in
pottery workers than in tin and tungsten miners (Chen et al., 2005,
Document ID 0985; Harrison et al., 2005, 1036), possibly reflecting
that pottery workers were exposed to silica particles having less
biologically-available, non-clay-occluded surface area than was the
case for miners.
Although it is evident that a number of factors can act to mediate
the toxicological potency of crystalline silica, it is not clear how
such considerations should be taken into account to evaluate lung
cancer and silicosis risks to exposed workers. After evaluating many in
vitro studies that investigated the surface characteristics of
crystalline silica particles and their influence on fibrogenic
activity, NIOSH concluded that further research is needed to associate
specific surface characteristics that can affect toxicity with specific
occupational exposure situations and consequent health risks to workers
(2002, Document ID 1110). Thus, OSHA preliminarily concluded that while
there was considerable evidence that several environmental influences
can modify surface activity to either enhance or diminish the toxicity
of silica, the available information was insufficient to determine in
any quantitative way how these influences may affect disease risk to
workers in any particular workplace setting.
3. Summary of the Preliminary QRA
OSHA presented in the Preliminary QRA estimates of the risk of
silica-related diseases assuming exposure over a working life (45
years, from age 20 to age 65) to the revised 8-hour time-weighted
average (TWA) PEL of 50 [micro]g/m\3\ respirable crystalline silica,
the new action level of 25 [micro]g/m\3\, and the previous PELs. OSHA's
previous general industry PEL for respirable quartz was expressed both
in terms of a particle count formula and a gravimetric concentration
formula; the previous construction and shipyard employment PELs for
respirable quartz were only expressed in terms of a particle count
formula. For general industry, as the quartz content increases, the
gravimetric PEL approached a limit of 100 [micro]g/m\3\ respirable
quartz. For construction and shipyard employment, OSHA's previous PELs
used a formula that limits exposure to respirable dust, depending upon
the quartz content, expressed as a respirable particle count
concentration. There was no single mass concentration equivalent for
the construction and shipyard employment PELs; OSHA reviewed several
studies that suggest that the previous construction/shipyard PEL likely
was between 250 and 500 [micro]g/m\3\ respirable quartz. In general
industry, for both the gravimetric and particle count PELs, OSHA's
previous PELs for cristobalite and tridymite were half the value for
quartz. Based upon these previous PELs and the new action level, OSHA
presented risk estimates associated with exposure over a working life
to 25, 50, 100, 250, and 500 [micro]g/m\3\ respirable silica
(corresponding to cumulative exposures over 45 years to 1.125, 2.25,
4.5, 11.25, and 22.5 mg/m\3\-yrs).
To estimate lifetime excess mortality risks at these exposure
levels, OSHA implemented each of the risk models in a life table
analysis that accounted for competing causes of death due to background
causes and cumulated risk through age 85. For these analyses, OSHA used
lung cancer, NMRD, or renal disease mortality and all-cause mortality
rates to account for background risks and competing risks (U.S. 2006
data for lung cancer and NMRD mortality in all males, 1998 data for
renal disease mortality, obtained from cause-specific death rate tables
published by the National Center for Health Statistics (2009, Document
ID 1104)). OSHA calculated these risk estimates assuming occupational
exposure from age 20 to age 65. The mortality risk estimates were
presented in terms of lifetime excess risk per 1,000 workers for
exposure over an 8-hour working day, 250 days per year, and a 45-year
working life.
For silicosis morbidity, OSHA based its risk estimates on
cumulative risk models used by various investigators to develop
quantitative exposure-response relationships. These models
characterized the risk of developing silicosis (as detected by chest
radiography) up to the time that cohort members (including both active
and retired workers) were last examined. Thus, risk estimates derived
from these studies represented less-than-lifetime risks of developing
radiographic silicosis. OSHA did not attempt to estimate lifetime risk
(i.e., up to age 85) for silicosis morbidity because the relationships
between age, time, and disease onset post-exposure have not been well
characterized.
a. Silicosis and NMRD Mortality
i. Exposure-Response Studies
In the Preliminary QRA, OSHA relied upon two published quantitative
risk studies of silicosis and NMRD mortality (Document ID 1711). The
first, Mannetje et al. (2002b, Document ID 1089) conducted a pooled
analysis of silicosis mortality in which there were 18,634 subjects,
150 silicosis deaths, and 20 deaths from unspecified pneumoconiosis.
Rates for silicosis adjusted for age, calendar time, and study were
estimated by Poisson regression and increased nearly monotonically with
deciles of cumulative exposure, from a mortality rate of 5/100,000
person-years in the lowest exposure category (0-0.99 mg/m\3\-yrs) to
299/100,000 person-years in the highest category (>28.10 mg/m\3\-yrs).
As previously discussed, the second, Park et al. (2002, Document ID
0405) analyzed the California diatomaceous earth cohort data from
Checkoway et al. (1997, Document ID 0326), and examined mortality from
chronic lung disease other than cancer (LDOC; also known as non-
malignant respiratory disease (NMRD)). Smoking information was
available for about 50 percent of the cohort and for 22 of the 67 LDOC
deaths available for analysis, permitting Park et al. (2002, Document
ID 0405) to partially adjust for smoking. Estimates of LDOC mortality
risks were derived via Poisson and Cox proportional hazards models; a
variety of relative rate model forms were fit to the data, with a
linear relative rate model selected for estimating risks.
ii. Risk Estimates
As silicosis is only caused by exposure to respirable crystalline
silica (i.e., there is no background rate of silicosis in the unexposed
population), absolute risks of silicosis mortality rather than excess
risks were calculated for the Mannetje et al. pooled analysis (2002b,
Document ID 1089). These risk estimates were derived from the rate
ratios incorporating simulated measurement error reported by
ToxaChemica (Document ID 0469). OSHA's estimate of lifetime risk of
silicosis mortality, for 45 years of exposure to the previous general
industry PEL, was 11 deaths per 1,000 workers for the pooled analysis
(Document ID 1711). At the revised PEL, the risk estimate was 7 deaths
per 1,000.
OSHA also calculated preliminary risk estimates for NMRD mortality.
These estimates were derived from Park et al. (2002, Document ID 0405).
For 45 years of exposure to the previous general industry PEL, OSHA
preliminarily estimated lifetime excess risk at 83 deaths per 1,000
workers. At the revised PEL, OSHA estimated 43 deaths per 1,000
workers.
OSHA noted that, for exposures up to 250 [micro]g/m\3\, the
mortality risk estimates based on Park et al. (2002, Document ID 0405)
are about 5 to 11 times as great as those calculated for the pooled
analysis of silicosis mortality (Mannetje et al., 2002b, Document ID
1089). These two sets of risk estimates, however, are not directly
comparable, as the endpoint for the Park et al. (2002, Document ID
0405) analysis was death from all non-cancer lung diseases, including
pneumoconiosis, emphysema, and chronic bronchitis, whereas the pooled
analysis by Mannetje et al. (2002b, Document ID 1089) included only
deaths coded as silicosis or other pneumoconiosis. Less than 25 percent
of the LDOC deaths in the Park et al. analysis were coded as silicosis
or other pneumoconiosis (15 of 67), suggesting that silicosis as a
cause of death may be misclassified as emphysema or chronic bronchitis.
Thus, Mannetje et al.'s (2002b, Document ID 1089) selection of deaths
may tend to underestimate the true risk of silicosis mortality, and
Park et al.'s (2002, Document ID 0405) analysis may more completely
capture the total respiratory mortality risk from all non-malignant
causes.
Since the time of OSHA's analysis, NCHS has released updated all-
cause mortality and NMRD mortality background rates from 2011
(http://wonder.cdc.gov/ucd-icd10.html); OSHA's final risk estimates for NMRD
mortality, which incorporate these updated rates (ICD10 codes J40-J47,
chronic lower respiratory diseases; J60-J66, J68, pneumoconiosis and
chemical effects), are available in Section VI, Final Quantitative Risk
Assessment and Significance of Risk.
b. Lung Cancer Mortality
i. Exposure-Response Studies
In 1997, when IARC determined that there was sufficient evidence to
regard crystalline silica as a human carcinogen, it also noted that
some epidemiological studies did not demonstrate an excess risk of lung
cancer and that exposure-response trends were not always consistent
among studies that were able to describe such trends (Document ID
1062). These findings led Steenland et al. (2001a, Document ID 0452) to
conduct a comprehensive exposure-response analysis--the IARC multi-
center study--of the risk of lung cancer associated with exposure to
crystalline silica. This study relied on all available cohort data from
previously-published epidemiological studies for which there were
adequate quantitative data on worker silica exposures to derive pooled
estimates of disease risk. In addition, as discussed previously, OSHA
identified four more recent studies suitable for quantitative risk
assessment: (1) An exposure-response analysis by Rice et al. (2001,
Document ID 1118) of a cohort of diatomaceous earth workers primarily
exposed to cristobalite; (2) an analysis by Attfield and Costello
(2004, Document ID 0285) of U.S. granite workers; (3) an exposure-
response analysis by Hughes et al. (2001, Document ID 1060) of U.S.
industrial sand workers; and (4) a risk analysis by Miller et al.
(2007, Document ID 1305) and Miller and MacCalman (2009, Document ID
1306) of British coal miners. OSHA thoroughly described each of these
studies in its Preliminary QRA (Document ID 1711); a brief summary of
the exposure-response models used in each study is provided here.
The Steenland et al. pooled exposure-response analysis was based on
data obtained from ten cohorts of silica-exposed workers (65,980
workers, 1,072 lung cancer deaths) (2001a, Document ID 0452). The
pooled analysis cohorts included U.S. gold miners (Steenland and Brown,
1995a, Document ID 0450), U.S. diatomaceous earth workers (Checkoway et
al., 1997, Document ID 0326), Australian gold miners (de Klerk and
Musk, 1998, Document ID 0345), Finnish granite workers (Koskela et al.,
1994, Document ID 1078), U.S. industrial sand employees (Steenland and
Sanderson, 2001, Document ID 0455), Vermont granite workers (Costello
and Graham, 1988, Document ID 0991), South African gold miners (Hnizdo
and Sluis-Cremer, 1991, Document ID 1051; Hnizdo et al.,1997, 1049),
and Chinese pottery workers, tin miners, and tungsten miners (Chen et
al., 1992, Document ID 0329).
Steenland et al. (2001a, Document ID 0452) performed a nested case-
control analysis via Cox regression. There were 100 controls chosen for
each case randomly from among cohort members who survived past the age
at which the case died; controls were matched on age (the time variable
in Cox regression), study, race/ethnicity, sex, and date of birth
within 5 years. Steenland et al. found that the use of any of the
following continuous exposure variables in a log linear relative risk
model resulted in positive statistically significant (p <= 0.05)
exposure-response coefficients: (1) Cumulative exposure with a 15-year
lag; (2) the log of cumulative exposure with a 15-year lag; and (3)
average exposure (2001a, Document ID 0452). The models that provided
the best fit to the data used cumulative exposure and log-transformed
cumulative exposure. Models that used log-transformed cumulative
exposure also showed no statistically significant heterogeneity among
cohorts (p = 0.36), possibly because they are less influenced by very
high exposures. At OSHA's request, Steenland (2010, Document ID 1312)
also conducted a categorical analysis of the pooled data set and
additional analyses using linear relative risk models (with and without
the log transformation of cumulative exposure) as well as a two-piece
spline model (see Document ID 1711, pp. 276-278).
Rice et al. (2001, Document ID 1118) applied a variety of exposure-
response models to the California diatomaceous earth cohort data
originally studied by Checkoway et al. (1993, Document ID 0324; 1996,
0325; 1997, 0326) and included in the Steenland et al. (2001a, Document
ID 0452) pooled analysis. The cohort consisted of 2,342 white males
employed for at least one year between 1942 and 1987 in a California
diatomaceous earth mining and processing plant. The cohort was followed
until 1994, and included 77 lung cancer deaths. Rice et al. reported
that exposure to crystalline silica was a significant predictor of lung
cancer mortality for nearly all of the models employed, with the linear
relative risk model providing the best fit to the data in the Poisson
regression analysis (2001, Document ID 1118).
Attfield and Costello (2004, Document ID 0285) analyzed the U.S.
granite cohort originally studied by Costello and Graham (1988,
Document ID 0991) and Davis et al. (1983, Document ID 0999) and
included in the Steenland et al. (2001a, Document ID 0452) pooled
analysis. The cohort consisted of 5,414 male granite workers who were
employed in the Vermont granite industry between 1950 and 1982 and who
had received at least one chest x-ray from the surveillance program of
the Vermont Department of Industrial Hygiene. The 2004 report by
Attfield and Costello extended follow-up from 1982 to 1994, and found
201 deaths (Document ID 0285). Using Poisson regression models, the
results of a categorical analysis showed a generally increasing trend
of lung cancer rate ratios with increasing cumulative exposure.
As mentioned previously, however, the rate ratio for the highest
exposure group in the Attfield and Costello analysis (cumulative
exposures of 6.0 mg/m\3\-yrs or higher) was substantially lower than
that for other exposure groups (2004, Document ID 0285). The authors
reported that the best-fitting model had a 15-year lag, untransformed
cumulative exposure, and the omission of this highest exposure group.
The authors argued that it was appropriate to omit the highest exposure
group for several reasons, including that the exposure estimates for
the highest exposure group were less reliable, and there was a greater
likelihood of cohort selection effects, competing causes of death, and
misdiagnosis (Document ID 0285, p. 136).
McDonald et al. (2001, Document ID 1091), Hughes et al. (2001,
Document ID 1060) and McDonald et al. (2005, Document ID 1092) followed
up on a cohort study of North American industrial sand workers included
in the Steenland et al. (2001a, Document ID 0452) pooled analysis. The
McDonald et al. cohort included 2,670 men employed before 1980 for
three years or more in one of nine North American (8 U.S. and 1
Canadian) sand-producing plants, including 1 large associated office
complex (2001, Document ID 1091). A nested case-control study based on
90 lung cancer deaths (through 1994) from this cohort was conducted by
Hughes et al. (2001, Document ID 1060). A subsequent update (through
2000, 105 lung cancer deaths) eliminated the Canadian plant, following
2,452 men from the eight U.S. plants (McDonald et al., 2005, Document
ID 1092). These nested case-control studies, Hughes et al. (2001,
Document ID 1060) and McDonald et al. (2005, Document ID 1092), allowed
for individual job, exposure, and smoking histories to be taken into
account in the exposure-response analysis. Hughes et al. (2001,
Document ID 1060) found statistically significant positive exposure-
response trends for lung cancer for both cumulative exposure (lagged 15
years) and average exposure concentration, but not for duration of
employment. With exposure lagged 15 years and after adjusting for
smoking, increasing quartiles of cumulative silica exposure were also
associated with lung cancer mortality (p-value for trend = 0.04).
McDonald et al. (2005, Document ID 1092) found very similar results,
with increasing quartiles of cumulative silica exposure (lagged 15
years) associated with lung cancer mortality (p-value for trend =
0.006). Because McDonald et al. (2005, Document ID 1092) did not report
the medians of the exposure categories, and given the similar results
of both case-control studies, OSHA chose to base its risk estimates on
the Hughes et al. (2001, Document ID 1060) study.
Miller et al. (2007, Document ID 1305) and Miller and MacCalman
(2009, Document ID 1306) continued a follow-up mortality study, begun
in 1970, of coal miners from 10 British coal mines initially followed
through the end of 1992 (Miller et al., 1997, Document ID 1304) and
extended it to 2005. In the analysis using internal controls and Cox
regression methods, the relative risk of lung cancer mortality,
adjusted for concurrent dust exposure and smoking status, at a
cumulative quartz exposure (lagged 15 years) equivalent of
approximately 55 [mu]g/m\3\ for 45 years was 1.14 (95% C.I., 1.04 to
1.25).
ii. Risk Estimates
In the Preliminary QRA, OSHA presented estimates of excess lung
cancer mortality risk from occupational exposure to crystalline silica,
based on data from the five epidemiology studies discussed above
(Document ID 1711). In its preliminary analysis, OSHA used background
all-cause mortality and lung cancer mortality rates from 2006, as
reported by the National Center for Health Statistics (NCHS) (Document
ID 1104). These rates were used in life table analyses to estimate
lifetime risks at the exposure levels of interest, ranging from 25 to
500 [mu]g/m\3\ respirable crystalline silica.
OSHA's preliminary estimates of lifetime excess lung cancer risk
associated with 45 years of exposure to crystalline silica at 100
[mu]g/m\3\ (approximately the previous general industry PEL) ranged
between 13 and 60 deaths per 1,000 workers, depending upon the study
used. For exposure to the revised PEL of 50 [mu]g/m\3\, the lifetime
risk estimates were in the range of between 6 and 26 deaths per 1,000
workers, depending upon the study used. For a 45 year exposure at the
new action level of 25 [mu]g/m\3\, OSHA estimated the risk to range
between 3 and 23 deaths per 1,000 workers. The Agency found that the
results from these preliminary assessments were reasonably consistent
despite the use of data from different cohorts and the reliance on
different analytical techniques for evaluating dose-response
relationships.
OSHA also estimated the lung cancer risk associated with 45 years
of exposure to the previous construction/shipyard PEL (in the range of
250 [mu]g/m\3\ to 500 [mu]g/m\3\) to range between 37 and 653 deaths
per 1,000 workers, depending upon the study used. OSHA acknowledges
that the 653 deaths is the upper limit for 45 years of exposure to 500
[mu]g/m\3\, and recognizes that actual risk, to the extent that workers
are exposed for less than 45 years or intermittently, is likely to be
lower. In addition, exposure to 250 or 500 [mu]g/m\3\ over 45 years
represents cumulative exposures of 11.25 and 22.5 mg/m\3\-yrs,
respectively. This range of cumulative exposure is well above the
median cumulative exposure for most of the cohorts used in the
preliminary risk assessment. Thus, OSHA explained that estimating lung
cancer excess risks over this higher range of cumulative exposures of
interest to OSHA required some degree of upward extrapolation of the
exposure-response function to model these high exposures, thus adding
uncertainty to the estimates.
Since the time of that original analysis, NCHS has released updated
all-cause mortality and lung cancer mortality background rates from
2011. OSHA's final risk estimates, which incorporate these updated
rates, are available in this preamble at Section VI, Final Quantitative
Risk Assessment and Significance of Risk.
c. Uncertainty Analysis of Pooled Studies of Lung Cancer Mortality and
Silicosis Mortality
In the Preliminary QRA, OSHA recognized that risk estimates can be
inherently uncertain and can be affected by confounding, selection
bias, and measurement error (Document ID 1711). OSHA presented several
reasons as to why it does not believe that confounding or selection
bias had a substantial impact on the risk estimates for lung cancer or
silicosis mortality (Document ID 1711, pp. 299-302). However, because
it was more difficult to assess the importance of exposure measurement
error, OSHA's contractor, ToxaChemica, Inc., commissioned Drs. Kyle
Steenland and Scott Bartell to perform an uncertainty analysis to
examine the effect of uncertainty due to measurement error in the
pooled studies (Steenland et al., 2001a, Document ID 0452; Mannetje
2002b, 1089) on the lung cancer and silicosis mortality risk estimates
(ToxaChemica, Inc., 2004, Document ID 0469).
There are two main sources of error in the silica exposure
measurements. The first arises from the assignment of individual
workers' exposures based on either exposure measurements for a sample
of workers in the same job or estimated exposure levels for specific
jobs in the past when no measurements were available, via a job-
exposure matrix (JEM) (Mannetje et al., 2002a, Document ID 1090). The
second arises from the conversion of historically-available dust
measurements, typically particle count concentrations, to gravimetric
respirable silica concentrations. ToxaChemica, Inc. conducted an
uncertainty analysis using the raw data from the IARC multi-centric
study to address these sources of error (2004, Document ID 0469).
i. Lung Cancer Mortality
To examine the effect of error in the assignment of individual
exposure values in the cohorts studied by Steenland et al. (2001a,
Document ID 0452), ToxaChemica, Inc. used a Monte Carlo analysis (a
type of simulation analysis that varies the values of an uncertain
input to an analysis--in this case, exposure estimates--to explore the
effects of different values on the outcome of the analysis) to randomly
sample new values for each worker's job-specific exposure levels from a
distribution that they believed characterized the variability in
exposures of individual workers in each job (see Document ID 1711, pp.
303-305). That is, ToxaChemica created a distribution of values for
each member of each cohort where the mean exposure for each member was
equal to the original exposure value and the distribution of exposure
values was based on a log-normal distribution having a standard
deviation that was based on the exposure variation observed in
industrial sand plants observed by Steenland and Sanderson (2001,
Document ID 0455). From this distribution, new sets of exposure values
from each cohort member were randomly drawn for 50 trials. This
simulation was designed to test whether sets of exposure values that
were plausibly different from the original estimates would lead to
substantially different results of the exposure-response analysis.
Except for the simulated exposure values and the correction of a few
minor errors in the original data sets, the simulation analysis used
the same data as the original analyses conducted by Steenland et al.
(2001a, Document ID 0452).
When an entire set of cumulative exposure values was assembled for
all workers based on these randomly sampled values, the set was used in
a conditional logistic regression to fit a new exposure-response model.
The extent to which altering the exposure values led to changes in the
results indicated how sensitive the previously presented risk estimates
may have been to error in the exposure estimates. Among the individual
cohorts, most of the mean regression coefficients resulting from the
simulation analysis were consistent with the coefficients from the
exposure-response analyses reported in Steenland et al. (2001, Document
ID 0455) and ToxaChemica, Inc. (2004, Document ID 0469) (following
correction for minor data entry and rounding errors). An exception was
the mean of the simulation coefficients based on the South Africa gold
cohort (0.26), which was lower than the previously calculated exposure
coefficient (0.582). ToxaChemica, Inc. (2004, Document ID 0469)
concluded that this error source probably did not appreciably change
the estimated exposure-response coefficient for the pooled data set.
To examine the effect of error in estimating gravimetric respirable
crystalline silica exposures from historical dust concentration data
(i.e., particle count data), ToxaChemica, Inc. (2004, Document ID 0469)
used a procedure similar to that used to assess uncertainties in
individual exposure value assignments. ToxaChemica, Inc. assumed that,
for each job in the dataset, a specific conversion factor existed that
related workers' exposures measured as particle concentrations to
gravimetric respirable silica exposures, and that this conversion
factor came from a normal distribution with a standard deviation
[sigma] = \1/2\ its mean [mu]. The use of a normal distribution was a
reasonable choice in that it allowed the sampled conversion factors to
fall above or below the original values with equal probability, as the
authors had no information to suggest that error in either direction
was more likely. The normal distribution also assigned higher
probability to conversion values closer to the original values. The
choice of the normal distribution therefore reflected the study
authors' judgment that their original conversion factors were more
likely to be approximately correct than not, while allowing for the
possibility of significant error in the original values.
A new conversion factor was then sampled for each job from the
appropriate distribution, and the complete set of sampled conversion
factors was then used to re-run the risk analysis used by Steenland et
al. (2001a, Document ID 0452). The results were similar to the
coefficients originally derived from each cohort; the only coefficient
substantially affected by the procedure was that for the South African
cohort, with an average value of 0.350 across ten runs compared to the
original value of 0.582 (see Table II-5, Document ID 1711, p. 307).
This suggests that the results of exposure-response analyses conducted
using the South African cohort are sensitive to error in exposure
estimates; therefore, there is greater uncertainty due to potential
exposure estimation error in an exposure-response model based on this
cohort than is the case for the other nine cohorts in Steenland et al's
analysis.
To explore the potential effects of both kinds of random
uncertainty described above, ToxaChemica, Inc. (2004, Document ID 0469)
used the distributions representing the error in job-specific exposure
assignment and the error in converting exposure metrics to generate 50
new exposure simulations for each cohort. A study-specific coefficient
and a pooled coefficient were fit for each new simulation, with the
assumption that the two sources of uncertainty were independent. The
results indicated that the only cohort for which the mean of the
exposure coefficients derived from the 50 simulations differed
substantially from the previously calculated exposure coefficient was
the South African gold cohort (simulation mean of 0.181 vs. original
coefficient of 0.582). For the pooled analysis, the mean coefficient
estimate from the simulations was 0.057, just slightly lower than the
previous estimate of 0.060. Based on these results, OSHA concludes
that random error in the underlying exposure estimates in the Steenland
et al. (2001a, Document ID 0452) pooled cohort study of lung cancer
is not likely to have substantially influenced the original risk
estimates derived from the pooled data set, although the model
coefficient for one of the ten cohorts (the South African gold miner
cohort) appeared to be sensitive to measurement errors (see Table II-5,
Document ID 1711, p. 307).
Drs. Steenland and Bartell also examined the effects of systematic
bias in conversion factors, considering the possibility that these may
have been consistently under-estimated or over-estimated for any given
cohort. They addressed possible biases in either direction, conducting
simulations where the true silica content was assumed to be either half
or double the estimated silica content of measured exposures. For the
conditional logistic regression model using log cumulative exposure
with a 15-year lag, doubling or halving the exposure for a specific
study resulted in virtually no change in the exposure-response
coefficient for that study or for the pooled analysis overall. This is
due to the use of log-transformed exposure metrics, which ensured that
any multiplicative bias in exposure would have virtually no effect on
conditional logistic regression coefficients (Document ID 0469, p. 17).
That is, for this model, a systematic error in exposure estimation for
any study had little effect on the lung cancer response rate for either
the specific study or the pooled analysis overall.
ii. Silicosis Mortality
Following the procedures described above for the lung cancer
analysis, Toxachemica, Inc. (2004, Document ID 0469) combined both
sources of random measurement error in a Monte Carlo analysis of the
silicosis mortality data from Mannetje et al. (2002b, Document ID
1089). Categorical analyses were performed with a nested case control
model, in contrast to the Poisson model used previously by Mannetje et
al. (2002b, Document ID 1089). The nested case control model was
expected to control more effectively for age. This model yielded
categorical rate ratio results using the original data (prior to
simulation of measurement error) which were approximately 20-25 percent
lower than those reported by Mannetje et al. (2002b, Document ID 1089).
The silicosis mortality dataset thus appeared to be more sensitive to
possible error in exposure measurement than the lung cancer dataset,
for which the mean of the simulation coefficients was virtually
identical to the original. OSHA notes that its risk estimates derived
from the pooled analysis (Mannetje et al., 2002b, Document ID 1089),
incorporated ToxaChemica, Inc.'s simulated measurement error (2004,
Document ID 0469). More information is provided in the Preliminary QRA
(Document ID 1711, pp. 310-314).
d. Renal Disease Mortality
i. Exposure-Response Studies
Steenland et al. (2002a, Document ID 0448) examined renal disease
mortality in a pooled analysis of three cohorts, as discussed
previously. These cohorts were chosen because data were available for
both underlying cause mortality and multiple cause mortality. The
combined cohort for the pooled analysis (Steenland et al., 2002a,
Document ID 0448) consisted of 13,382 workers with exposure information
available for 12,783 (95 percent). SMRs (compared to the U.S.
population) for renal disease (acute and chronic glomerulonephritis,
nephrotic syndrome, acute and chronic renal failure, renal sclerosis,
and nephritis/nephropathy) were statistically significantly elevated
using multiple cause data (SMR 1.29, 95% CI 1.10-1.47, 193 deaths) and
underlying cause data (SMR 1.41, 95% CI 1.05-1.85, 51 observed deaths).
ii. Risk Estimates
As detailed in the Preliminary QRA, OSHA estimated that exposure to
the previous (100 [mu]g/m\3\) and revised (50 [mu]g/m\3\) general
industry PELs, over a 45-year working life, would result in a lifetime
excess renal disease mortality risk of 39 and 32 deaths per 1,000
workers, respectively. For exposure to the previous construction/
shipyard PELs, OSHA estimated the lifetime excess risk to range from 52
to 63 deaths per 1,000 workers at exposures of 250 and 500 [mu]g/m\3\,
respectively. These risks reflect the 1998 background all-cause
mortality and renal mortality rates for U.S. males. Background rates
were not adjusted for the renal disease risk estimates because the CDC
significantly changed the classification of renal diseases after 1998;
they are now inconsistent with those used by Steenland et al. (2002a,
Document ID 0448) to ascertain the cause of death of workers in their
study.
e. Silicosis Morbidity
i. Exposure-Response Studies
OSHA summarized, in its Preliminary QRA, the principal cross-
sectional and cohort studies that quantitatively characterized
relationships between exposure to crystalline silica and the
development of radiographic evidence of silicosis (Document ID 1711).
Each of these studies relied on estimates of cumulative exposure to
evaluate the relationship between exposure and silicosis prevalence.
The health endpoint of interest in these studies was the appearance of
opacities on chest radiographs indicative of pulmonary fibrosis. Most
of the studies reviewed by OSHA considered a finding consistent with an
ILO classification of 1/1 to be a positive diagnosis of silicosis,
although some also considered an x-ray classification of 1/0 or 0/1 to
be positive. OSHA noted its belief, in the Preliminary QRA, that the
most reliable estimates of silicosis morbidity, as detected by chest
radiographs, come from the studies that evaluated radiographs over
time, included radiographic evaluation of workers after they left
employment, and derived cumulative or lifetime estimates of silicosis
disease risk. OSHA also pointed out that the low sensitivity of chest
radiography in detecting silicosis suggests that risk estimates derived
from radiographic evidence likely underestimate the true risk.
Hnizdo and Sluis-Cremer (1993, Document ID 1052) described the
results of a retrospective cohort study of 2,235 white gold miners in
South Africa. A total of 313 miners had developed silicosis (x-ray with
ILO 1/1 or greater) and had been exposed for an average of 27 years at
the time of diagnosis. The average latency for the cohort was 35 years
(range of 18-50 years) from the start of exposure to diagnosis. The
average respirable dust exposure for the cohort overall was 290 [mu]g/
m\3\ (range 110-470), corresponding to an estimated average respirable
silica concentration of 90 [mu]g/m\3\ (range 33-140). The average
cumulative dust exposure for the overall cohort was 6.6 mg/m\3\-yrs
(range 1.2-18.7). Silicosis risk increased exponentially with
cumulative exposure to respirable dust in models using log-logistic
regression. Using the exposure-response relationship developed by
Hnizdo and Sluis-Cremer (1993, Document ID 1052), and assuming a quartz
content of 30 percent in respirable dust, Rice and Stayner (1995,
Document ID 0418) estimated the risk of silicosis to be 13 percent for
a 45-year exposure to 50 [mu]g/m\3\ respirable crystalline silica.
Steenland and Brown (1995b, Document ID 0451) studied 3,330 South
Dakota gold miners who had worked at least a year underground between
1940 and 1965. Chest x-rays were obtained in cross-sectional surveys in
1960 and 1976 and used along with death certificates to ascertain cases
of silicosis; 128 cases were found via death certificate, 29 were found
by x-ray (defined as ILO 1/1 or greater), and 13 were found by both.
OSHA notes that the inclusion of death certificate diagnoses
complicates interpretation of the risk estimate from this study since,
as noted by Finkelstein (2000, Document ID 1015), it is not known how
well such diagnoses correlate with ILO radiographic interpretations; as
such, the risk estimates derived from this study may not be directly
comparable to others that rely exclusively on radiographic findings to
evaluate silicosis morbidity risk. The mean exposure concentration was
50 [mu]g/m\3\ for the overall cohort, with those hired before 1930
exposed to an average of 150 [mu]g/m\3\. The average duration of
exposure for workers with silicosis was 20 years (s.d. = 8.7) compared
to 8.2 years (s.d. = 7.9) for the rest of the cohort. This study found
that cumulative exposure was the best disease predictor, followed by
duration of exposure and average exposure. Lifetime risks were
estimated from Poisson regression models using standard life table
techniques; the results indicated an estimated risk of 47 percent
associated with 45 years of exposure to 90 [mu]g/m\3\ respirable
crystalline silica, which reduced to 35 percent after adjustment for
age and calendar time.
OSHA used the same life table approach as described for estimating
lung cancer and NMRD mortality risks to estimate lifetime silicosis
risk based on the silicosis rates, adjusted for age and calendar time,
calculated by Steenland and Brown (1995b, Table 2, Document ID 0451).
Silicosis risk was estimated through age 85, assuming exposure from age
20 through 65, and assuming that the silicosis rate remains constant
after age 65. All-cause mortality rates to all males for calendar year
2006 were used to account for background competing risk. From this
analysis, OSHA estimated the risk from exposure to the previous general
industry PEL of 100 [mu]g/m\3\ to be 43 percent; this is somewhat
higher than estimated by Steenland and Brown (1995b) because of the use
by OSHA of more recent mortality data and calculation of risk through
age 85 rather than 75. For exposure to the revised PEL of 50 [mu]g/
m\3\, OSHA estimated the lifetime risk to be 7 percent. Since the time
of the original analysis, NCHS has released updated all-cause mortality
background rates from 2011; OSHA's final risk estimates, which
incorporate these updated rates, are available in Section VI, Final
Quantitative Risk Assessment and Significance of Risk.
Miller et al. (1995, Document ID 1097; 1998, 0374) and Buchanan et
al. (2003, Document ID 0306) reported on a follow-up study conducted in
1990 and 1991 of 547 survivors of a 1,416 member cohort of Scottish
coal workers from a single mine. These men all worked in the mine
during a period between early 1971 and mid-1976, during which they had
experienced "unusually high concentrations of freshly cut quartz in
mixed coalmine dust" (Document ID 0374, p.52). Thus, this cohort
allowed for the study of exposure-rate effects on the development of
silicosis. The men all had radiographs dating from before, during, or
just after this high concentration period, and the 547 participating
survivors received follow-up chest x-rays between November 1990 and
April 1991.
Buchanan et al. (2003, Document ID 0306) presented logistic
regression models in stages. In the first stage they compared the
effect of pre- vs. post-1964 cumulative quartz exposures on odds
ratios; this yielded a statistically significant odds ratio estimate
for post-1964 exposures. In the second stage they added total dust
levels both pre- and post-1964, age, smoking status, and the number of
hours worked pre-1954; only post-1964 cumulative exposures remained
significant. Finally, in the third stage, they started with only the
statistically significant post-1964 cumulative exposures, and separated
these exposures into two quartz bands, one for exposure to
concentrations less than 2,000 [mu]g/m\3\ respirable quartz and the
other for concentrations greater than or equal to 2,000 [mu]g/m\3\.
Both concentration bands were highly statistically significant in the
presence of the other, with the coefficient for exposure concentrations
greater than or equal to 2000 [mu]g/m\3\ being three times that of the
coefficient for concentrations less than 2000 [mu]g/m\3\. From this,
the authors concluded that their analysis showed that "the risks of
silicosis over a working lifetime can rise dramatically with exposure
to such high concentrations over a timescale of merely a few months"
(Buchanan et al. 2003, Document ID 0306, p. 163). The authors then used
the model to estimate the risk of acquiring a chest x-ray classified as
ILO category 2/1+, 15 years after exposure, as a function of both low
(<2000 [mu]g/m\3\) and high (>2000 [mu]g/m\3\) quartz concentrations.
OSHA chose to use this model to estimate the risk of radiological
silicosis consistent with an ILO category 2/1+ chest x-ray for several
exposure scenarios; in each, it assumed 45 years of exposure, 2000
hours/year of exposure, and no exposure above a concentration of 2000
[mu]g/m\3\. The results showed that occupational exposures to the
revised PEL of 50 [mu]g/m\3\ led to an estimated risk of 55 cases per
1,000 workers. Exposure at the previous general industry PEL of 100
[mu]g/m\3\ increased the estimate to 301 cases per 1,000 workers. At
higher exposure levels the risk estimates rose quickly to near
certainty.
Chen et al. (2001, Document ID 0332) reported the results of a
retrospective study of a Chinese cohort of 3,010 underground miners who
had worked in tin mines at least one year between 1960 and 1965. They
were followed through 1994, by which time 2,426 (80.6 percent) workers
had either retired or died, and only 400 (13.3 percent) remained
employed at the mines. Annual radiographs were taken beginning in 1963
and cohort members continued to have chest x-rays taken every 2 or 3
years after leaving work. Silicosis was diagnosed when at least 2 of 3
radiologists classified a radiograph as being a suspected case or at
Stage I, II, or III under the 1986 Chinese pneumoconiosis roentgen
diagnostic criteria, which the authors reported agreed closely with ILO
categories 0/1, Category 1, Category 2, and Category 3, respectively.
Silicosis was observed in 33.7 percent of the group; 67.4 percent of
the cases developed after exposure ended.
Chen et al. (2001, Document ID 0332) found that a Weibull model
provided the best fit to relate cumulative silicosis risk to eight
categories of cumulative total dust exposure. The risk of silicosis was
strongly related to cumulative silica exposure. The investigators
predicted a 55-percent risk of silicosis associated with 45 years of
exposure to 100 [mu]g/m\3\. The paper did not report the risk
associated with a 45-year exposure to 50 [mu]g/m\3\, but OSHA estimated
the risk to be about 17 percent (based on the parameters of the Weibull
model).
In a later study, Chen et al. (2005, Document ID 0985) investigated
silicosis morbidity risks among three cohorts to determine if the risk
varied among workers exposed to silica dust having different
characteristics. The cohorts consisted of 4,547 pottery workers, 4,028
tin miners, and 14,427 tungsten miners, all employed after January 1,
1950 and selected from a total of 20 workplaces. The approximate
mean cumulative exposures to respirable silica for pottery, tin, and
tungsten workers were 6.4 mg/m\3\-yrs, 2.4 mg/m\3\-yrs, and 3.2 mg/
m\3\-yrs, respectively. Measurement of particle surface occlusion
(presence of a mineral coating that may affect the biological
availability of the quartz component) indicated that, on average, 45
percent of the surface area of respirable particles collected from
pottery factory samples was occluded, compared to 18 percent of the
particle surface area for tin mine samples and 13 percent of particle
surface area for tungsten mines. When cumulative silica exposure was
adjusted to reflect exposure to surface-active quartz particles (i.e.,
not occluded), the estimated cumulative risk among pottery workers more
closely approximated those of the tin and tungsten miners, suggesting
to the authors that alumino silicate occlusion of the crystalline
particles in pottery factories at least partially explained the lower
risk seen among pottery workers, despite their having been more heavily
exposed. Based on Chen et al. (2005, Document ID 0985), OSHA estimated
the cumulative silicosis risk associated with 45 years of exposure to
100 [mu]g/m\3\ respirable crystalline silica to be 6 percent for
pottery workers, 12 percent for tungsten miners, and 40 percent for tin
miners. For 45 years of exposure to 50 [mu]g/m\3\, cumulative silicosis
morbidity risks were estimated to be 2 percent for pottery workers, 2
percent for tungsten miners, and 10 percent for tin miners.
ii. Risk Estimates
OSHA's risk estimates for silicosis morbidity ranged between 60 and
773 per 1,000 workers for a 45-year exposure to the previous general
industry PEL of 100 [mu]g/m\3\, and between 20 and 170 per 1,000
workers for a 45-year exposure to the revised PEL of 50 [mu]g/m\3\,
depending upon the study used. OSHA recognizes that actual risk, to the
extent that workers are exposed for less than 45 years or
intermittently, is likely to be lower, but also recognizes that
silicosis can progress for years after exposure ends. Also, given the
consistent finding of a monotonic exposure-response relationship for
silicosis morbidity with cumulative exposure in the studies reviewed,
OSHA continues to find that cumulative exposure is a reasonable
exposure metric upon which to base risk estimates in the exposure range
of interest.
D. Comments and Responses Concerning Silicosis and Non-Malignant
Respiratory Disease Mortality and Morbidity
In this section, OSHA focuses on comments pertaining to the
literature used by the Agency to assess risk for silicosis and non-
malignant respiratory disease (NMRD) mortality and morbidity. As
discussed in the Review of Health Effects Literature and Preliminary
QRA (Document ID 1711) and in Section V.C, Summary of the Review of
Health Effects Literature and Preliminary QRA, of this preamble, OSHA
used two studies (ToxaChemica, 2004, Document ID 0469; Park et al.,
2002, 0405) to determine lifetime risk for silicosis and NMRD mortality
and five studies (Buchanan et al., 2003, Document ID 0306; Chen et al.,
2001, 0332; Chen et al., 2005, 0985; Hnizdo and Sluis-Cremer, 1993,
1052; and Steenland and Brown, 1995b, 0451) to determine cumulative
risk for silicosis morbidity. OSHA discussed the reasons for selecting
these scientific studies for quantitative risk assessment in its Review
of Health Effects Literature and Preliminary QRA (Document ID 1711, pp.
340-342). Briefly, OSHA concluded that the aforementioned studies used
scientifically accepted techniques to measure silica exposures and
health effects in order to determine exposure-response relationships.
The Agency believed, and continues to believe, that these studies, as a
group, provide the best available evidence of the exposure-response
relationships between silica exposure and silicosis morbidity,
silicosis mortality, and NMRD mortality and that they constitute a
solid and reliable foundation for OSHA's final risk assessment.
OSHA received both supportive and critical comments and testimony
regarding these studies. Comments largely focused on how the authors of
these studies analyzed their data, and concerns expressed by commenters
generally focused on exposure levels and measurement, potential biases,
confounding, statistical significance of study results, and model
forms. This section does not include extensive discussion on exposure
measurement error, potential biases, thresholds, confounding factors,
and the use of the cumulative exposure metric, which are discussed in
depth in other sections of this preamble, including V.J Comments and
Responses Concerning Biases in Key Studies and V.K Comments and
Responses Concerning Exposure Estimation Error and ToxaChemica's
Uncertainty Analysis. OSHA addresses comments on general model form and
various other issues here and concludes that these comments do not
meaningfully affect OSHA's reliance on the studies discussed herein or
the results of the Agency's final risk assessment.
1. Silicosis and NMRD Mortality
There are two published studies that report quantitative risk
assessments of silicosis and NMRD mortality (see Document ID 1711, pp.
292-298). The first is an exposure-response analysis of diatomaceous
earth (DE) workers (Park et al., 2002, Document ID 0405). Park et al.
quantified the relationship between cristobalite exposure and mortality
caused by NMRD, which includes silicosis, pneumoconiosis, emphysema,
and chronic bronchitis (Park et al. refers to these conditions as
"lung disease other than cancer (LDOC)," while OSHA uses the term
"NMRD"). Because NMRD captures much of the silicosis
misclassification that results in underestimation of the disease and
includes risks from other lung diseases associated with crystalline
silica exposures, OSHA believes the risk estimates derived from the
Park et al. study reasonably reflect the risk of death from silica-
related respiratory diseases, including silicosis (Document ID 1711,
pp. 297-298). The second study (Mannetje et al. 2002b, Document ID
1089) is a pooled analysis of six epidemiological studies that were
part of an IARC effort. OSHA's contractor ToxaChemica later conducted a
reanalysis and uncertainty analysis using these data (ToxaChemica,
2004, Document ID 0469). OSHA believes that the estimates from the
pooled study represent credible estimates of mortality risk from
silicosis across a range of industrial workplaces, but are likely to
understate the actual risk because silicosis is under-reported as a
cause of death.
a. Park et al. (2002)
The American Chemistry Council (ACC) submitted several comments
pertaining to the Park et al. (2002, Document ID 0405) study, including
comments on the cohort's exposure concentrations. In its post-hearing
brief, the ACC noted that the mean crystalline silica exposure in
Park's DE cohort was estimated to be more than three times the former
general industry PEL of 100 [mu]g/m\3\ and the mean estimated exposure
of the workers with silicosis could have been close to 10 times that
level. According to the ACC, extrapolating risks from the high exposure
levels in this cohort to the much lower levels relevant to OSHA's risk
assessment (the previous general industry PEL of 100 [mu]g/m\3\ and
the revised PEL of 50 [mu]g/m\3\) is "fraught with uncertainty"
(Document ID 4209, pp. 84-85).
OSHA acknowledges that there is some uncertainty in using models
heavily influenced by exposures above the previous PEL due to potential
deviance at areas of the relationship with fewer data points. However,
OSHA believes that the ACC's characterization of exposures in the Park
et al. (2002) study as vastly higher than the final and former PELs is
incorrect. The ACC focused on mean exposure concentrations, reported by
Park et al. as 290 [mu]g/m\3\, to make this argument (Document ID 0405,
p. 37). However, in the Park et al. study, the mean cumulative exposure
of the cohort was 2.16 mg/m\3\-yrs, lower than what the final rule
would permit over 45 years of exposure (2.25 mg/m\3\-yrs) (Document ID
0405, p. 37). Thus, whereas some participants in the Park et al. study
had higher average-8-hour exposures than were typical under the
previous PEL, they were quite comparable to the exposures workers might
accumulate over their working lives under the final PEL of 50 [mu]g/
m\3\. In addition, as discussed in Section V.M, Comments and Responses
Concerning Working Life, Life Tables, and Dose Metric, OSHA believes
that the evidence in the rulemaking record, including comments and
testimony from NIOSH (Document ID 3579, Tr. 127), Kyle Steenland, Ph.D.
(Document ID 3580, Tr. 1227), and OSHA peer reviewer Kenneth Crump,
Ph.D. (Document ID 1716, p. 166), points to cumulative exposure as a
reasonable and appropriate dose metric for deriving exposure-response
relationships. In sum, OSHA does not agree that the Park study should
be discounted based on the ACC's concerns about the estimated exposure
concentrations in the diatomaceous earth cohort.
The ACC also criticized the Park study for its treatment of
possible confounding by smoking and exposure to asbestos. The ACC
commented in its pre-hearing brief that data on smoking was available
for only half of the cohort (Document ID 2307, Attachment A, p. 108).
The Panel also wrote that, "while Park et al. dismissed asbestos as a
potential confounder and omitted asbestos exposure in their final
models, the situation is not as clear-cut as they would have one
believe" (Document ID 2307, Attachment A, p. 109). The Panel
highlighted that Checkoway et al. (1997), the study upon which Park
relied to dismiss asbestos as a potential confounder, noted that
"misclassification of asbestos exposure may have hindered our ability
to control for asbestos as a potential confounder" (Document ID 0326,
p. 685; 2307, Attachment A, p. 109).
OSHA has reviewed the ACC's concerns, and maintains that Park et
al. adequately addressed the issues of possible confounding by smoking
and exposure to asbestos in this data set. Smoking habits of a third of
the individuals who died from NMRD were known in the Park et al. (2002)
study. Based on that partial knowledge of smoking habits, Park et al.
presented analyses indicating that confounding by smoking was unlikely
to significantly impact the observed relationship between cumulative
exposure to crystalline silica and NMRD mortality (Document ID 0405, p.
41). Specifically, Park et al. (2002) performed internally standardized
analyses, which tend to be less susceptible to confounding by smoking
since they compare the mortality experience of groups of workers within
the cohort rather than comparing the mortality experience of the cohort
with an external population (such as by using national mortality
rates); the authors found that the internally standardized models
yielded only slightly lower exposure-response coefficients than
externally adjusted models (Document ID 0405; 1711, p. 302). These
results suggested that estimates of NMRD mortality risks based on this
cohort are not likely to be exaggerated due to cohort members' smoking
habits. Park et al. also stated that the authors' findings regarding
possible confounding by smoking were consistent with those of Checkoway
et al., who also concluded there it was "very unlikely" that smoking
could explain the association between mortality from NMRD and silica
exposure in this cohort (Document ID 0405, p. 41; 0326, p. 687). NIOSH
noted that "[r]esidual confounding from poorly characterized smoking
could have an effect," but that effect could be either positive or
negative (Document ID 4233, pp. 32-33). While OSHA agrees that
comprehensive smoking data would be ideal, the Agency believes that the
approach taken by Park et al. to address this issue was reasonable.
Asbestos exposure was estimated for all workers in Park et al.,
which enabled the researchers to directly test confounding. They
"found no confounding by asbestos" and, accordingly, omitted asbestos
exposure in their final modeling (Document ID 0405, p. 41). As
discussed in the Review of Health Effects Literature and Preliminary
QRA (Document ID 1711, pp. 301-302), exposure to asbestos was
particularly prevalent among workers employed prior to 1930; after
1930, asbestos was presumably no longer used in the process (Gibbs,
1998, Document ID 1024, p. 307; Checkoway et al., 1998, 0984, p. 309).
Checkoway et al. (1998), who evaluated the issue of asbestos
confounding for the same cohort used by Park et al., found that the
risk ratio for the highest silica exposure group after excluding the
workers employed before 1930 from the cohort (Relative Risk (RR) =
1.73) was almost identical to the risk ratio of the high-exposure group
before excluding those same workers (RR = 1.74) (Document ID 0984, p.
309). In addition, Checkoway's reanalysis of the original cohort study
(Checkoway et al., 1993) examined those members of the cohort for whom
there was quantitative information on asbestos exposure, based on a
mixture of historical exposure monitoring data, production records, and
recorded quantities of asbestos included in mixed products of the plant
(Checkoway et al., 1996, Document ID 0325). The authors found an
increasing trend in lung cancer mortality with exposure to crystalline
silica after controlling for asbestos exposure and found only minor
changes in relative risk estimates after adjusting for asbestos
exposure (1996, Document ID 0325). Finally, Checkoway et al. (1998)
reported that the prevalence of pleural abnormalities (indicators of
asbestos exposure) among workers hired before 1930 (4.2 percent) was
similar to that of workers hired after 1930 who presumably had no
asbestos exposure (4.9 percent), suggesting that asbestos exposure was
not a confounder for lung abnormalities in this group of workers
(Document ID 0984, p. 309). Therefore, Checkoway et al. (1998)
concluded that asbestos was not likely to significantly confound the
exposure-response relationship observed between lung cancer mortality
and exposure to crystalline silica in diatomaceous earth workers.
Rice et al. also utilized Checkoway's (1997, Document ID 0326) data
to test for confounding by asbestos in their Poisson and Cox
proportional hazards models. Finding no evidence of confounding, Rice
et al. did not include asbestos exposure as a variable in the final
models presented in their 2001 paper (Document ID 1118, p. 41). Based
on these numerous assessments of the effects of exposure to asbestos in
the diatomaceous earth workers cohort used by Park et al. (2002), OSHA
concludes that concerns about asbestos confounding in this cohort have
been adequately addressed and that the additional analyses performed by
Park et al. on this issue confirmed the findings of prior researchers
that confounding by asbestos exposure was not likely to have a large effect
on exposure-response relationships.
The ACC also expressed concern about model selection. Louis Anthony
Cox, Jr., Ph.D., of Cox Associates, on behalf of the ACC, was concerned
that the linear relative rate model was not appropriate because it is
not designed to test for exposure-response thresholds and, similarly,
the ACC has argued that threshold models are appropriate for
crystalline silica-related diseases (Document ID 2307, Attachment 4,
pp. 91). The ACC claimed that the Park et al. (2002) study is "fully
consistent" with a threshold above the 100 [mu]g/m\3\ concentration
for NMRD, including silicosis, mortality (Document ID 2307, Attachment
A, p. 107).
In its post-hearing comments, NIOSH explained that categorical
analysis for NMRD indicated no threshold existed with cumulative
exposure corresponding to 25 [mu]g/m\3\ over 40 years of exposure,
which is below the cumulative exposure equivalent to the new PEL over
45 years (Document ID 4233, p. 27). Park et al. did not estimate a
threshold below that level because the data lacked the power needed to
discern a threshold (Document ID 4233, p. 27). OSHA agrees with NIOSH's
assessment. In addition, as discussed extensively in Section V.I,
Comments and Responses Concerning Thresholds for Silica-Related
Diseases, OSHA has carefully reviewed the issue of thresholds and has
concluded, based on the best available evidence, that workers with
cumulative and average exposure levels permitted under the previous PEL
of 100 [mu]g/m\3\ are at risk of silica-related disease (that is, there
is unlikely to be an exposure-response threshold at or near 100 [mu]g/
m\3\). For these reasons, OSHA disagrees with Dr. Cox's criticism of
Park et al.'s reliance on the linear relative rate model.
The ACC then questioned the use of unlagged cumulative exposures as
the metric in Park et al. (2002). Dr. Cox noted that "[u]nlagged
models are not very biologically plausible for dust-related NMRD deaths
(if any) caused by exposure concentrations in the range of interest.
Unresolved chronic inflammation and degradation of lung defenses takes
years to decades to manifest" (Document ID 2307, Attachment 4, p. 92).
OSHA considers this criticism overstated. Park et al. considered a
range of lag periods, from two years to 15. They found that
"[u]nlagged models seemed to provide the best fit to the data in
Poisson analyses although lagged models performed almost as well"
(Document ID 0405, p. 37). Based on those findings, as well as
acknowledgments that NMRD effects other than silicosis (e.g., chronic
bronchitis) may be observable without a relatively long lag time
(unlike cancer) and that the majority of deaths observed in the cohort
were indeed NMRD other than silicosis, the researchers decided to use
an unlagged model. Because Park found the differences between the
lagged and unlagged models for this cohort and the NMRD endpoint to be
insignificant, OSHA finds that Park's final choice to use an unlagged
model does not detract from OSHA's decision to utilize lagged models in
its risk assessment.
The ACC was also concerned about the truncation of cumulative
exposures in the Park et al. (2002) paper. Peter Morfeld, Dr. rer.
medic, stated that Park et al.:
suffers from a methodological drawback....The authors truncated
the cumulative RCS dust exposures before doing the final analyses
based on their observation of where the cases were found. The
maximum in the study was 62.5 mg/m\3\-years but exposures were only
used up to 32 mg/m\3\-years because no LDOC deaths occurred at
exposures higher than that level. Such a selection distorts the
estimated exposure-response relationship because it is based on the
outcome of the study and on the exposure variable. Because high
exposures with no effects were deliberately ignored, the exposure-
response effect estimates are biased upward (Document ID 2307,
Attachment 2, p. 27).
OSHA acknowledges this concern about the truncation of data in the
study, and asked Mr. Park about it at the public hearing. Mr. Park
testified that there were good reasons to truncate the part of the
exposed workforce at the high end of cumulative exposure. He noted
several plausible reasons for the drop-off in the number of cases at
high exposures (attenuation), including random variance in
susceptibility to disease among different people and the healthy worker
survivor effect \6\ (Document ID 3579, Tr. 242-243). He also stated
that this attenuation is a common occurrence in studies of workers
(Document ID 3579, Tr. 242). Mr. Park then emphasized that how one
describes the higher end of the exposure-response relationship is
inconsequential for the risk assessment process because the
relationship at the lower end of the spectrum, where the PEL was
determined, is more important for rulemaking (Document ID 3579, Tr.
242-243). He also stated, in a post-hearing comment, that "[f]or the
purpose of low exposure extrapolation, adding a quadratic term [to
better describe the entirety of the exposure-response relationship]
would result in loss of precision with no advantage [gained] over
truncation of high cumulative exposure observation time" (Document ID
4233, p. 26). To summarize, Mr. Park stated that there are good
scientific reasons to expect attenuation of exposure-response at the
high end of the cumulative exposure range and that use of higher-
exposure data affected by healthy worker survivor effect or other
issues could reduce precision of the exposure-response model at the
lower exposures that are more relevant to the final silica standard.
OSHA finds that Mr. Park's approach in his study, along with his
explanations in the rulemaking record, are reasonable and that he has
fully responded to the concerns of the ACC.
---------------------------------------------------------------------------
\6\ Briefly, if individuals cease working due to illness, then
those individuals will not be represented in cohort subgroups having
the highest cumulative exposures. That exclusion may enable
individuals with greater physiological resilience to silica
exposures to be overrepresented in cohorts exposed to greater
amounts of silica. Further discussion on the healthy worker survivor
effect can be found in Section V.F, Comments and Responses on Lung
Cancer Mortality.
---------------------------------------------------------------------------
Dr. Morfeld also noted that alternative techniques that do not
require truncation are available to account for a healthy worker
survivor effect (Document ID 2307, Attachment 2, pp. 27-28). OSHA
believes such techniques, such as g-estimation, to be relatively new or
not yet in standard use in occupational epidemiology. As discussed
above, OSHA finds Mr. Park's approach in his study to be reasonable.
Finally, Dr. Cox stated in his comments that:
key studies relied on by OSHA, such as Park et al. (2002), do not
correct for biases in reported ER [exposure-response] relations due
to residual confounding by age (within age categories), i.e., the
fact that older workers may tend to have both higher lung cancer
risks and higher values of occupational exposure metrics, even if
one does not cause the other. This can induce a non-causal
association between the occupational exposure metrics and the risk
of cancer (Document ID 2307, Attachment 4, p. 29).
Confounding occurs in an epidemiological study when the
contribution of a causal factor cannot be separated from the effect of
another variable (e.g., age) not accounted for in the analysis.
Residual confounding occurs when attempts to control for confounding
are not precise enough (e.g., controlling for age by using groups with
age spans that are too wide), or subjects are misclassified with
respect to confounders (Document ID 3607, p. 1). However, the Park et
al. (2002) study of non-malignant respiratory disease mortality, which
Dr. Cox cited as not considering residual confounding by age, actually
addressed this issue by using 13 five-year age groups
(<25, 25-29, 30-34, etc.) in the models (Document ID 0405, p. 37).
Further discussion on residual confounding bias is found in Section V.J,
Comments and Responses Concerning Biases in Key Studies.
The inclusion of Park et al. (2002) (Document ID 0405) in OSHA's
risk assessment has additional support in the record. OSHA's expert
peer-review panel supported including the Park et al. study in the risk
assessment, with Gary Ginsberg, Ph.D., stating that it "represents a
reasonable estimate of silica-induced total respiratory mortality"
(Document ID 3574, p. 29). In addition, as OSHA noted in its Review of
Health Effects Literature and Preliminary QRA (Document ID 1711, pp.
355-356), the Park et al. study is complemented by the Mannetje et al.
multi-cohort silicosis mortality pooled study, which included several
cohorts that had exposure concentrations in the range of interest for
this rulemaking and also showed clear evidence of significant risk of
silicosis and other NMRD at the previous general industry and
construction PELs (2002b, Document ID 1089).
b. Mannetje et al. (2002b) and ToxaChemica (2004)
The ACC also submitted several comments on the Mannetje et al.
(2002b) study of silicosis mortality; the data from Mannetje et al.
were used in the ToxaChemica (2004) re-analysis. As noted above, the
Mannetje et al. (2002b) study was a pooled analysis of silicosis
mortality data from six epidemiological cohorts. This study showed a
statistically significant association between silicosis mortality and
workers' cumulative exposure, as well as with average exposure and
exposure duration. The ACC's pre-hearing brief stated that the study
"provided no justification for the relative rate model forms [Mannetje
et al.] used to evaluate exposure-response" (Document ID 2307,
Attachment A, p. 113). The concern expressed was that the study may not
have considered all potential exposure-response relationships and was
unable to discern differences between monotonic and non-monotonic
characteristics (Document ID 2307, Attachment A, p. 113-114).
Mannetje et al. (2002b, Document ID 1089) did not discuss whether
models other than relative rate models were tested. However, Mannetje's
data was reexamined by ToxaChemica, Inc. on request from OSHA and the
reexamined data was used by OSHA to help estimate lifetime risk for
silicosis mortality (2004, Document ID 0469; 1711, pp. 310-314). The
ToxaChemica reanalysis of the data included a categorical analysis and
a five-knot restricted spline analysis, in addition to a logistic
model, using the log of cumulative exposure (Document ID 0469, p. 50).
ToxaChemica also corrected some errors found in the original data set
and used a nested case-control approach, which they stated would
control more precisely for age than the Poisson regression approach
used by Mannetje et al. (Document ID 0469, p. 18). As shown in Figure 5
of ToxaChemica's report, the restricted spline model (which has
considerable flexibility to represent non-monotonic features of
exposure-response data) appeared to be monotonic, while the categorical
analysis appeared largely monotonic but for one exposure group
(Document ID 0469, p. 40, 50). When not adjusted for measurement error,
the second highest exposure group deviated from the monotonic
relationship existing between the other groups. However, the deviation
was resolved when two sources of measurement error were accounted for
(Document ID 0469, p. 40). The categorical analysis, restricted spline
model, and logistic model yielded roughly similar exposure-response
curves (Document ID 0469, p. 50). OSHA concludes that the ToxaChemica
reanalysis addresses the concerns raised by the ACC by finding similar
exposure-response relationships regardless of the model as well as
providing greater validation of a monotonic curve.
The ACC next questioned the odds ratios generated in the Mannetje
et al. (2002b) study (Document ID 2307, p. 114; 4209, p. 88). The Panel
noted that "the exposure-response relationship is not even fully
monotonic" and that the silica odds ratios in the pooled analysis have
overlapping confidence intervals, suggesting no statistically
significant difference (Document ID 2307, p. 114). The Panel concluded
that "the data indicate that there is no clear effect of exposure on
odds ratios over the entire range considered by the authors; hence, the
study provides no basis for concluding that reducing exposures will
reduce the odds ratio for silicosis mortality" (Document ID 4209, p.
88). Essentially, the ACC argued that the data do not appear to fit a
monotonic relationship and that the confidence intervals for each
exposure level overlap too much to discern any differences in risk
ratios between those exposures.
OSHA believes that the ACC overstated its contention about
confidence interval overlap between groups in the Mannetje et al.
(2002b) paper. Although the original data set reported in the study
lacks a monotonic relationship on the upper end of the exposure
spectrum (>9.58 mg/m\3\-yrs) (possibly due to a healthy worker survivor
effect, as explained above), OSHA notes that the 95 percent confidence
intervals reported do not contradict the presence of a monotonic
relationship (Document ID 1089). First, the confidence intervals of the
lower exposed groups did not overlap with those of the higher exposed
groups in that study (Document ID 1089). Second, even if they did,
overlap in confidence intervals does not mean that there is not a
significant difference between those groups. While it is true that, if
95 percent confidence intervals do not overlap, the represented
populations are statistically significantly different, the converse--
that, if confidence intervals do overlap, there is no statistically
significant difference--is not always true (Nathaniel Schenker and Jane
F. Gentleman. "On Judging the Significance of Differences by Examining
the Overlap Between Confidence Intervals." The American Statistician.
55(3): 2001. 182-186. (http://www.tandfonline.com/doi/abs/10.1198/000313001317097960).
Finally, as discussed above and in detail in Section V.K, Comments
and Responses Concerning Exposure Estimation Error and ToxaChemica's
Uncertainty Analysis, the ToxaChemica et al. (2004) re-analysis of the
corrected Mannetje et al. (2002b) data adjusting for two sources of
measurement error resulted in a monotonic relationship for the risk
ratios (Document ID 0469).
2. Silicosis Morbidity
OSHA relied on five studies for determining risk for silicosis
morbidity: Buchanan et al., 2003 (Document ID 0306), Chen et al., 2001
(Document ID 0332), Chen et al., 2005 (Document ID 0985), Hnizdo and
Sluis-Cremer, 1993 (Document ID 1052), and Steenland and Brown, 1995b
(Document ID 0451). OSHA finds that the most reliable estimates of
silicosis morbidity, as detected by chest radiographs, come from these
five studies because they evaluated radiographs over time, included
post-employment radiographic evaluations, and derived cumulative or
lifetime estimates of silicosis disease risk. OSHA received several
comments about these studies.
a. Buchanan et al. (2003)
Buchanan et al. (2003) reported on a cohort of Scottish coal
workers (Document ID 0306). The authors found a statistically
significant relationship between silicosis and cumulative
exposure acquired after 1964 (Document ID 0306). They also
found that the risks of silicosis over a working lifetime can
rise dramatically with exposure to high concentrations over
a timescale of merely a few months (Document ID 0306). In the
Preliminary QRA, OSHA considered this study to be of the highest
overall quality of the studies relied upon to assess silicosis
morbidity risks, in large measure because the underlying exposure data
was based on modern exposure measurement methods and avoided the need
to estimate historical exposures. The risk estimates derived from this
study were lower than those derived from any of the other studies
criticized by the ACC. One reason for this is because Buchanan et al.
only included cases with chest x-ray findings having an ILO score of 2/
1 or higher, whereas the other studies included cases with less damage,
having a lower degree of perfusion on x-ray (ILO 1/0 or 1/1) (Document
ID 0306). Thus, OSHA considered the risk estimates derived from the
Buchanan et al. study to be more likely to understate risks.
Dr. Cox commented that age needed to be included for modeling in
Dr. Miller's 1998 paper, the data from which were used in the Buchanan
et al. (2003) paper (Document ID 2307, Attachment 4, p. 97). However,
the Miller et al. (1998) study explicitly states that age was one of
several variables that were tried in the model but did not improve the
model's fit, as was time spent working in the poorly characterized
conditions before 1954 (Document ID 0374, p. 57). OSHA concludes that
the original paper did assess these variables and how they related to
the exposure-response relationship. Buchanan et al. (2003) also noted
their own finding that differences in age and exposure both failed to
improve fit, in agreement with Miller et al.'s conclusion (Document ID
0306, p. 161). OSHA therefore finds no credible reason that age should
have been included as a variable in Miller et al. (1998).
Dr. Cox also questioned the modeling methods in the Buchanan paper,
which presented logistic regression in progressive stages to search for
significance (Document ID 2307, Attachment 4, pp. 97-98; 0306, pp. 161-
163). Dr. Cox claimed that this is an example of uncorrected multiple
testing bias where the post hoc selection of data, variables, and
models can make independent variables appear to be statistically
significant in the prediction model. He suggested that corrections for
bias are needed to determine if the reported significance is causal or
statistical (Document ID 2307, Attachment 4, pp. 97-98). OSHA peer
reviewer Brian Miller, Ph.D., stated that Dr. Cox's claim that the
model was affected by multiple testing bias is unfounded (Document ID
3574, pp. 31-32). He noted that the model was based on a detailed
knowledge of the history of exposures at that colliery, and represented
the researchers' attempt to build "a reality-driven and `best-fitting'
model," (Document ID 3574, p. 31, quoting 2307, Attachment 4, p. 4).
Furthermore, none of OSHA's peer reviewers raised any concerns about
the approach taken by Buchanan et al. to develop their exposure-
response model and none suggested that corrections needed to be made
for multiple testing bias; all of them supported the study's inclusion
in OSHA's risk assessment (Document ID 3574). Finally, the cumulative
risk for silicosis morbidity derived from this study is similar to
values from other papers reported in the QRA (see OSHA's Final
Quantitative Risk Assessment in Section VI). Therefore, for the reasons
discussed above, OSHA is not convinced by Dr. Cox's arguments and finds
no credible reason to remove Buchanan et al. (2003) from consideration.
b. Chen et al. (2001, 2005), Steenland and Brown (1995), and Hnizdo and
Sluis-Cremer (1993)
The ACC also commented on several other studies used by OSHA to
estimate silicosis morbidity risks; these were the studies by Chen et
al. (2001, Document ID 0332; 2005, 0985), Steenland and Brown (1995b,
Document ID 0451), and Hnizdo and Sluis-Cremer (1993, Document ID
1052). The ACC's comments focus on uncertainties in estimating the
historical exposures of cohort members (Document ID 2307, Attachment A,
pp. 117-122, 124-130, 132-136). Section V.K, Comments and Responses
Concerning Exposure Estimation Error and ToxaChemica's Uncertainty
Analysis, discusses the record in detail with respect to the general
issue of uncertainties in estimating historical exposures to respirable
crystalline silica in epidemiological studies. The issues specific to
the studies relied upon by OSHA in its risk estimates for silicosis
morbidity will be discussed below.
In the Chen et al. studies, which focused on mining (i.e., tin,
tungsten) and pottery cohorts, high volume area samplers collected dust
and the respirable crystalline silica concentration was determined from
those samples (2001, Document ID 0332; 2005, 0985). However, according
to the ACC, the rest of the collected dust was not assessed for
chemicals that potentially could also cause radiographic opacities
(Document ID 2307, Attachment A, pp. 132-135). Neither study expressed
reason to be concerned about the non-silica portion of the dust
samples. OSHA recognizes that uncertainty about potential unknown
exposures exists in retrospective studies, which describes most
epidemiological research. However, OSHA emphasizes that the risk values
derived from the Chen et al. studies do not differ remarkably from
other silicosis morbidity studies used in the risk assessment (Document
ID 0306, 1052, 0451). Therefore, OSHA concludes that it is unlikely
that an unknown compound significantly impacted the exposure-response
relationships reported in both Chen studies.
The study on gold miners (Steenland and Brown, 1995b, Document ID
0451), which found that cumulative exposure was the best disease
predictor, followed by duration of exposure and average exposure, was
also criticized by the ACC, which alleged that the exposure assessment
suffered from "enormous uncertainty" (Document ID 2307, Attachment A,
pp. 146-147). The ACC noted that exposure measurements were not
available for the years prior to 1937 or after 1975 and that this
limitation of the exposure information may have resulted in an
underestimation of exposures (Document ID 2307, Attachment A, pp. 124-
126). OSHA agrees that these are potential sources of uncertainty in
the exposure estimates, but recognizes exposure uncertainty to be a
common occurrence in occupational epidemiology studies. OSHA believes
that the authors used the best measurement data available to them in
their study.
The ACC also took issue with Steenland and Brown's conversion
factor for converting particle count to respirable silica mass (10
mppcf = 100 [mu]g/m\3\), which was somewhat higher than that used in
the Vermont granite worker studies (10 mppcf = 75 [mu]g/m\3\) (Document
ID 2307, Attachment A, p. 126). OSHA notes that the study's reasoning
for adopting that specific particle count conversion factor was to
address the higher percentage of silica found in the gold mine samples
applicable to their cohort in comparison to the Vermont granite study
(Document ID 0451, p. 1373). OSHA finds this decision, which was based
on the specific known exposure conditions of this cohort, to be
reasonable.
With respect to the Hnizdo and Sluis-Cremer (1993, Document ID
1052) study, which found that silicosis risk increased exponentially with
cumulative exposure to respirable dust (Document ID 1052, p. 447), the
ACC questioned three assumptions the study made about exposures. First,
exposures were assumed to be static from the 1930s to the 1960s, based
on measurements from the late 1950s to mid-1960s, an assumption that,
according to the ACC, might underestimate exposure for workers employed
before the late 1950s (Document ID 2307, Attachment A, pp. 117-119).
Second, although respirable dust, by definition, includes particles up
to 10 [mu]m, the study only considered particles sized between 0.5 and
5 [mu]m in diameter (Document ID 1052, p. 449). The ACC contends this
exclusion may have resulted in underestimated exposure and
overestimated risk (Document ID 2307, Attachment A, p. 119). OSHA
agrees that uncertainty in exposure estimates is an important issue in
the silica risk assessment, and generally discusses the issue of
exposure measurement uncertainty in depth in a quantitative uncertainty
analysis described in Section V.K, Comments and Responses Concerning
Exposure Estimation Error and ToxaChemica's Uncertainty Analysis. As
discussed there, after accounting for the likely effects of exposure
measurement uncertainty in the risk assessment, OSHA affirms the
conclusion of the risk assessment that there is significant risk of
silicosis to workers exposed at the previous PELs.
Thirdly, the ACC challenged the authors' estimate of the quartz
content of the dust as 30 percent when it should have been 54 percent
(Document ID 1052, p. 450; 2307, Attachment A, p. 120). According to
the ACC, the 30 percent estimate was based on an incorrect assumption
that the samples had been acid-washed (resulting in a reduction in
silica content) before the quartz content was measured (Document ID
2307, Attachment A, pp. 120-122). This assumption would greatly
underestimate the exposures of the cohort and the exposures needed to
cause adverse effects, thus overestimating actual risk (Document ID
2307, Attachment A, pp. 121-122). The ACC recommended that the quartz
content in the Hnizdo and Sluis-Cremer study be increased from 30 to 54
percent, based on the Gibbs and Du Toit study (2002, Document ID 1025,
p. 602).
OSHA considered this issue in the Preliminary QRA (Document ID
1711, p. 332). OSHA noted that the California Environmental Protection
Agency's Office of Environmental Health Hazard Assessment reviewed the
source data for Hnizdo and Sluis-Cremer, located in the Page-Shipp and
Harris (1972, Document ID 0583) study, and compared them to the quartz
exposures calculated by Hnizdo and Sluis-Cremer (OEHHA, 2005, Document
ID 1322, p. 29). OEHHA concluded after analyzing the data that the
samples likely were not acid-washed and that the Hnizdo and Sluis-
Cremer paper erred in describing that aspect of the samples.
Additionally, OEHHA reported data that suggests that the 30 percent
quartz concentration may actually overestimate the exposure. It noted
that recent investigations found the quartz content of respirable dust
in South African gold mines to be less than 30 percent (Document ID
1322). In summary, OSHA concludes that no meaningful evidence was
submitted to the rulemaking record that changes OSHA's original
decision to include the Hnizdo and Sluis-Cremer study in its risk
assessment.
Despite the uncertainties inherent in estimating the exposures of
occupational cohorts in silicosis morbidity studies, the resulting
estimates of risk for the previous general industry PEL of 100 [mu]g/
m\3\ are in reasonable agreement and indicate that lifetime risks of
silicosis morbidity at this level, and, by extension, risks at the
higher previous PELs for maritime and construction (see section VI,
Final Quantitative Risk Assessment and Significance of Risk) are in the
range of hundreds of cases per 1,000 workers. Even in the unlikely
event that exposure estimates underlying all of these studies were
systematically understated by several fold, the magnitude of resulting
risks would likely still be such that OSHA would determine them to be
significant.
3. Conclusion
After carefully considering all of the comments on the studies
relied on by OSHA to estimate silicosis and NMRD mortality and
silicosis morbidity risks, OSHA concludes that the scientific evidence
used in its quantitative risk assessment substantially supports the
Agency's finding of significant risk for silicosis and non-malignant
respiratory disease. In its risk estimates in the Preliminary QRA, OSHA
acknowledged the uncertainties raised by the ACC and other commenters,
but the Agency nevertheless concluded that the assessment was
sufficient for evaluating the significance of the risk. After
evaluating the evidence in the record on this topic, OSHA continues to
conclude that its risk assessment (see Final Quantitative Risk
Assessment in Section VI.C of this preamble) provides a reasonable and
well-supported estimate of the risk faced by workers who are exposed to
respirable crystalline silica.
E. Comments and Responses Concerning Surveillance Data on Silicosis
Morbidity and Mortality
As discussed above in this preamble, OSHA has relied on
epidemiological studies to assess the risk of silicosis, a debilitating
and potentially fatal occupationally-related lung disease caused by
exposure to respirable crystalline silica. In the proposed rule (78 FR
56273, 56298; also Document ID 1711, pp. 31-49), OSHA also discussed
data from silicosis surveillance programs that provide some information
about the number of silicosis-associated deaths or the extent of
silicosis morbidity in the U.S. (78 FR at 56298). However, as OSHA
explained, the surveillance data are not sufficient for estimating the
risks of health effects associated with exposure to silica, nor are
they sufficient for estimating the benefits of any potential regulatory
action. This is because silicosis-related surveillance data are only
available from a few states and do not provide exposure data that can
be matched to surveillance data. Consequently, there is no way of
knowing how much silica a person was exposed to before developing fatal
silicosis (78 FR at 56298).
In addition, the available data likely understate the resulting
death and disease rates in U.S. workers exposed to crystalline silica
(78 FR 56298). This understatement is due in large part to: (1) The
passive nature of these surveillance systems, which rely on healthcare
providers' awareness of a reporting requirement and submission of the
appropriate information on standardized forms to health departments;
(2) the long latency period of silicosis; (3) incomplete occupational
exposure histories, and (4) other factors that result in a lack of
recognition of silicosis by healthcare providers, including the low
sensitivity, or ability of chest x-rays to identify cases of silicosis
(78 FR 56298). Specific to death certificate data, information on usual
industry and occupation are available from only 26 states for the
period 1985 to 1999, and those codes are not verifiable (Document ID
1711). Added to these limitations is the "lagging" nature of
surveillance data; it often takes years for cases to be reported,
confirmed, and recorded. Furthermore, in many cases, the available
surveillance systems lack information about actual exposures or even
information about the usual occupation or industry of the deceased
individual, which could provide some information about occupational
exposure (see 78 FR at 56298). Therefore, the Agency did not use these
surveillance data to estimate the risk of silicosis for the purpose of
meeting its legal requirements to prove a significant risk of material
impairment of health (see 29 U.S.C. 655(b)(5); Benzene, 448 U.S. 607,
642 (1980)).
Comments and testimony focusing on the silicosis surveillance data
alleged that OSHA should have used the surveillance data in its risk
estimates. Stakeholders argued that the declining numbers of reported
silicosis deaths prove the lack of necessity for a new silica standard.
Commenters also claimed that the surveillance data prove that OSHA
overestimated both the risks at the former permissible exposure limits
(PELs) and the benefits of the new rule.
After reviewing the rulemaking record, OSHA maintains its view that
these silicosis surveillance data, although useful for providing
context and an illustration of a significant general trend in the
reduction of deaths associated with silicosis over the past 4-5
decades, are not sufficient for estimating the magnitude of the risk or
the expected benefits. In the case of silicosis, surveillance data are
useful for describing general trends nationally and a few states have
the ability to use the data at the local or state level to identify
"sentinel events" that would justify initiating an inspection of a
workplace, for example. The overall data, however, are inadequate and
inappropriate for estimating risks or benefits associated with various
exposure levels, as is required of OSHA's regulatory process, in part
because they significantly understate the extent of silicosis in
workers in the United States and because they lack information about
exposure levels, exposure sources (e.g., type of job), controls, and
health effects that is necessary to examine the effects of lowering the
PEL. Thus, for these reasons and the ones discussed below, OSHA has
continued to rely on epidemiological data to meet its burden of
demonstrating that workers exposed to respirable crystalline silica at
the previous PELs face a significant risk of developing silicosis and
that risk will be reduced when the new limit is fully implemented.
Another related concern identified by stakeholders is the apparent
inconsistency between surveillance data and risk and benefits estimates
derived from modeling epidemiological data (Document ID 4194, pp. 7-10;
4209, pp. 3-4). However, this difference is not an inconsistency, but
the result of comparing two distinctly different items. Surveillance
data, primarily death certificate data, are known to be under-reported
and lack associated exposure data necessary to model relationships
between various exposure levels and observance of health effects. For
these reasons, OSHA relied on epidemiologic studies with detailed
exposure-response relationships to evaluate the significance of risk at
the preceding and new PELs. Thus, the silicosis mortality data derived
from death certificates and estimates of silica-related mortality risks
derived from well-conducted epidemiologic studies cannot be directly
compared in any meaningful way. With respect to silicosis morbidity,
OSHA notes that the estimates by Rosenman et al. (2003, Document ID
0420) of the number of cases of silicosis estimated to occur in the
U.S. (between 2,700 and 5,475 estimated to be in OSHA's jurisdiction
(i.e., excluding miners)) each year is in reasonable agreement with the
estimates derived from epidemiologic studies, assuming either a 13-year
or 45-year working life (see Chapter VII, Table VII-2 of the FEA).
1. Surveillance Data on Silicosis Mortality
The principal source of data on annual silicosis mortality in the
U.S. is the National Institute for Occupational Safety and Health
(NIOSH) Work-Related Lung Disease (WoRLD) Surveillance System (e.g.,
NIOSH, 2008c, Document ID 1308), which compiles cause-of-death data
from death certificates reported to state vital statistics offices and
collected by the National Center for Health Statistics (NCHS). Paper
copies were published in 2003 and 2008 (Document ID 1307; 1308) and
data are updated periodically in the electronic version on the CDC Web
site (http://www.cdc.gov/eworld). NIOSH also developed and manages the
National Occupational Respiratory Mortality System (NORMS), a data-
storage and interactive data retrieval system that reflects death
certificate data compiled by NCHS (http://webappa.cdc.gov/ords/norms.html).
From 1968 to 2002, silicosis was recorded as an underlying or
contributing cause of death on 16,305 death certificates; of these, a
total of 15,944 (98 percent) deaths occurred in males (CDC, 2005,
Document ID 0319). Over time, silicosis-related mortality has declined
in the U.S., but has not been eliminated. Based on the death
certificate data, the number of recognized and coded deaths for which
silicosis was an underlying or contributing cause decreased from 1,157
in 1968 to 161 in 2005, corresponding to an 86-percent decline
(Document ID 1711, p. 33; 1308, p. 55) (http://wwwn.cdc.gov/eworld).
The crude mortality rate, expressed as the number of silicosis deaths
per 1,000,000 general population (age 15 and higher) fell from about
8.9 per million to about 0.5 per million over that same time frame, a
decline of 94 percent (Document ID 1711, p. 33; 1308, p. 55) (http://wwwn.cdc.gov/eworld).
OSHA's Review of Health Effects Literature and Preliminary QRA
included death certificate statistics for silicosis up to and including
2005 (Document ID 1711, p. 33). OSHA has since reviewed the more recent
NORMS and NCHS data, up to and including 2013, which appear to show a
general downward trend in mortality, as presented in Table V-1.
However, more detailed examination of the most recent data
collected through NCHS (Table V-2) indicates that the decline in the
number of deaths with silicosis as an underlying or contributing cause
has leveled off in more recent years, suggesting that the number of
silicosis deaths being recorded and captured by death certificates may
be stabilizing after 30 or more years of decline.
Robert Cohen, M.D., representing the American Thoracic Society,
noted this apparent plateau effect, testifying that "[t]he data from
the NIOSH work-related lung disease surveillance report and others show
a plateau in silicosis mortality since the 1990s, and we are concerned
that that has been the same without any further reduction for more than
20 years. So we think that we still have work to do" (Document ID 3577, p. 775).
Some commenters raised the question about whether decedents who
died more recently were exposed to high levels of silica (pre-1970s)
and therefore wouldn't necessarily reflect mortalities relevant to the
current OSHA standard (Document ID 4194, p. 9; 4209, pp. 7-8). OSHA has
no information on the age of these decedents, or the timing of their
exposure to silica. If we assume that workers born in 1940-1950 would
have started working around 1960, at the earliest, and into the 1970's,
and life expectancy in general of 70 years, or 60-70 years to account
for years of life lost due to silicosis, most of these workers' working
life would have been spent after the 1971 PEL went into effect. It is
likely that some of the more recent decedents were exposed to silica
prior to 1971; however, it is less likely that all were exposed prior
to 1971. At the end of the day, there is no actual exposure information
on these decedents, and this generalization does not account for
overexposures, which have persisted over time.
2. Surveillance Data on Silicosis Morbidity
There is no nation-wide system for collecting silicosis morbidity
case data. The data available are from three sources: (1) The National
Hospital Discharge Survey (Document ID 1711, p. 40-43); (2) the Agency
for Healthcare Research and Quality's (AHRQ) Nationwide Inpatient
Survey (Document ID 3425, p. 2; https://www.hcup-us.ahrq.gov/nisoverview.jsp); and (3) states that administer silicosis and/or
pneumoconiosis disease surveillance (see Document ID 1711, p. 40-43;
http://www.cdc.gov/niosh/topics/surveillance/ords/StateBasedSurveillance/stateprograms.html).
Both of the first two sources of data on silicosis morbidity cases
are surveys that provide estimates of hospital discharges. The first is
the National Hospital Discharge Survey (NHDS), which was conducted
annually from 1965-2010. The NHDS was a national probability survey
designed to meet the need for information on characteristics of
inpatients discharged from non-Federal short-stay hospitals in the
United States (see http://www.cdc.gov/nchs/nhds.htm). Estimates of
silicosis listed as a diagnosis on hospital discharge records are
available from the NHDS for the years 1985 to 2010 (see http://www.cdc.gov/nchs/nhds.htm). National estimates were rounded to the
nearest 1,000, and the NHDS has consistently reported approximately
1,000 discharges/hospitalizations annually since 1980 (e.g., Document
ID 1307; 1308). The second survey, the National (Nationwide) Inpatient
Sample (NIS), is conducted annually by the AHRQ. Dr. Kenneth Rosenman,
Division Chief and Professor of Medicine at Michigan State University
and who oversees one of the few occupational disease surveillance
systems in the U.S., testified that data from the NIS indicated that
the nationwide number of hospitalizations where silicosis was one of
the discharge diagnoses has remained constant, with 2,028
hospitalizations reported in 1993 and 2,082 in 2011 (Document ID 3425,
p. 2).
Morbidity data are also available from the states that administer
silicosis and/or pneumoconiosis disease surveillance. These programs
rely primarily on hospital discharge records and also may get some
reports of cases from the medical community and workers' compensation
programs. Currently, NIOSH funds the State-Based Occupational Safety
and Health Surveillance cooperative agreements (Document ID 1711, p.
40-41; http://www.cdc.gov/niosh/topics/surveillance/ords/StateBasedSurveillance.html). All states funded under a cooperative
agreement conduct population-based surveillance for pneumoconiosis
(hospitalizations and mortality), and a few states (currently Michigan
and New Jersey) have expanded surveillance specifically for silicosis
(Document ID 1711, p. 40-42; http://www.cdc.gov/niosh/topics/surveillance/ords/StateBasedSurveillance/stateprograms.html).
State-based hospital discharge data are a useful population-based
surveillance data source for quantifying pneumoconiosis (including
silicosis), even though only a small number of individuals with
pneumoconiosis are hospitalized for that condition (Document ID 0996),
and the data refer to hospitalizations with a diagnosis of silicosis,
and not specific people. In addition to mortality data, NIOSH has
updated its WoRLD Surveillance System with some state-based morbidity
case data (http://wwwn.cdc.gov/eworld/Grouping/Silicosis/94). State-
based surveillance systems can provide more detailed information on a
few cases of silicosis.
NIOSH has published aggregated state case data in its WoRLD Reports
(Document ID 1308; 1307) for two ten-year periods that overlap, 1989 to
1998 and 1993 to 2002. State morbidity case data are compiled and
evaluated by variables such as ascertainment source, primary industry,
and occupations. For the time period 1989 to 1998, Michigan reported
589 cases of silicosis, New Jersey 191 cases, and Ohio 400 cases
(Document ID 1307, p. 69). In its last published report, for the later
and partially overlapping time period 1993 to 2002, Michigan reported
465 cases, New Jersey 135, and Ohio 279 (Document ID 1308, p. 72). Data
for the years 2003 to 2011, from the CDC/NIOSH electronic report,
eWoRld, show a modest decline in the number of cases of silicosis in
these three states; however, decreases are not nearly as substantial as
are those seen in the mortality rates (see Table V-3). Annual averages
for the two ten-year periods and the nine-year time period were
calculated by OSHA solely for the purpose of comparing cases of
silicosis reported over time.
3. Critical Comments Received on Surveillance Data
Industry representatives, including ACC's Crystalline Silica Panel
and Dr. Jonathan Borak, representing the Chamber of Commerce (Chamber),
contended that the steep decline seen in the number and rate of
silicosis deaths since 1968 proves that OSHA cannot meet its burden of
demonstrating that a more protective standard is necessary (e.g.,
Document ID 4209, p. 10; 2376, p. 8; 4016, p. 9). Similarly, other
commenters, such as the American Petroleum Institute, the Independent
Petroleum Association of America, the National Mining Association, the
American Foundry Society (AFS), the National Utility & Excavating
Contractors Association, Acme Brick, the National Ready Mixed Concrete
Association, and the Small Business Administration's Office of Advocacy
stated that surveillance data demonstrate that the previous OSHA PEL
was sufficiently effective in reducing the number of deaths from
silicosis (Document ID 3589, Tr. 4041; 4122; 2301, pp. 3, 7-9; 2211, p.
2; 2379, pp. 23-25; 2171, p. 1; 3730, p. 5; 3586, Tr. 3358-3360; 3589,
Tr. 4311; 2349, pp. 3-4). Industry commenters also argued that the
number of recorded silicosis-related deaths in recent years, as
reflected in the surveillance data, is far lower than the number of
lives that OSHA projected would be saved by a more stringent rule,
indicating that OSHA's risk assessment is flawed (e.g., Document ID
3578, Tr. 1074-1075; 4209, p. 3-4).
The Chamber, along with others, declared that OSHA ignored steep
declines in silicosis mortality, which in its view indicates that there
is no further need to reduce the PEL (Document ID 4194, pp. 7-8). OSHA
has not ignored the fact that the available surveillance data indicate
a decline in silicosis mortality. As discussed above and in the
proposal, the Agency has acknowledged that the available surveillance
data do show a decline in the silicosis mortality since 1968.
Furthermore, OSHA has no information on whether underreporting has
increased or decreased over time, and does not believe that differing
rates of reporting and underreporting of silicosis on death
certificates explains the observed decline in silicosis mortality. OSHA
believes that the reductions in deaths attributable to silicosis are
real, and not a statistical artifact. However, OSHA disagrees with
commenters' argument that this trend shows the lack of a need for this
new rule. First, as explained above, there is strong evidence that the
death certificate data do not capture the entirety of silicosis
mortality that actually exists, due to underreporting of silicosis as a
cause of death. Second, the stakeholders' argument assumes that
mortality will continue to decline, even in the absence of a stronger
silica standard, and that OSHA and workers should wait for this decline
to hit bottom (e.g., Document ID 4209, p. 7). However, testimony in the
record suggests that the decline in the number of deaths has leveled
off since 2000, probably because of the deaths of those historically
exposed to higher levels of silica occurred before then (e.g., Document
ID 3577, p. 775).
Third, the decline in silicosis deaths recorded over the past
several decades cannot be solely explained by improved working
conditions, but also reflects the decline in employment in industries
that historically were associated with high workplace exposures to
crystalline silica. One of OSHA's peer reviewers for the Review of
Health Effects Literature and Preliminary QRA, Bruce Allen, commented
that the observed decline in mortality "...in no way adjusts for
the declining employment in jobs with silica exposure," making "its
interpretation problematic. To emphasize the contribution of historic
declines in exposure as the underlying cause is spurious; no
information is given to allow one to account for declining employment"
(Document ID 3574, p. 7). The CDC/NIOSH also identified declining
employment in heavy industries where silica exposure was prevalent as a
"major factor" in the reduction over time in silicosis mortality
(Document ID 0319, p. 2). As discussed below, however, some silica-
generating operations or industries are new or becoming more prevalent.
In his written testimony, Dr. Rosenman pointed out that there are
"two aspects to the frequency of occurrence of disease (1)...the
risk of disease based on the level of exposure and (2) the number of
individuals at risk" (Document ID 3425, pp. 3-4). Dr. Rosenman
estimated the decline in the number of workers in Michigan foundries
(75 percent) and the number of abrasive blasting companies in Michigan
(71 percent), and then compared these percentages to the percentage
decline in the number of recorded silicosis deaths (80 percent) over a
similar time period. The similarities in these values led him to
attribute "almost all" of the decrease in silicosis deaths to a
decrease in the population at risk (Document ID 3425, pp. 3-4).
Finally, OSHA's reliance on epidemiological data for its risk
assessment purposes does not suggest that the Agency ignored the
available surveillance data. As discussed above, the data are
inadequate and inappropriate for estimating risks or benefits
associated with various exposure levels, as is required of OSHA's
regulatory process. Even in the limited cases where surveillance data
are available, OSHA generally relies on epidemiological data, to the
extent they include sufficiently detailed information on exposures,
exposure sources (e.g., type of job), and health effects, to satisfy
its statutory requirement to use the best available evidence to
evaluate the significance of risk associated with exposure to hazardous
substances.
Some stakeholders provided comments to the rulemaking record
consistent with OSHA's assessment. For example, Dr. Borak stated that
the surveillance data "provide little or no basis" (Document ID 2376,
p. 8) for OSHA to evaluate the protectiveness of the previous PELs.
Similarly, NIOSH asserted that relying on the surveillance data to show
that there is no need for a lower PEL or that there is no significant
risk at 100 [mu]g/m\3\ would be "a misuse of surveillance data"
(Document ID 3579, Tr. 167). NIOSH also added that, because the
surveillance data do not include information about exposures, it is not
the kind of data that could be used for a quantitative risk assessment.
NIOSH concluded that surveillance data are, in fact, "really not
germane to the risk assessment" (Document ID 3579, Tr. 248). OSHA
agrees with both Dr. Borak and NIOSH that the surveillance data cannot
and do not inform the Agency on the need for a lower PEL, nor is there
a role for surveillance data in making its significant risk findings.
Therefore, for its findings of significant risk at the current PEL, the
Agency relied on evidence derived from detailed exposure-response
relationships from well-conducted epidemiologic studies, and not
surveillance data, which have no associated exposure information. In
this case, epidemiologic data provided the best available evidence.
In its testimony, the AFL-CIO pointed out that a recent U.S.
Government Accountability Office (GAO) report on the Mine Safety and
Health Administration's (MSHA) proposed coal dust standard references
the National Academy of Sciences (NAS) conclusion that risk assessments
based on epidemiological data, not surveillance data, were an
appropriate means to assess risk for coal-dust exposures (Document ID
4204, p. 21; 4072, Attachment 48, pp. 7-8). The NAS emphasized that the
surveillance data available to MSHA did not include individual miners'
levels of exposure to coal mine dust and, therefore, could not be used
for the purpose of estimating disease risk for miners.
"Based on principles of epidemiology and statistical modeling, measures
of past exposures to coal mine dust are critical to assessing the
relationship between miners' cumulative coal mine dust exposure and
their risk of developing [pneumoconiosis]" (Document ID 4072,
Attachment 48, p. 8). The same rationale applies here. Thus, OSHA's
decision to rely on epidemiological data is well supported by the
record.
Commenters from companies and industry groups also argued that they
had no knowledge of workers acquiring silicosis in their companies or
industry (e.g., Document ID 2384, p. 2; 2338, p. 3; 2365, p. 2; 2185,
p. 3; 2426, p. 1). OSHA received similar comments as part of a letter
campaign in which over 100 letters from brick industry representatives
claimed there to be little or no silicosis observed in the industry
despite historical exposures above the PEL (e.g., Document ID 2009).
OSHA considered these comments and believes that many companies,
including companies in the brick industry, may not have active medical
surveillance programs for silicosis. Silicosis may not develop until
after retirement as a result of its long latency period. In addition,
silica exposures in some workplaces may be well below the final PEL as
a result of the environment in which workers operate, including
existing controls. Thus, OSHA believes that it is difficult to draw
conclusions about the rate of silicosis morbidity in specific
workplaces without having detailed information on medical surveillance,
silica exposures, and follow-up. This is why OSHA relies heavily on
epidemiological studies with detailed exposure data and extended
follow-up, and uses these data to evaluate exposure-response
relationships to assess health risks at the preceding and new PELs.
Commenters also argued that, due to the long latency of the
disease, silicosis cases diagnosed today are the result of exposures
that occurred before the former PELs were adopted, and thus reflect
exposures considerably higher than the previous PELs (e.g., Document ID
2376, p. 3; 2307, p. 12; 4194, p. 9; 3582, Tr. 1935). OSHA notes that
the evidence shows that the declining trend in silicosis mortality does
not provide a complete picture with regard to silicosis trends in the
United States. Although many silicosis deaths reported today are likely
the result of higher exposures (both magnitude and duration), some of
which may have occurred before OSHA adopted the previous PELs,
silicosis cases continue to occur today--some in occupations and
industries where exposures are new and/or increasing. For example, five
states reported cases of silicosis in dental technicians for the years
1994 to 2000 (CDC, MMWR Weekly, 2004, 53(09), pp. 195-197), for the
first time. For the patients described in this report, the only
identified source of crystalline silica exposure was their work as
dental technicians. Exposure to respirable crystalline silica in dental
laboratories can occur during procedures that generate airborne dust
(e.g., mixing powders, removing castings from molds, grinding and
polishing castings and porcelain, and using silica sand for abrasive
blasting). In 2015, the CDC reported the first case of silicosis
(progressive massive fibrosis) associated with exposure to quartz
surfacing materials (countertop fabrication and installation) in the
U.S. The patient was exposed to dust for 10 years from working with
conglomerate or quartz surfacing materials containing 70%-90%
crystalline silica. Cases had previously been reported in Israel, Italy
and Spain (MMWR, 2015, 64(05); 129-130). Recently, hazardous silica
exposures have been newly documented during hydraulic fracturing of gas
and oil wells (Bang et al., MMWR, 2015, 64(05); 117-120).
Dr. Rosenman's testimony provides support for this point. He
testified that newer industries with high silica exposures may also be
under-recognized because workers in those industries have not yet begun
to be diagnosed with silicosis due to the latency period (Document ID
3577, p. 858). Dr. Rosenman submitted to the record a study by Valiante
et al. (2004, Document ID 3926) that identified newly exposed
construction workers in the growing industry of roadway repair, which
began using current methods for repair in the 1980s. These methods use
quick-setting concrete that generates dust containing silica above the
OSHA PEL when workers perform jackhammering, and sawing and milling
concrete operations. State surveillance systems identified 576
confirmed silicosis cases in New Jersey, Michigan, and Ohio that were
reported to NIOSH for the years 1993 through 1997. Of these, 45 (8
percent) cases were in construction workers, three of which had been
engaged in highway repair.
Sample results for this study indicated a significant risk of
overexposure to crystalline silica for workers who performed the five
highway repair tasks involving concrete. Sample results in excess of
the OSHA PEL were found for operating a jackhammer (88 percent of
samples), sawing concrete and milling concrete tasks (100 percent of
samples); cleaning up concrete tasks (67 percent of samples); and
drilling dowels (100 percent of samples). No measured exposures in
excess of the PEL were found for milling asphalt and cleaning up
asphalt; however, of the eight samples collected for milling asphalt,
six (55 percent) results approached the OSHA PEL, and one was at 92
percent of the PEL. No dust-control measures were in place during the
sampling of these highway repair operations.
The authors pointed out that surveillance systems such as those
implemented by these states are limited in their ability to detect
diseases with long latencies in highway repair working populations
because of the relatively short period of time that modern repair
methods had been in use when the study was conducted. Nevertheless, a
few cases were identified, although the authors explain that the work
histories of these cases were incomplete, and the authors recommended
ongoing research to evaluate the silicosis disease potential among this
growing worker population (Document ID 3926, pp. 876-880). In
construction, use of equipment such as blades used on handheld saws to
dry-cut masonry materials have increased both efficiency and silica
exposures for workers over the past few decades (Document ID 4223, p.
11-13). Exposure data collected by OSHA as part of its technological
feasibility analysis demonstrates that exposures frequently exceed
previous exposure limits for these operations when no dust controls are
used (see Chapter IV of the FEA). Another operation seeing new and
increasing exposures to respirable crystalline silica is hydraulic
fracturing in the oil and gas industry (Document ID 3588, p. 3773).
Information in the record from medical professionals noted that lung
diseases caused by silica exposures are "not relics of the past," and
that they continue to see cases of silicosis and other related
diseases, even among younger workers who entered the workforce after
the former PEL was enacted (see Document ID 3577, Tr. 773).
Furthermore, the general declining trend seen in the death
certificate data is considerably more modest in silicosis morbidity
data. In his written testimony, Dr. Rosenman stated that the nationwide
number of hospitalizations where silicosis was one of the discharge
diagnoses has remained constant, with 2,028 hospitalizations reported
in 1993 and 2,082 in 2011 (Document ID 3425, p. 2). It is the opinion of
medical professionals including the American Thoracic Society and the
American College of Chest Physicians that these hospitalizations likely
represent "the tip of the iceberg" (of silicosis cases) since milder
cases are not likely to be admitted to the hospital (Document ID 2175,
p. 3). Again, this evidence shows that the declining trend observed in
silicosis mortality statistics does not provide a complete picture with
regard to silicosis trends in the United States. While silicosis
mortality has decreased substantially since records were first
available in 1968, the number of silicosis related deaths appears to
have leveled off (see Table V-2; Document ID 3577, Tr. 775). Workers
are still dying from silicosis today, and new cases are being
identified by surveillance systems, where they exist.
Based on the testimony and evidence described above, OSHA finds
that the surveillance data describing trends in silicosis mortality and
morbidity provide useful evidence of a continuing problem, but are not
suitable for evaluating either the adequacy of the previous PELs or
whether a more protective standard is needed. In fact, it would not be
possible to derive estimates of risk at various exposure levels from
the available surveillance data for silica. OSHA therefore
appropriately continues to rely on epidemiological data and its
quantitative risk assessment to support the need to reduce the previous
PELs in its final rule.
Commenters also argued that OSHA has failed to prove that a new
standard is necessary because silica-associated deaths are due to
existing exposures in excess of the previous PELs; therefore, the
Agency should focus on better enforcing the previous PELs, rather than
enacting a new standard (e.g., Document ID 2376, p. 8; 2307, p. 12;
4016, pp. 9-10; 3582, Tr. 1936). OSHA does not find this argument
persuasive. First, many of the commenters used OSHA's targeted
enforcement data to make this point. These data were obtained during
inspections where OSHA suspected that exposures would be above the
previous PELs. Consequently, the data by their very nature are skewed
in the direction of exceeding the previous PELs, and such enforcement
serves a deterrence function, encouraging future compliance with the
PEL.
Second, not all commenters agreed that overexposures were
"widespread." A few other commenters (e.g., AFS) thought that OSHA
substantially overstated the number of workers occupationally exposed
above 100 [mu]g/m\3\ in its PEA (Document ID 2379, p. 25). However
OSHA's risk analyses evaluated various exposure levels in determining
risks to workers, and did not rely on surveillance data, which rarely
have associated exposure data. Although OSHA relied on exposure data
from inspections to assess technological feasibility, it did not rely
on inspection data for its risk assessment because these exposure data
are not tied to specific health outcomes. Instead, the exposure data
used for risk assessment purposes is found in the scientific studies
discussed throughout this preamble section.
The surveillance data are also not comparable to OSHA's estimate of
deaths avoided by the final rule because, as is broadly acknowledged,
silicosis is underreported as a cause of death on death certificates.
Thus, the surveillance data capture only a portion of the actual
silicosis mortality. This point was raised by several rulemaking
participants, including Dr. Rosenman; Dr. James Cone, MD, MPH,
Occupational Medicine Physician at the New York City Department of
Health, the AFL-CIO; and the American Thoracic Society (ATS) (Document
ID 3425, p. 2; 3577, Tr. 855, 867; 4204, p. 17; 2175, p. 3; 3577, Tr.
772).
The rulemaking record includes one study that evaluated
underreporting of silicosis mortality. Goodwin et al. (2003, Document
ID 1030) estimated, through radiological confirmation, the prevalence
of unrecognized silicosis in a group of decedents presumed to be
occupationally exposed to silica, but whose causes of death were
identified as respiratory diseases other than silicosis. In order to
assess whether silicosis had been overlooked and under-diagnosed by
physicians, the authors looked at x-rays of decedents whose underlying
cause of death was listed as tuberculosis, cor pulmonale, chronic
bronchitis, emphysema, or chronic airway obstruction, and whose usual
industry was listed as mining, construction, plastics, soaps, glass,
cement, concrete, structural clay, pottery, miscellaneous mineral/
stone, blast furnaces, foundries, primary metals, or shipbuilding and
repair.
Any decedent found to have evidence of silicosis on chest x-ray
with a profusion score of 1/0 was considered to be a missed diagnosis.
Of the 177 individuals who met study criteria, radiographic evidence of
silicosis was found in 15 (8.5 percent). The authors concluded that
silicosis goes undetected even when the state administers a case-based
surveillance system. Goodwin et al. (2003, Document ID 1030) also cites
mortality studies of Davis et al. (1983, Document ID 0999) and Hughes
(1982, Document ID 0362) who reported finding decedents with past chest
x-ray records showing evidence of silicosis but no mention of silicosis
on the death certificate.
The Goodwin et al. (2003) study illustrates the importance of
information about the decedent's usual occupation and usual industry on
death certificates. Yet for the years 1985 to 1999, only 26 states
coded this information for inclusion on death certificates. If no
occupational information is available, recognizing exposure to silica,
which is necessary to diagnose silicosis, becomes even more difficult,
further contributing to possible underreporting.
Dr. Rosenman, a physician, epidemiologist and B-reader, testified
that in his research he found silicosis recorded on only 14 percent of
the death certificates of individuals with confirmed silicosis
(Document ID 3425, p. 2; 3577, Tr. 854; see also 3756, Attachment 11).
This means that as much as 86 percent of deaths related to silicosis
are missing from the NIOSH WoRLD database, substantially compromising
the accuracy of the surveillance information. Dr. Rosenman also found
that silicosis is listed as the cause of death in a small percentage of
individuals who have an advanced stage of silicosis; 18 percent in
those with progressive massive fibrosis (PMF) and 10 percent in those
with category 3 profusion.
As noted above, factors that contribute to underreporting by health
care providers include lack of information about exposure histories and
difficulty recognizing occupational illnesses that have long latency
periods, like silicosis (e.g., Document ID 4214, p. 13; 3584, Tr.
2557). Dr. Rosenman's testimony indicated that many physicians are
unfamiliar with silicosis and this lack of recognition is one factor
that contributes to the low recording rate for silicosis on death
certificates (Document ID 3577, Tr. 855). In order to identify cases of
silicosis, a health care provider must be informed of the patient's
history of occupational exposure to dust containing respirable silica,
a critical piece of information in identifying and reporting cases of
silicosis. However, information on a decedent's usual occupation and/or
industry is often not available at the time of death or is too general
to be useful. If the physician completing the death certificate is
unaware of the decedent's occupational exposure history to crystalline
silica, and does not have that information available to her/him on a
medical record, a diagnosis of silicosis on the death certificate is
unlikely. According to a study submitted by the Laborers' Health and
Safety Fund of North America, (Wexelman et al., 2010), a sample of
physician residents surveyed in New York City did not believe that
cause of death reporting is accurate; this was a general finding, and
not specific to silicosis (Document ID 3756, Attachment 7).
The ATS and the American College of Chest Physicians commented that
physicians often fail to recognize or misdiagnose silicosis as another
lung disease on the death certificate, leading to under-reporting on
death certificates (3577, Tr. 821, 826-827) and under-recognize and
underreport cases of silicosis (Document ID 2175, p. 3). As Dr.
Weissman from NIOSH responded:
...it's well known that death certificates don't capture all
of the people that have a condition when they pass away, and so
there would be many that probably would not be captured if the
silicosis didn't directly contribute to the death and depending on
who filled out the death certificate, and the conditions of the
death and all those kinds of things. So it's an under-representation
of people who die with the condition.... (Document ID 3579, pp.
166-167).
Although there is little empirical evidence describing the extent
to which silicosis is underreported as a cause of death, OSHA finds,
based on this evidence as well as on testimony in the record, that the
available silicosis surveillance data are likely to significantly
understate the number of deaths that occur in the U.S. where silicosis
is an underlying or contributing cause. This is in large part due to
physicians and medical residents who record causes of death not being
familiar or having access to the patient's work or medical history (see
Wexelman et al., 2010, Document ID 3756, Attachment 7; Al-Samarri et
al., Prev. Chronic Dis. 10:120210,2013). According to Goodwin et al.
(2003, Document ID 1030, p. 310), most primary care physicians do not
take occupational histories, nor do they receive formal training in
occupational disease. They further stated that, since it is likely that
a person would not retain the same health care provider over many
years, even if the presence of silicosis in a patient might have been
known by a physician who cared for them, it would not necessarily be
known by another physician or resident who recorded cause of death
years or decades later and who did not have access to the patient's
medical or work history. OSHA finds the testimony of Dr. Rosenman
compelling, who found that silicosis was not recorded as an underlying
or contributing cause of death even where there was chest x-ray
evidence of progressive massive fibrosis related to exposure to
crystalline silica.
Some commenters stated that the decline in silicosis mortality
demonstrates that there is a threshold for silicosis above the prior
PEL of 100 [mu]g/m\3\ (Document ID 4224, p. 2-5; 3582, Tr. 1951-1963).
OSHA finds this argument irrelevant as the threshold concept does not
apply to historical surveillance data. As noted above and discussed in
Section V.I, Comments and Responses Concerning Threshold for Silica-
Related Diseases, OSHA believes that surveillance data should not be
used for quantitative risk analysis (including determination of
threshold effects) because it lacks an exposure characterization based
on sampling. Thus, the surveillance data cannot demonstrate the
existence of a population threshold.
There is also evidence in the record that silicosis morbidity
statistics reviewed earlier in this section are underreported. This can
be due, in part, to the relative insensitivity of chest roentgenograms
for detecting lung fibrosis. Hnizdo et al. (1993) evaluated the
sensitivity, specificity and predictive value of radiography by
correlating radiological and pathological (autopsy) findings of
silicosis. "Sensitivity" and "specificity" refer to the ability of
a test to correctly identify those with the disease (true positive
rate), and those without the disease (true negative). Because
pathological findings are the most definitive for silicosis, findings
on biopsy and autopsy provide the best comparison for determining
sensitivity and specificity of chest imaging.
The study used three readers and defined a profusion score of 1/1
as positive for silicosis. Sensitivity was defined as the probability
of a positive radiological reading (ILO category >1/1) given that
silicotic nodules were found in the lungs at autopsy. Specificity was
defined as the probability of a negative radiological reading (ILO
category < 1/1) given that no, or only an insignificant number of
silicotic nodules were found at autopsy. The average sensitivity values
were low for each of the three readers (0.39, 0.37, and 0.24), whereas
the average specificity values were high (0.99, 0.97, and 0.98). For
all readers, the proportion of true positive readings (i.e., the
sensitivity) increased with the extent of silicosis found at autopsy
(Document ID 1050).
In the only published study that quantified the extent of
underreporting of silicosis mortality and morbidity, Rosenman et al.
estimated the number of new cases of silicosis occurring annually in
the U.S. at between 3,600 and 7,300 based on the ratio of living to
deceased persons identified and confirmed as silicotics in the Michigan
surveillance data and extrapolating that ratio using the number of
deaths due to silicosis for the U.S. as a whole (2003, Document ID
0420). OSHA reviewed the study in its Review of the Health Effects
Literature (Document ID 1711, p. 48). Patrick Hessel, Ph.D., criticized
the methods used by Dr. Rosenman, and deemed the resulting estimates
unreliable, stating that the actual number of new silicosis cases
arising each year is likely to be lower than the authors estimated
(Document ID 2332, p. 2; 3576, Tr. 323-331).
OSHA disagrees with the criticisms that Dr. Hessel, commenting on
behalf of the Chamber, offered on the study by Rosenman et al. (2003,
Document ID 0420). Specifically, Dr. Hessel argued: (1) That the
silicosis-related deaths used by Rosenman et al. occurred during the
period 1987 through 1996, and do not reflect the declining numbers
after that time period; (2) that the Michigan surveillance system
relied on a single B-reader who was biased toward finding silicosis in
patients who were brought to his attention for suspected silicosis; and
(3) that the Michigan population was not representative of the rest of
the country, since about 80 percent of the workers diagnosed with
silicosis worked in foundries, which are not prevalent in most other
states. Finally, in his hearing testimony, Dr. Hessel criticized the
capture-recapture analysis used by Rosenman et al. to estimate the
extent of underreporting of cases, stating that a number of underlying
assumptions used in the analysis were not met (Document ID 3576, Tr.
323-332).
Dr. Rosenman addressed many of these criticisms in the study and at
the rulemaking hearing. Regarding the fact that the number of
silicosis-related deaths does not reflect the decline in deaths after
1996, Dr. Rosenman testified that, although the number of recorded
silicosis deaths have declined since then, the ratio of cases to deaths
has increased because the number of cases has not declined. "The
living to dead ratio that we reported in our published study in 2003
was 6.44. This ratio has actually increased in recent years to 15.2. A
similar ratio...[was] found in the New Jersey surveillance data,
which went from 5.97 to 11.5 times" (Document ID 3577, Tr. 854). If
one were to apply the more recent ratio from Michigan (more than double
the ratio used by Rosenman et al.) to the more recent number of deaths
in the country (about half that recorded in the mid-1990s; see Table V-
1) to extrapolate the number of silicosis cases for the U.S. overall,
the result would be even greater than the estimate in Rosenman et al. (2003).
At the hearing, Dr. Rosenman testified that he was the sole B-
reader of lung x-rays for the study, and that he received the x-ray
films from other radiologists who suspected but did not confirm the
presence of silicosis (Document ID 3577, Tr. 877-878). Dr. Rosenman,
while acknowledging that there could be differences between readers in
scoring x-ray films, argued that such differences in scoring--for
example, whether a film is scored a 3/3, 3/2, or 2/3--did not affect
this study since the study design only required that a case be
identified and confirmed (diagnosis requires a chest radiograph
interpretation showing rounded opacities of 1/0 or greater profusion)
(Document ID 3577, Tr. 877-878; 0420, p. 142).
Dr. Rosenman also addressed the criticism that Michigan's worker
population with silica exposure is significantly different from the
rest of the country. In the study, Rosenman et al. reported that the
ratio of cases to deaths was about the same for Ohio as for Michigan
and, during the public hearing, Dr. Rosenman testified that the ratio
of cases to deaths for New Jersey was also similar to Michigan's (11.5
vs. 15.2) (Document ID 0420, p. 146; 3577, Tr. 854). This similarity
was despite the fact that New Jersey had a different industrial mix,
with fewer foundries (Document ID 3577, Tr. 878). Furthermore, the
estimates made by Rosenman et al. depended on the ratio of cases to
deaths in Michigan, rather than just the number of cases in that state.
The authors believed that the ratio would be unaffected by the level of
industrialization in Michigan (Document ID 0420, p. 146).
Finally, regarding the capture-recapture analysis, OSHA notes that
Dr. Hessel acknowledged that this technique has been used in
epidemiology to estimate sizes of populations identified from multiple
overlapping sources (Document ID 2332, p. 2), which is the purpose for
which Rosenman et al. used the approach. In addition, the Rosenman et
al. study noted that the assumptions used in capture-recapture analysis
could not be fully met in most epidemiological study designs, but that
the effect of violating these assumptions was either negligible or was
evaluated using interaction terms in the regression models employed.
The investigators also reported that the capture-recapture analysis
used on Ohio state surveillance data found that the total number of
cases estimated for the state was between 3.03 and 3.18 times the
number of cases identified, a result that is comparable to that for
Michigan (Document ID 0420, pp. 146-147). After considering Dr.
Hessel's written testimony, Dr. Rosenman testified that "...overall
I don't think his comments make a difference in my data" (Document ID
3577, Tr. 877).
OSHA finds all of Dr. Rosenman's responses to Dr. Hessel's
criticisms to be reasonable. And based on Dr. Rosenman's comments and
testimony, OSHA continues to believe that the Rosenman et al. (2003)
analysis and resulting estimates of the number of new silicosis cases
that arise each year are reasonable. Additionally, Dr. Rosenman, in
updating his data for his testimony for this rulemaking, found that the
ratio had increased from 6.44 in the published study to 15.2 times in
more recent years (Document ID 3577, Tr. 854). The study supports
OSHA's hypothesis that silicosis is a much more widespread problem than
the surveillance data suggest and that OSHA's estimates of the non-
fatal illnesses that will be avoided as a result of this new silica
standard are not unreasonable. Regardless, even assuming commenters'
criticisms have merit, they do not significantly affect OSHA's own
estimates from the epidemiological evidence of the risks of silicosis.
Accordingly, after careful consideration of the available
surveillance data, stakeholders' comments and testimony, and the
remainder of the record as a whole, OSHA has determined that the
available silicosis surveillance data are useful for providing context
and an illustration of a significant general trend in the reduction of
deaths associated with silicosis over the past four to five decades. As
discussed above, and in large part because the data themselves are
limited and incomplete, OSHA believes reliance upon them for the
purpose of estimating the magnitude of the risk would be inappropriate.
The Agency has chosen instead to follow its well-established practice
of relying on epidemiological data to meet its burden of demonstrating
that workers exposed to respirable crystalline silica at the previous
PELs face a significant risk of developing silicosis and that such risk
will be reduced when the new limit is fully implemented.
F. Comments and Responses Concerning Lung Cancer Mortality
OSHA received numerous comments regarding the carcinogenic
potential of crystalline silica as well as the studies of lung cancer
mortality that the Agency relied upon in the Preliminary Quantitative
Risk Assessment (QRA). Many of these comments, particularly from the
ACC, asserted that (1) OSHA should have relied upon additional
epidemiological studies, and (2) the studies that the Agency did rely
upon (Steenland et al., 2001a, as re-analyzed in ToxaChemica, 2004;
Rice et al., 2001; Attfield and Costello, 2004; Hughes et al., 2001;
and Miller and MacCalman, 2009) were flawed or biased. In this section,
OSHA presents these comments and its responses to them.
1. Carcinogenicity of Crystalline Silica
As discussed in the Review of Health Effects Literature and
Preliminary QRA (Document ID 1711, pp. 76-77), in 1997, the World
Health Organization's International Agency for Research on Cancer
(IARC) conducted a thorough expert committee review of the peer-
reviewed scientific literature and classified crystalline silica dust,
in the form of quartz or cristobalite, as Group 1, "carcinogenic to
humans" (Document ID 2258, Attachment 8, p. 211). IARC's overall
finding for silica was based on studies of nine occupational cohorts
that it considered to be the least influenced by confounding factors
(Document ID 1711, p. 76). In March of 2009, 27 scientists from eight
countries participated in an additional IARC review of the scientific
literature and subsequently, in 2012, IARC reaffirmed that respirable
crystalline silica dust is a Group 1 human carcinogen that causes lung
cancer (Document ID 1473, p. 396). Additionally, in 2000, the National
Toxicology Program (NTP) of HHS concluded that respirable crystalline
silica is a known human carcinogen (Document ID 1164, p. 1).
The ACC, in its pre-hearing comments, questioned the carcinogenic
potential of crystalline silica, asserting that IARC's 1996
recommendation that crystalline silica be classified as a Group 1
carcinogen was controversial (Document ID 2307, Attachment A, p. 29).
The ACC cited Dr. Patrick Hessel's 2005 review of epidemiological
studies, published after the initial IARC determination, in which he
concluded that "the silica-lung cancer hypothesis remained
questionable" (Document ID 2307, Attachment A, p. 31). The ACC
reasserted this position in its post-hearing brief, contending that
"epidemiological studies have been negative as often as they have been
positive" (Document ID 4209, pp. 33-34).
After the publication of Dr. Hessel's 2005 review article, IARC
reaffirmed in 2012 its earlier Group 1 classification for crystalline
silica dust (Document ID 1473). As pointed out by Steenland and
Ward, IARC is one of "2 agencies that are usually considered to be
authoritative regarding whether a substance causes cancer in humans,"
the other being the NTP, which has also determined crystalline silica
to be carcinogenic on two separate occasions (2013, article included in
Document ID 2340, p. 5). David Goldsmith, Ph.D., who coauthored one of
the first published articles linking silica exposure to lung cancer,
echoed Steenland and Ward:
It is important to recognize that evidence for silica's
carcinogenicity has been reviewed three times by the International
Agency for Research on Cancer, once in 1987, 1997, and 2012. It has
been evaluated by California's Proposition 65 in 1988, by the
National Toxicology Program in 2000 and reaffirmed in 2011, and by
the National Institute for Occupational Safety and Health in 2002
(Document ID 3577, Tr. 861-862).
Multiple organizations with great expertise in this area, including
the American Cancer Society, submitted comments supporting the thorough
and authoritative nature of IARC's findings regarding silica's
carcinogenicity (e.g., Document ID 1171; 1878). OSHA likewise places
great weight on the IARC and NTP classifications and, based on their
findings, concludes that the carcinogenic nature of crystalline silica
dust has been well established. Further support for this finding is
discussed in Section V.L, Comments and Responses Concerning Causation.
2. Silicosis and Lung Cancer
In addition to debating the conclusions of IARC, Peter Morfeld, Dr.
rer. medic, testifying on behalf of the ACC Crystalline Silica Panel,
concluded that OSHA's risk estimates for lung cancer are "unreliable"
because they "ignore threshold effects and the apparent mediating role
of silicosis" (Document ID 2307, Attachment 2, p. 16). Dr. Morfeld
argued that silicosis is a necessary prerequisite for silica-related
lung cancer. Commenters' arguments about silicosis being a prerequisite
for lung cancer and silicosis having a threshold are linked; if it were
shown both that silicosis requires a certain threshold of exposure and
that only persons with silicosis get lung cancer, then silica-related
lung cancer would also have an exposure threshold. As discussed in
Section V.I, Comments and Responses Concerning Thresholds for Silica-
Related Diseases, commenters claimed that there is a threshold for
silicosis above the previous PEL for general industry, which would make
any threshold for lung cancer above that level as well. OSHA discusses
these comments in detail in that section, and has determined that even
if lung cancer does not occur in the absence of silicosis, the record
strongly supports the conclusion that workers exposed to respirable
crystalline silica would still be at risk of developing lung cancer as
a result of their exposure because silicosis can develop among workers
whose average and cumulative exposures are below the levels permitted
by the previous PELs.
OSHA received comments from other stakeholders, including Robert
Glenn, representing the Brick Industry Association, and the AFS on the
possible mediating role of silicosis in the development of lung cancer
(Document ID 2307, pp. 29-35; 2343, Attachment 1, pp. 42-45; 2379,
Attachment 2, pp. 24-25). The ACC cited several review articles in
support of its claim that "silica exposures have not been shown to
increase the risk of lung cancer in the absence of silicosis"
(Document ID 2307, Attachment A, pp. 29, 32, 35). These articles
included: A 2004 review of studies by Kurihara and Wada that found that
while silicosis is a risk factor for lung cancer, exposure to silica
itself may not be a risk factor (Document ID 1084); a 2006 review by
Pelucchi et al. that determined that the issue of whether silica itself
increases lung cancer risk in the absence of silicosis has not been
resolved (Document ID 0408); and a 2011 review by Erren et al. that
concluded it is unclear whether silica causes lung cancer in persons
who do not already have silicosis (Document ID 3873). Similarly, the
AFS cited a review by the Health and Safety Executive (2003) that
concluded that increased risks of lung cancer are restricted to those
groups with the highest cumulative exposures, with evidence tending to
show that excess lung cancer mortality is restricted to those with
silicosis (Document ID 2379, Attachment 2, pp. 24-25). Having reviewed
the studies cited by commenters, OSHA has come to the conclusion that
none of the cited studies demonstrates that silicosis is a necessary
precursor to lung cancer, but acknowledges that uncertainty remains
about what percentage of lung cancers in silica-exposed workers are
independent of silicosis.
Similarly, the ACC stated that none of the studies of lung cancer
mortality that OSHA relied upon in the Preliminary QRA demonstrates
that silica exposure causes lung cancer in the absence of silicosis
(Document ID 2307, Attachment A, p. 66). During the rulemaking hearing,
NIOSH scientists addressed the issue of whether silicosis is a
necessary precursor to the development of lung cancer. They stated that
it is a difficult issue to resolve because the two diseases may have a
similar pathway, such that they can develop independently but still
appear correlated. Mr. Robert Park also added that:
[S]ilicosis isn't detectable until there's splotches on the lung
that are visible in x-rays. So prior to that point, somebody could
have [been] developing lung disease and you just can't see it. So,
of course, people that have silicosis are going to have higher lung
cancer, and it's going to look like a threshold because you didn't
see the silicosis in other people that have lower lung cancer risk.
To really separate those two, you'd have to do a really big study.
You'd have to have some measures, independent measures of lung
physiological pathology, and see what's going on with silicosis as a
necessary condition for development of lung cancer (Document ID
3579, Tr. 245-247).
Similarly, David Weissman, MD, concurred that "there's quite a bit
of reason as Bob [Park] said to think that the two processes
[development of silicosis and development of lung cancer] don't require
each other, and it would be extraordinarily difficult to sort things
out in human data" (Document ID 3579, Tr. 247). Indeed, Checkoway and
Franzblau (2000) reviewed the epidemiological literature addressing
this topic, and found that the "limitations of existing epidemiologic
literature that bears on the question at hand suggest that prospects
for a conclusive answer are bleak" (Document ID 0323, p. 257). The
authors concluded that silicosis and lung cancer should be treated in
risk assessments as "separate entities whose cause/effect relations
are not necessarily linked" (Document ID 0323, p. 257). Brian Miller,
Ph.D., a peer reviewer of OSHA's Review of Health Effects Literature
and Preliminary QRA, likewise wrote in his post-hearing comments, "I
consider this issue unanswerable, given that we cannot investigate for
early fibrotic lesions in the living, but must rely on radiographs"
(Document ID 3574, p. 31).
During the public rulemaking hearing, several stakeholders pointed
to a recent study of Chinese pottery workers and miners by Liu et al.
(2013, article included in Document ID 2340) as evidence that exposure
to crystalline silica is associated with lung cancer even in the
absence of silicosis (Document ID 3580, Tr. 1232-1235; 3577, Tr. 803-
804, 862-863). In this study, the authors excluded 15 percent of the
cohort (including 119 lung cancer deaths) with radiographic evidence of
silicosis and found that the risk of lung cancer mortality still
increased with cumulative exposure to crystalline silica, suggesting
that clinically-apparent silicosis is not a prerequisite for
silica-related lung cancer
(article included in Document ID 2340, pp. 3, 7).
The ACC argued that it is "premature to draw that conclusion,"
stating that the Liu study's conclusions are not supported by the data
and raising questions about uncertainty in the exposure estimates,
modeling and statistics, confounding, and the silicosis status of
cohort members (Document ID 2307, Attachment A, p. 48; 4027, pp. 35-36;
4209, pp. 40-51). With regard to exposure estimates, the ACC had a
number of concerns, including that conversion factors determined by
side-by-side sampling in 1988-1989 were used to convert Chinese total
dust concentrations to respirable crystalline silica exposures
(Document ID 4209, pp. 40-41). Dr. Cox expressed concern that these
conversion factors from 1988-1989 might not have been applicable to
other time periods, as particle size distributions could change over
time (Document ID 4027, p. 32). OSHA acknowledges this concern, but
given the "insufficient historical particle size data...to analyze
whether there were changes in particle size distributions from the
1950s to the 1990s," believes that the authors were justified in
making their exposure assumptions (Document ID 4027, p. 32). Dr. Cox's
concerns involving modeling and statistics (see Document ID 4027, pp.
33-36) in the study, including the absence of model diagnostics, the
use of inappropriate or misspecified models, the lack of a discussion
of residual confounding and model uncertainty, and the use of
inappropriate data adjustments and transformations, are discussed in
detail in Section V.J, Comments and Responses Concerning Biases in Key
Studies.
On the issue of confounding, the ACC noted that Liu et al. (2013)
used a subcohort of 34,018 participants from 6 tungsten mines, 1 iron
mine, and 4 potteries derived from a total cohort of 74,040
participants from 29 mines and pottery factories studied previously by
Chen et al. (2007, Document ID 1469; 2307, Attachment A, pp. 48-50).
Liu et al. (2013) excluded participants in the original cohort if
detailed information on work history or smoking was not available, or
if they worked in copper mines or tin mines where the analysis could be
confounded by other exposures, namely radon and carcinogenic polycyclic
aromatic hydrocarbons (PAHs) in the former and arsenic in the latter
(article included in Document ID 2340, p. 2). The ACC's main concern
was that Liu et al. (2013) did not adjust for these confounders in
their analyses, but rather claimed that there were no confounding
exposures in their smaller cohort on the basis of the exclusion
criteria (Document ID 2307, Attachment A, p. 49).
The ACC also noted that Chen et al. (2007) stated that the Chinese
pottery workers were exposed to PAHs, and some of the iron-copper
miners were exposed to PAHs and radon progeny (Document ID 2307,
Attachment A, p. 49). Chen et al. (2007) initially found an association
between respirable silica and lung cancer mortality in the pottery
workers and iron-copper miners, but it disappeared after adjusting for
PAH exposures (Document ID 1469). In the tungsten miners, Chen et al.
(2007) found no significant association for lung cancer mortality,
while Liu et al. (2013) did. Similarly, the ACC pointed out that a
subsequent study by Chen et al. (2012, article included in Document ID
2340) also failed to find a statistically significant increase in the
hazard ratio for lung cancer, meaning that there was no significant
positive exposure-response relationship between cumulative silica
exposure and lung cancer mortality (Document ID 4209, p. 45). Dr.
Morfeld concluded, "Unless and until these issues are resolved, Liu et
al. (2013) should not be used to draw conclusions regarding exposure-
response relationships between RCS [respirable crystalline silica],
silicosis and lung cancer risk" (Document ID 2307, Attachment 2, pp.
15-16).
During the public hearing, counsel to the ACC asked Dr. Steenland,
a co-author on the Liu et al. (2013) study, if he would provide
measurement data on the PAH exposures in the potteries, as well as
present the data from the Liu et al. (2013) study separately for
pottery factories and tungsten mines, as they were in Chen et al.
(2007, Document ID 1469) (Document ID 3580, Tr. 1237-1240). Dr.
Steenland subsequently provided the requested data for inclusion in the
rulemaking record (Document ID 3954).
With respect to the PAH data for the potteries, Dr. Weihong Chen,
the study's first author, reported that, in measurements in 1987-1988
in the four potteries that were excluded from the Liu et al. (2013)
analysis, the mean total PAHs was 38.9 [micro]g/m\3\ and the mean
carcinogenic PAHs was 4.7 [micro]g/m\3\. In the four potteries that
were included in the Liu et al. (2013) analysis, the mean total and
carcinogenic PAHs, as measured in 1987-1988, were substantially lower
at 11.6 and 2.5 [micro]g/m\3\, respectively. When the measurements were
repeated in 2006, the mean total and carcinogenic PAHs in the four
potteries included in the analysis were still lower, at 2.2 and 0.08
[micro]g/m\3\, levels that were "not much higher than environmental
PAH in many [Chinese] cities" (Document ID 3954, p. 2). Dr. Chen also
reported that, when comparing levels within six job titles, there was
no significant correlation between total or carcinogenic PAHs (based on
the 2006 measurements) and respirable silica dust. When the results
were presented separately for the mines and potteries, in analyses
using continuous cumulative exposure, the relationship between silica
exposure and lung cancer mortality remained significant for the pottery
factories, but not the metal mines. In the categorical analyses using
quartiles of cumulative exposure, the results were mixed: The
association between silica exposure and lung cancer mortality was
statistically significant in some exposure quartiles for both metal
mines and pottery factories (Document ID 3954, p. 2).
Based upon these subsequent data, the ACC concluded that PAHs were
likely present in the potteries but not in the mines (Document ID 4209,
p. 45). OSHA believes this conclusion, although plausible, to be
speculative. What is known is that the potteries that were excluded had
a higher average level of PAHs, and that a significant association
between cumulative silica exposure and lung cancer mortality remained
in the included potteries even after the analysis was separated by
potteries and mines. However, the association was less clear in the
metal mines.
The ACC also raised concerns about the silicosis status of lung
cancer cases in the Liu cohort, asserting that some workers may not
have had post-employment radiography given that social health insurance
only recently began to pay for it. As such, the ACC asserted that some
workers who developed lung cancer post-employment may have also had
undiagnosed silicosis (Document ID 4209, pp. 49-50). OSHA acknowledges
the limitations of the study, as with any retrospective study, but also
notes that no evidence was put forth to indicate that workers with
silicosis were misclassified in the study as workers without silicosis.
Further, Dr. Goldsmith testified that the method used by Liu et al. for
excluding workers with silicosis (x-ray findings) was "very eminently
reasonable," given that the only foolproof means of proving the
absence of silicosis--autopsy--was not available for this particular
cohort (Document ID 3577, Tr. 874-875).
Thus, OSHA concludes that the Liu et al. (2013) study preliminarily
suggests that silicosis is not required for the development of lung cancer;
however, no one study will settle the question of the role of silicosis
in the carcinogenicity of crystalline silica. As acknowledged by Dr.
Cox, the Agency did not rely upon the Liu et al. (2013) study in its
preliminary or final QRA (Document ID 2307, Attachment 4, p. 37).
Overall, after giving lengthy consideration to all evidence in the
record regarding whether silicosis is a necessary precursor to the
development of lung cancer, including the Liu study, the NIOSH
testimony, and the mechanistic evidence for the carcinogenicity of
crystalline silica discussed in Section V.H, Mechanisms of Silica-
Induced Adverse Health Effects, OSHA concludes that the mediating role
of silicosis in the development of lung cancer is not "apparent," as
suggested by Dr. Morfeld and the ACC (Document ID 2307, Attachment 2,
p. 16). As such, OSHA continues to believe that substantial evidence
supports the Agency's decision to consider lung cancer as a separate,
independent health endpoint in its risk analysis. The Agency also notes
that even if lung cancer does not occur in the absence of silicosis,
the record strongly supports the conclusion that workers exposed to
respirable crystalline silica would still be at risk of developing lung
cancer as a result of their exposure because silicosis can develop from
average and cumulative exposures below the levels allowed at the
previous PEL (see Section V.I, Comments and Responses Concerning
Thresholds for Silica-Related Diseases.)
3. Additional Studies
Stakeholders also suggested several additional studies that they
believe OSHA should include in its QRA on lung cancer. The AFS
commented that OSHA's Preliminary QRA overlooked a 2003 report by the
Health and Safety Executive (HSE, Document ID 1057), asserting that
over 40 percent of the references cited by HSE were omitted in OSHA's
review (Document ID 4035, p. 2). OSHA disagrees with this assessment of
overlooking the report, noting that the Agency reviewed and referenced
the HSE report in its Review of Health Effects Literature and
Preliminary QRA (Document ID 1711, p. 77). As discussed in Section V.C,
Summary of the Review of Health Effects Literature and Preliminary QRA,
OSHA used a weight-of-evidence approach to evaluate the scientific
studies in the literature to determine their overall quality. In so
doing, OSHA thoroughly reviewed approximately 60 published, peer-
reviewed primary epidemiological studies covering more than 30
occupational cohorts in over a dozen industrial sectors, as well as the
IARC pooled study and several meta-analyses (Document ID 1711, pp. 75-
172).
The AFS also submitted a 2011 review of 30 foundry epidemiology
studies by the Industrial Industries Advisory Council (IIAC) and noted
that only 7 of those 30 studies were included in OSHA's Review of
Health Effects Literature and Preliminary QRA (Document ID 2379, p.
24). AFS wrote:
The PQRA largely dismisses the foundry epidemiology studies,
based on assertions of positive confounding. However, a study
showing that there is no adverse effect despite a positive
confounder is not only still relevant to the question, but should be
more persuasive than a study without positive confounders because
the data then show that even with an additive risk, there is no
increase in effect at the reported exposure levels (Document ID
2379, p. 24).
In response to this comment, OSHA gathered the remaining 23 foundry
studies cited in the submitted report and placed them in the rulemaking
docket during the post-hearing comment period. OSHA notes, in the first
instance, that most of these studies were not designed to study the
effects of silica exposure on foundry workers, and did not even attempt
to do so; rather, their purpose was to examine lung cancer mortality
and/or morbidity in foundry work, which involves many toxic and
otherwise harmful substances besides silica. Therefore, OSHA would
likely be unable to suitably use these studies as a basis for a
quantitative risk assessment regarding respirable crystalline silica by
itself.
With respect to AFS's assertions of studies showing "no adverse
effect," OSHA notes that the summary section of the IIAC review
report, submitted as evidence by AFS, stated that, "The cohort
mortality studies and two morbidity studies suggest an increased risk
of lung cancer in foundry workers when considered overall, but do not
support a doubling of risk....Findings in the case-control studies,
the majority of which adjust for the effects of smoking...tend to
support those of the cohort studies" (Document ID 3991, p. 5). As
such, this review of 30 foundry epidemiology studies showed an
increased excess risk of lung cancer from foundry work; the fact that
the excess risk was not increased by a factor of two is irrelevant to
the current proceedings. The factor of two appears to be used by the
IIAC in determining whether monetary benefits should be paid to foundry
workers in Great Britain and is completely unrelated to OSHA's
statutory requirements for determining whether workers exposed to
silica are at a significant risk of material impairment of health.
Given that excess lung cancer was observed in many of these studies,
OSHA rejects the AFS's assertion that, even with positive confounding,
there was no increase in adverse effect (i.e., lung cancer).
OSHA also notes that the IIAC's finding of an elevated risk of lung
cancer in foundries is not surprising. As Dr. Mirer stated during his
testimony, IARC categorized foundry work as Group 1, carcinogenic to
humans, in 1987 based on observed lung cancer (Document ID 2257,
Attachment 3, p. 5). IARC reaffirmed its Group 1 classification for
foundry work in 2012 (Document ID 4130). However, as noted by OSHA in
its Review of Health Effects Literature, the foundry epidemiology
studies were profoundly confounded by the presence of exposures to
other carcinogens, including PAHs, aromatic amines, and metals
(Document ID 1711, p. 264). Because of this confounding, as well as the
fact that most of these studies did not specifically study the effects
of silica exposure on foundry workers, OSHA has decided not to include
them in its QRA.
The ACC likewise cited several individual studies that it believed
found no relationship between silica exposure and lung cancer risk
(Document ID 2307, Attachment A, pp. 33-35). These included studies by:
(1) Yu et al. (2007), which found no consistent exposure-response
relationship between silica exposure and lung cancer death in workers
with silicosis in Hong Kong (Document ID 3872); (2) Chen et al. (2007),
which found, as mentioned in relation to the Liu et al. (2013) study,
no relationship between silica exposure and lung cancer after adjusting
for confounders in a study of Chinese tungsten miners, tin miners,
iron-copper miners, and pottery workers (Document ID 1469); (3) Birk et
al. (2009), which found the standardized mortality ratio (SMR) for lung
cancer was not elevated in a subgroup of men who worked in areas of
German porcelain plants with the highest likely silica exposures
(Document ID 1468); (4) Mundt et al. (2011), which found, in a
subsequent analysis of the German porcelain industry, that cumulative
silica exposure was not associated with lung cancer mortality,
mortality from kidney cancer, or any other cause of death other than
silicosis (Document ID 1478); and (5) Westberg et al. (2013), which
found that cumulative silica exposure was not associated with lung
cancer morbidity (Document ID 4054).
Briefly, Chen et al. (2007) examined a cohort of male workers in 29
Chinese mines and factories, and initially found a significant trend
between cumulative silica exposure and lung cancer mortality in pottery
workers and tin miners; this trend was no longer significant after
adjustment for occupational confounders (carcinogenic PAHs in
potteries, arsenic in tin mines) (Document ID 1469, pp. 320, 323-324).
On the contrary, Liu et al. (2013) demonstrated a statistically
significant association between cumulative silica exposure and lung
cancer mortality after excluding mines and factories with confounding
exposures (article included in Document ID 2340). As noted previously,
there are questions of how confounding exposures to radon, PAHs, and
arsenic were handled in both the Chen et al. (2007) and Liu et al.
(2013) studies. One important difference between the two studies,
however, was the follow-up time. While Chen et al. (2007) had follow-up
to 1994 and identified 511 lung cancer deaths in a cohort of 47,108
workers (Document ID 1469, pp. 321-322), Liu et al. (2013) had follow-
up to 2003 and identified 546 lung cancer deaths in a cohort of 34,018
workers (article included in Document ID 2340, pp. 2-4).
OSHA discussed the Birk et al. (2009, Document ID 1468) and Mundt
et al. (2011, Document ID 1478) studies of the German porcelain
industry in its Supplemental Literature Review, noting several
limitations that are applicable to both studies and might preclude the
conclusion that there was no association between silica exposure and
lung cancer (Document ID 1711, Attachment 1, pp. 6-12). One such
limitation was the mean age of subjects--35 years--at the start of
follow-up, making this a relatively young cohort in which to observe
lung cancer. The mean follow-up period of 19 years per subject was also
a limitation, given the long latency for lung cancer and the young age
of the cohort at the start of follow-up; only 9.2 percent of the cohort
was deceased by the end of the follow-up period. OSHA noted that Mundt
et al. (2011) acknowledged that additional follow-up of the cohort may
be valuable (Document ID 1711, Attachment 1, pp. 10-11; 1478, p. 288).
In addition, Mundt et al. (2011) had only 74 male lung cancer deaths,
some of whom had possible or probable prior silica exposure that could
have resulted in cumulative exposure misclassification (Document ID
1478, pp. 285, 288). The authors also reported statistically
significantly elevated lung cancer hazard ratios for some categories of
average silica exposure, but did not present any trend analysis data
(Document ID 1478, p. 285). It also does not appear that Mundt et al.
performed any lagged analyses for lung cancer to account for the
latency period of lung cancer.
Following the ACC's citation of the Yu et al. (2007) and Westberg
et al. (2013) studies in its pre-hearing comments, OSHA obtained and
reviewed these studies, and added them to the rulemaking docket
(Document ID 3872; 4054). Yu et al. (2007) followed a cohort of 2,789
workers in Hong Kong diagnosed with silicosis between 1981 and 1998.
The average follow-up time was 9 years, with 30.6 percent of the cohort
deceased when the study ended in 1999. The SMR for lung cancer was not
statistically significantly elevated following indirect adjustment for
cigarette smoking; similarly, the authors did not find a significant
exposure-response relationship between cumulative silica exposure and
lung cancer mortality (Document ID 3872). Westberg et al. (2013)
studied a group of 3,045 male Swedish foundry workers to determine lung
cancer incidence and morbidity. Although the lung cancer incidence was
statistically significantly elevated, the authors did not find a
significant exposure-response relationship with cumulative quartz
exposure (Document ID 4054, p. 499).
Regarding these studies, OSHA notes that the Westberg et al. (2013)
study, like other foundry studies, is confounded by other carcinogenic
substances present in foundries, including, as the authors pointed out,
phenol, formaldehyde, furfuryl alcohols, PAHs, carbon black,
isocyanates, and asbestos (Document ID 4054, p. 499). The Yu et al.
(2007) study had an average follow-up period of only 9 years (Document
ID 3872, p. 1058, Table 1), which is a short follow-up period when
considering the latency period for the development of cancer. In
addition, the Yu et al. study (2007), as described in the earlier Tse
et al. (2007) study, used a job exposure matrix developed from expert
opinion to assign estimated past levels of silica exposure to
individuals based on self-reported work history; changes in exposure
intensity with calendar year were not considered because of limited
data (Document ID 3841, p. 88; 3872, p. 1057). OSHA notes that this
exposure estimation may have included considerable misclassification
due to inaccuracies in self-reported work history, the use of expert
opinion to estimate past exposure levels rather than actual
measurements for the subjects under study, and the failure to
incorporate any changes in exposure levels over calendar time into the
exposure estimates. Although these exposure estimates were used in an
analysis that found a significant exposure-response for NMRD mortality
among workers with silicosis (Tse et al., 2007, Document ID 3841), an
exposure-response for lung cancer mortality may not be as strong and
may be harder to detect, requiring more accurate exposure information.
OSHA also notes that NMRD mortality is likely to be a competing cause
of death with lung cancer, such that some workers may have died from
NMRD before developing lung cancer. The workers with silicosis in this
study also had high exposures (mean cumulative exposure of 10.89 mg/
m\3\-yrs) (Document ID 3872, p. 1058), possibly making it difficult to
detect an exposure-response for lung cancer when exposures are
relatively homogenous and high. Selection effects would have been
extreme in these highly-exposed workers, whose all-cause mortality was
double what would be expected (853 deaths observed, 406 expected) in
the general population of males in Hong Kong and whose respiratory
disease mortality was an astounding six times the expected level (445
deaths observed, 75 expected) (Document ID 3872, p. 1059).
OSHA acknowledges that not every study reaches the same results and
conclusions. This is typically true in epidemiology, as there are
different cohorts, measurements, study designs, and analytical methods,
among other factors. As a result, scientists critically examine the
studies, both individually and overall, in the body of literature to
draw weight-of-evidence conclusions. IARC noted, with respect to its
1997 carcinogenicity determination:
[N]ot all studies reviewed demonstrated an excess of cancer of
the lung and, given the wide range of populations and exposure
circumstances studied, some non-uniformity of results had been
expected. However, overall, the epidemiological findings at the time
supported an association between cancer of the lung and inhaled
crystalline silica ([alpha]-quartz and cristobalite) resulting from
occupational exposure (Document ID 1473, p. 370).
Given IARC's re-affirmation of this finding in 2012, OSHA does not
believe that the individual studies mentioned above fundamentally
change the weight of evidence in the body of literature supporting the
carcinogenicity of crystalline silica. The best available evidence in
the rulemaking record continues to indicate that exposure to respirable
crystalline silica causes lung cancer. OSHA acknowledges, however, that
there is some uncertainty with respect to the exact magnitude of the
lung cancer risk, as each of the key studies relied upon provides
slightly different risk estimates, as indicated in Table VI-1.
Further, the ACC focused extensively on and advocated for a study
by Vacek et al. (2011) that found no significant association between
respirable silica exposure and lung cancer mortality in a cohort of
Vermont granite workers (Document ID 1486, pp. 75-81). Included in the
rulemaking docket are the peer-reviewed published version of the study
(Document ID 1486) and the earlier Final Report to the ACC, whose
Crystalline Silica Panel funded the study (Document ID 2307, Attachment
6), as well as comments from two of the authors of Vacek et al. (2011)
responding to OSHA's treatment of the study in its Supplemental
Literature Review (Document ID 1804). The ACC stated:
Perhaps of most interest and relevance for present purposes--
because the cohort has been studied so extensively in the past and
because the present PEL is based indirectly on experience in the
Vermont granite industry--is the mortality study of Vermont granite
workers published in 2011. While the Vermont granite workers cohort
has been studied on a number of previous occasions, this is the most
comprehensive mortality study of Vermont granite workers to date
(Document ID 2307, Attachment A, p. 36).
The ACC criticized OSHA for rejecting the Vacek et al. (2011) study
in its Supplemental Literature Review and instead relying upon the
Attfield and Costello (2004, Document ID 0284) study of Vermont granite
workers (Document ID 2307, Attachment A, pp. 36-47; 4209, pp. 34-36).
The ACC asserted several differences between the studies. First, while
Attfield and Costello had 5,414 workers (201 lung cancer deaths) in the
cohort, Vacek et al. had 7,052 workers (356 lung cancer deaths) as they
extended the follow-up period by 10 years to 2004. Vacek et al. also
claimed to have more complete mortality data, finding that "162
workers, whom Attfield assumed were alive in 1994, had died before that
time and some decades earlier" (Document ID 2307, Attachment A, p.
38). In addition, Vacek et al. used exposure measurements and raw data
not used by Attfield and Costello; for example, Vacek et al. used
pension records and interviews from other studies to account for gaps
in employment and changes in jobs, while Attfield and Costello assumed
that a person remained in the same job between chest x-rays at the
Vermont Department of Industrial Health surveillance program. Different
conversion factors to estimate gravimetric concentrations from particle
count data were also used: Attfield and Costello used a factor of 10
mppcf = 75 [micro]g/m\3\ while Vacek et al. used a factor of 10 mppcf =
100 [micro]g/m\3\ (Document ID 2307, Attachment A, pp. 36-39; 1804, p.
3). OSHA notes that this discrepancy in gravimetric conversion factors
should not affect the detection of an exposure-response relationship,
as all exposures would differ by a constant factor.
The ACC also pointed out that Attfield and Costello's exposure
estimate for sandblasters was 60 [micro]g/m\3\ prior to 1940, 50
[micro]g/m\3\ from 1940-1950, and 40 [micro]g/m\3\ after 1950,
maintaining these numbers were too low compared to Vacek et al.'s
estimates of 240, 160, and 70 [micro]g/m\3\, respectively (Document ID
2307, Attachment A, p. 39; 1486, p. 313). Attfield and Costello took
these estimates for sand blasters from the Davis et al. (1983, Document
ID 0999) study, discussed in detail below; the estimates were based on
six published industrial hygiene measurement studies.
Lastly, the ACC posited that Attfield and Costello inappropriately
excluded the highest exposure group, stating:
Vacek et al. used all their data in evaluating potential E-R
[exposure-response] trends with increasing exposure. Attfield and
Costello did not. Instead, on a post hoc basis, they excluded the
highest exposure category from their analysis when they discovered
that the E-R trend for lung cancer was not significant if that group
was included (even though the trends for non-malignant respiratory
diseases were significant when all the data were used). This is an
example of both data selection bias and confirmation bias (Document
ID 2307, Attachment A, p. 40).
Based upon these assertions, the ACC concluded, "In sum, when
judged without a result-oriented confirmation bias, the larger, more
recent, more comprehensive, and more detailed study by Vacek et al.
(2011) must be deemed to supersede Attfield and Costello (2004) as the
basis for evaluating potential silica-related lung cancer risks in the
Vermont granite industry" (Document ID 2307, Attachment A, p. 41).
OSHA initially discussed some issues surrounding the Vacek et al.
(2011) study in its Supplemental Literature Review (Document ID 1711,
Attachment 1, pp. 2-5). Specifically, OSHA noted that (1) the
cumulative exposure quintiles used in the Vacek et al. (2011) analysis
were higher than the values used in the Attfield and Costello (2004)
analysis; (2) the regression models used in the Vacek et al. (2011)
study exhibited signs of uncontrolled confounding, as workers in the
second lowest cumulative exposure stratum in the models (except for
silicosis) exhibited a lower risk than those in the lowest stratum,
while all outcomes (except NMRD) in the highest exposure stratum showed
a decline in the odds ratio (a measure of the association between
silica exposure and health outcome) compared to the next lower stratum;
and (3) Vacek et al. (2011) found a statistically significant excess of
lung cancer (SMR = 1.37, with almost 100 excess lung cancer deaths) in
the cohort when compared to U.S. white males (Document ID 1486, p.
315). Regarding the excess lung cancer deaths, although they were
unable to obtain information on smoking for many of the cohort members,
Vacek et al. suggested that the elevated SMR for lung cancer was due,
at least in part, to the differences between the smoking habits of the
cohort and reference populations (Document ID 1486, p. 317). OSHA noted
that although the SMR for other NMRD was elevated, there was no
significant SMR elevation for other smoking-associated diseases,
including cancers of the digestive organs, larynx, and bladder, as well
as bronchitis, emphysema, and asthma (Document ID 1711, Attachment 1,
p. 5). Elevated SMRs for these diseases would be expected if workers in
the study population smoked more than those in the reference
population; in fact, for all heart disease, the mortality in the study
population (SMR = 0.89) was statistically significantly lower than the
reference population (Document ID 1486, p. 315). These data do not
support Vacek et al.'s assertion that smoking was responsible for the
increased lung cancer SMR in the cohort. In addition, Davis et al.
(1983) noted that granite shed workers employed during the 1970's
smoked only slightly more than U.S. white males (Document ID 0999, p.
717). OSHA also pointed out that the SMR may have been understated, as
Vacek et al. did not account for a healthy worker effect (HWE).
The ACC did not agree with OSHA's review of the Vacek et al. study,
noting that OSHA "rejects Vacek et al. (2011) on grounds that are
confusing and unfounded" (Document ID 2307, Attachment A, p. 41). The
ACC argued that the quintiles of cumulative exposure used by Vacek et
al. were not higher than typical values for lung cancer, and that OSHA,
in its Supplemental Literature Review, compared the Vacek et al.
quintiles of cumulative exposure for silicosis with the Attfield and
Costello groups used for both silicosis and lung cancer (Document ID
2307, Attachment A, pp. 41-42). OSHA acknowledges this discrepancy and,
given that Vacek et al. used quintiles of cumulative exposure that
differed for each health endpoint, agrees that the quintiles for lung
cancer used by Vacek et al. were not appreciably higher than the
exposure groups used by Attfield and Costello, though the Agency recognizes
that there may be alternative explanations for the patterns observed in
the Vacek et al. data. Regarding uncontrolled confounding, the ACC
stated that "The Vermont granite worker cohort, after all, supposedly is
free of confounding exposures," (Document ID 2307, Attachment A, p. 43
(citing Attfield and Costello, 2004, 0284)). Vacek et al. also pointed out
that although the odds ratios for the second lowest exposure stratums were
lower than those for the lowest categories for each of the diseases,
they were not statistically significantly lower (Document ID 1804, pp.
1-2).
Although OSHA notes that this latter phenomenon, in which the odds
ratio for the second lowest exposure stratum is lower than that for the
lowest stratum, is commonly observed and often attributable to some
form of selection confounding, the Agency recognizes that there may be
alternative explanations for the patterns observed in the Vacek et al.
data. One such explanation for the decreased odds ratios in the highest
exposure group is potential attenuation resulting from a HWE.
The HWE, as defined by Stayner et al. (2003), has two components:
(1) A healthy initial hire effect, in which bias is "introduced by the
initial selection of workers healthy enough to work...and the use
of general population rates for the comparison group, which includes
people who are not healthy enough to work," and (2) a healthy worker
survivor effect, referring "to the tendency of workers with ill health
to drop from the workforce and the effect this dropout may have on
exposure-response relationships in which cumulative exposure is the
measure of interest" (Document ID 1484, p. 318). Thus, the healthy
initial hire effect occurs in the scenario in which the death rate in a
worker group is compared to that in the general population; because the
general population has many people who are sick, the death rate for
workers may be lower, such that a direct comparison of the two death
rates results in a bias. The healthy worker survivor effect occurs in
the scenario in which less healthy workers transfer out of certain jobs
into less labor-intensive jobs due to decreased physical fitness or
illness, or leave the workforce early due to exposure-related illness
prior to the start of follow-up in the study. As a result, the
healthier workers accumulate the highest exposures such that the risk
of disease at higher exposures may appear to be constant or decrease.
OSHA disagrees with the ACC's statement that "the possibility of a
potential HWE in this cohort could not have affected the E-R analyses"
in Vacek et al. (2011) (Document ID 2307, Attachment A, p. 46), and
with the similar statement by study authors Pamela Vacek, Ph.D. and
Peter Callas, Ph.D., both of the University of Vermont, who asserted
that the HWE could not have impacted their exposure-response analyses
"because they were not based on an external reference population"
(Document ID 1804, p. 2). This explanation only considers one component
of the HWE, the healthy initial hire effect. An internal control
analysis, such as that performed by Vacek et al., will generally
minimize the healthy initial hire effect but does not address the
healthy worker survivor effect (see Document ID 1484, p. 318 (Stayner
et al. (2003)). Thus, the statement by the ACC that there could be no
HWE in the internal case control analysis of Vacek et al. (2011) is
incorrect, as it considered only the healthy initial hire effect and
not the healthy worker survivor bias.
In contrast, Attfield and Costello's stated rationale for excluding
the highest exposure group is related to the healthy worker survivor
effect:
We do know that this group is distinctive in entering the cohort
with substantial exposures--83% had worked for 20 years or more in
the high dust levels prevalent prior to controls. They were,
therefore, a highly selected healthy worker group. A further reason
may be that in the days when tuberculosis and silicosis were the
main health concerns in these workers, lung cancer may have been
obscured in this group as a cause of death in some cases" (Document
ID 0284, p. 136).
Support for Attfield and Costello's reasoning is provided by a
study by Applebaum et al. (2007), which re-analyzed the data from the
Attfield and Costello (2004) paper and concluded that there was a
healthy worker survivor effect present (study cited by Vacek et al.,
2009, Document ID 2307, Attachment 6, p. 3). Applebaum et al. (2007)
split the cohort of Vermont granite workers into two groups: (1) Those
that began working before the start of the study follow-up, i.e.,
prevalent hires; and (2) those that began working after the start of
the study follow-up, i.e., incident hires. The rationale for splitting
the cohort into these two groups was to examine if a healthy worker
survivor effect was more likely in the prevalent hire group, as this
group would be affected by workers that were more susceptible to health
effects and left the industry workforce prior to the start of the study
follow-up (Applebaum et al., 2007, pp. 681-682). Using spline models to
examine exposure-response relationships without forcing a particular
form (e.g., linear, linear-quadratic) on the observed data, the authors
found that the inclusion of prevalent hires in the analysis weakened
the association between cumulative silica exposure and lung cancer
because of bias from the healthy worker survivor effect. The bias can
be reduced by including only incident hires, or keeping the date of
hire close to the start of follow-up (Applebaum et al., 2007, pp. 685-
686). An alternative explanation for this trend offered by Applebaum et
al. may be that, assuming that there was more measurement error in the
older data, the prevalent hires had more exposure misclassification
(2007, p. 686); in such a case, however, the inclusion of prevalent
hires would still bias the results towards the null. Given the findings
of the Applebaum et al. (2007) study, OSHA believes that Attfield and
Costello (2004) had good reasons for removing the highest exposure
group, which was composed mostly of prevalent workers (83 percent of
workers in the highest exposure group had worked at least 20 years
prior to the start of the follow-up period) (Document ID 0284, p. 136).
Vacek et al. (2011), on the other hand, excluded 609 workers in the
design of their study cohort due to insufficient information. However,
the majority of the workers excluded from the cohort were incident
hires who began work after 1950 (Document ID 2307, Attachment 6, p. 12;
1486, p. 314). The final Vacek et al. (2011) cohort included 2,851
prevalent hires (began employment before 1950) compared to 4,201
incident hires (began employment in or after 1950) (Document ID 2307,
Attachment 6, p. 12; 1486, p. 314). By composing about 40 percent of
their cohort with prevalent hires and excluding many incident hires,
Vacek et al. (2011) may have introduced additional healthy worker
survivor effect bias into their study. Interestingly, Vacek et al.
described the Applebaum et al. (2007) results in their 2009 report,
stating, "They [Applebaum et al.] found that decreasing the relative
proportion of prevalent to incident hires [in the data used by Attfield
and Costello] resulted in a stronger association between cumulative
silica exposure and lung cancer mortality" (Document ID
2307, Attachment 6, p. 3). Despite their acknowledgement of the
Applebaum et al. (2007) findings, Vacek et al. (2011) did not conduct
any analysis of only the incident hires, or use statistical methods to
better determine the presence and effect of a healthy worker survivor
effect in their study.
The ACC also commented on Vacek et al.'s suggestion that the
elevated SMR observed for lung cancer in the cohort (when compared to a
reference population of U.S. white males) was due to differences in the
smoking habits of the cohort and reference population, which OSHA
criticized in its Supplemental Literature Review (Document ID 1486, p.
317; 1711, Attachment 1, p. 5). The ACC stated, "OSHA suggests that
the lack of complete smoking data for the cohort is a problem and
contends that smoking could not explain the elevated SMR for lung
cancer. This criticism, as Dr. Vacek explains, is overstated, and, in
any event, does not detract from the study's findings regarding the
absence of an association between silica exposure and lung cancer"
(Document ID 2307, Attachment A, pp. 46-47; 1804, p. 2).
Vacek et al. (2011) estimated the relative smoking prevalence in
the cohort to be 1.35 times that in the reference population; using
this estimated relative smoking prevalence, the authors estimated that
"the expected number of lung cancer deaths in the cohort after
adjusting the reference rates for smoking would be 353, yielding a
[non-significant] SMR of 1.02" (Document ID 1486, p. 317). OSHA notes
that this method used by Vacek et al. to adjust the SMR for smoking
neglects the healthy worker survivor effect (i.e., smokers may leave
the workforce sooner than nonsmokers because smoking is a risk factor
for poor health). Absent control for the healthy worker survivor
effect, smoking would (and perhaps did) become a negative confounder
because long duration--high cumulative exposure--workers would tend
toward lower smoking attributes. The method used by Vacek et al. is
also inconsistent with the frequently cited Axelson (1978) method,
which is used to adjust the SMR when the exposed population has a
higher percentage of smokers than the reference population (Checkoway
et al. 1997, Document ID 0326; Chan et al. 2000, 0983). As a result,
Vacek et al. (2011) likely overestimated the confounding effect of
smoking in this cohort.
In addition, as previously noted by OSHA, the SMRs for cancers
largely attributable to smoking, such as those of the buccal cavity and
pharynx (SMR = 1.01), larynx (SMR = 0.99), and esophagus (SMR = 1.15)
were not significant in the Vacek et al. study (Document ID 1486, p.
315; 2307, Attachment 6, p. 14). The SMR of 0.94 for bronchitis,
emphysema, and asthma also was not significant. If smoking were truly
responsible for the highly statistically significant SMR (1.37)
observed for lung cancer, the SMRs for these other diseases should be
significant as well. OSHA likewise notes that other studies have found
that smoking does not have a substantial impact on the association
between crystalline silica exposure and lung cancer mortality (e.g.,
Checkoway et al., 1997, Document ID 0326; Steenland et al., 2001a,
0452, p. 781) and that crystalline silica is a risk factor for lung
cancer independent of smoking (Kachuri et al., 2014, Document ID 3907,
p. 138; Preller et al., 2010, 4055, p. 657).
OSHA is also concerned about some features of the study design and
exposure assessment in Vacek et al. (2011). Regarding the study design,
in their nested case-control analyses, Vacek et al. sorted cases into
risk sets based on year of birth and year of death, and then matched
three controls to each risk set; from the data presented in Table 5 of
the study, the actual number of controls per lung cancer case can be
calculated as 2.64 (Document ID 1486, p. 316). Vacek et al.'s decision
to use such a small number of controls per case was unnecessarily
restrictive, as there were additional cohort members who could have
been used as controls for the lung cancer deaths. Typically, if the
relevant information is available, four or more (or all eligible)
controls are used per case to increase study power to detect an
association. OSHA notes that Steenland et al. (2001a), in their nested
case-control pooled analysis, used 100 controls per case (Document ID
0452, p. 777).
In addition, Vacek et al. stated that for the categorical analysis,
cut points on cumulative exposure were based on quintiles of the
combined distribution for cases and controls (Document ID 1486, p.
314). Therefore, there should be an approximately equal total number of
subjects (cases plus controls) in each group (or quintile). OSHA's
examination of Table 5 in the Vacek et al. (2011) study shows that
there is an approximately equal distribution of subjects for all
endpoints except lung cancer; for example, the silicosis groups each
had 43-44 subjects, the NMRD groups each had 125-130 subjects, the
kidney cancer groups each had 22-23 subjects, and the kidney disease
groups each had 25 subjects. However, the lung cancer groups, ranging
from the lowest to the highest exposure, had 325, 232, 297, 241, and
202 subjects (Document ID 1486, p. 316). OSHA could find no explanation
for this discrepancy in the text of the Vacek et al. (2011) study, and
questions how the lung cancer groups were composed.
With respect to the different job exposure matrices, OSHA has
reason to believe that the exposure data reported in the Attfield and
Costello study are more accurate than the data Vacek et al. used. OSHA
is particularly concerned that Vacek et al.'s pre-1940 exposure
estimate of 150 [micro]g/m\3\ for one job (channel bar operator) was
much lower than Attfield and Costello's estimate, from the Davis et al.
(1983) matrix, of 1070 [micro]g/m\3\ (Document ID 1486, p. 313; 0284,
p. 131). As NIOSH observed in its post-hearing comments, changing the
exposure estimate for channel bar operators could have "major
consequences" on the exposure-response analysis, as the job occurred
frequently (Document ID 4233, p. 22). NIOSH then pointed out that the
Attfield and Costello (2004) exposure estimate for channel bar
operators was based on multiple exposure measurements conducted by
Davis et al. (1983), whereas Vacek et al. based their exposure estimate
"on only three dust measurements" in which "only wet drilling was
used. Thus, their study used not only very limited sampling data but
also values that were biased towards low levels, since the samples were
taken when water was being used to control dust," a practice that was
not typically used for this occupation at the time (Document ID 4233,
p. 22). In fact, photographs from Hosey et al. (1957) showed channel
bar drilling in 1936 and 1937 with and without dust control; the
caption for the photo without dust control states that the "operator
in background is barely visible through dust cloud" (Document ID 4233,
p. 24, citing 3998, Attachment 14b). As NIOSH explained,
If there is a true [linear] relationship between exposure to
silica dust and lung cancer mortality, classifying highly exposed
workers incorrectly as low-exposed shifts the elevated risks to the
low exposure range. The impact is to spuriously elevate risks at low
exposures and lower them at high exposures, resulting in the
exposure-response trend being flattened or even obscured.
Ultimately, the true relationship may not be evident, or if it is,
may be attenuated (Document ID 4233, p. 22, n. 1).
Vacek et al. reported in their study that they conducted a
sensitivity analysis that did not change the exposure-response
relationship between silica exposure and lung cancer risk,
even when Attfield and Costello's pre-1940 exposure estimates were used
for channel bar operators (Document ID 2340, pp. 317-318; 2307,
Attachment 6, p. 31). Part of the problem may be the way that channel
bar operators were defined by Vacek et al. As noted by NIOSH, "Leyner
driller and channel bar operator or driller are synonyms" (Document ID
4233, p. 22, n. 3). Attfield and Costello defined channel bar operators
in that way, with a pre-1940 exposure estimate of 1070 [micro]g/m\3\
(Document ID 0284, p. 131). Vacek et al., on the contrary, assigned
channel bar operators to a category called "channel bar (wet)" and
assigned a pre-1940 exposure estimate of 150 [micro]g/m\3\ (Document ID
2307, Attachment 6, Appendix B, pp. 7, 15). They included Leyner
drillers under a general category called "driller" with a pre-1940
exposure estimate of 1070 [micro]g/m\3\ (Document ID 2307, Attachment
6, Appendix B, pp. 7, 15). Included in the Vacek et al. (2009) category
of "drillers" were plug drillers (Document ID 2307, Attachment 6,
Appendix B, p. 15); OSHA notes that Attfield and Costello used a lower
pre-1940 exposure estimate of 650 [micro]g/m\3\ for plug drillers, as
defined by Davis et al. (1983). OSHA believes that Vacek et al.
underestimated the exposures of some channel bar operators, and
overestimated the exposures of plug drillers, which may have
contributed to the lack of association, and that the categorization
used by Attfield and Costello, with the synonymous channel bar
operators and Leyner drillers in one category, and plug drillers in a
separate category, was more appropriate. Thus, even in Vacek et al's
sensitivity analysis, in which they used Attfield and Costello's
exposure estimate of 1070 [micro]g/m\3\ for channel bar operators and
drillers, the plug drillers would still have had a higher exposure
estimate (1070 [micro]g/m\3\ versus Attfield and Costello's 650
[micro]g/m\3\), making the analysis different from that of Attfield and
Costello.
For the reasons discussed herein, OSHA has decided not to reject
the Attfield and Costello (2004) study in favor of the Vacek et al.
(2011) study as a basis for risk assessment. OSHA maintains that it has
performed an objective analysis of the Attfield and Costello (2004) and
Vacek et al. (2011) studies. OSHA agrees with some of the ACC's
criticisms regarding the Agency's initial evaluation of the exposure
groupings and confounding in the Vacek et al. (2011) study. OSHA is
concerned, however, as discussed above, about several aspects of Vacek
et al. (2011), including a potential bias from the healthy worker
survivor effect, which was shown to exist in this cohort (see Applebaum
et al., 2007, cited in Document ID 2307, Attachment 6, p. 3), as well
as about job categorization that may have resulted in exposure
misclassification for certain job categories (e.g., the synonymous
channel bar operators and Leyner drillers). Despite its concerns with
the Vacek et al. study, OSHA acknowledges that comprehensive studies,
such as Attfield and Costello (2004) and Vacek et al. (2011), in the
Vermont granite industry have shown conflicting results with respect to
lung cancer mortality (Document ID 0284; 1486). As discussed earlier,
conflicting results are often observed in epidemiological studies due
to differences in study designs, analytical methods, exposure
assessments, populations, and other factors. In addition, the exposure-
response relationship between silica and lung cancer may be easily
obscured by bias, as crystalline silica is a comparably weaker
carcinogen (i.e., the increase in risk per unit exposure is smaller)
than other well-studied, more potent carcinogens such as hexavalent
chromium (Steenland et al., 2001, Document ID 0452, p. 781). Although
OSHA believes that the Attfield and Costello (2004) study is the most
appropriate Vermont granite study to use in its QRA, the Agency notes
that, even in the absence of the Attfield and Costello (2004) study,
the risk estimates for lung cancer mortality based on other studies
still provide substantial evidence that respirable crystalline silica
poses a significant risk of serious health conditions to exposed
workers.
4. Comments on Specific Studies Relied Upon by OSHA in Its QRA
a. Attfield and Costello (2004)
As stated above, OSHA disagrees with the ACC's contention that
Vacek et al. provides a more reliable scientific basis for estimating
risk than Attfield and Costello. While it is true that the final risk
estimate (54 deaths per 1,000 workers) derived from the Attfield and
Costello study for an exposure level of 100 [micro]g/m\3\ is the
highest when compared to the other studies, it is not true that the
final risk estimate (22 deaths per 1,000 workers) derived from the
Attfield and Costello study is the highest for the final rule's PEL of
50 [micro]g/m\3\. In fact, it is within the range of risk estimates
derived from the ToxaChemica (2004) pooled analysis of 16 to 23 deaths
per 1,000 workers at the final PEL. Thus OSHA has decided to retain its
reliance on the Attfield and Costello (2004) study and, again, notes
that, even without the Attfield and Costello (2004) study, all of the
other studies in the Final QRA demonstrate a clearly significant risk
of lung cancer mortality (11 to 54 deaths per 1,000 workers) at an
exposure level of 100 [micro]g/m\3\, with a reduced, albeit still
significant, risk (5 to 23 deaths per 1,000 workers) at an exposure
level of 50 [micro]g/m\3\ (see Table VI-1 in Section VI, Final
Quantitative Risk Assessment and Significance of Risk). Excluding
Attfield and Costello (2004), in other words, would not change OSHA's
final conclusion regarding the risk of death from lung cancer.
b. Miller and MacCalman (2009)
According to the ACC, OSHA's risk estimates based on the Miller and
MacCalman (2009, Document ID 1306) study are "more credible than the
others--because [the study] involved a very large cohort and was of
higher quality in terms of design, conduct, and detail of exposure
measurements," and also adjusted for smoking histories (Document ID
2307, Attachment A, p. 73). Although the risk estimates generated from
the Miller and MacCalman data were the lowest of the lung cancer
mortality estimates, the ACC next asserted that they were biased
upwards for several reasons. First, the ACC stated that exposure
information was lacking for cohort members after the mines closed in
the mid-1980's, and quoted OSHA as stating, "Not accounting for this
exposure, if there were any, would bias the risk estimates upwards"
(Document ID 2307, Attachment A, p. 74 (quoting 1711, p. 289)). OSHA,
however, does not believe there to have been additional substantial
quartz exposures. As the study authors wrote, "Because of the steep
decline of the British coal industry, the opportunities for further
extensive coal mine exposure were vanishingly small" (Document ID
1306, p. 11). Thus OSHA believes it to be unlikely that the risk
estimates are biased upwards to any meaningful degree based on lack of
exposure information at the end of the study period.
The ACC also stated that the unrestricted smoking of cohort members
after the closure of the mines would have resulted in risk estimates
that were biased upwards (Document ID 2307, Attachment A, p. 74). OSHA
has no reason to believe, nor did the ACC submit any evidence in
support of its contention, that unrestricted smoking occurred, however,
and notes that the authors stated that the period after the mines
closed was one of "greater anti-smoking health promotion campaigns"
(Document ID 1306, p. 11).
Finally, the ACC noted that Miller and MacCalman did not adjust
significance levels for the multiple comparisons bias with respect to
lag selection that Dr. Cox alleged affected their study (Document ID
2307, Attachment A, p. 74). Dr. Cox claimed that trying multiple
comparisons of alternative approaches, such as different lag periods,
and then selecting a final choice based on the results of these
multiple comparisons, leads to a multiple comparisons bias that could
result in false-positive associations (Document ID 2307, Attachment 4,
p. 28; see Section V.J, Comments and Responses Concerning Biases in Key
Studies). He argued that the authors should have reduced the
significance level (typically p = 0.05) at which a result is considered
to be significant. "Lag" refers to the exclusion of the more recent
years of exposure (e.g., 10-year lag, 15-year lag) to account for the
fact that diseases like cancer often have a long latency period (i.e.,
that the cancer may not be detected until years after the initiating
exposure, and exposures experienced shortly before detection probably
did not contribute to the development of disease). "Lag selection,"
therefore, refers to the choice of an appropriate lag period. As
addressed later in the Section V.J, Comments and Responses Concerning
Biases in Key Studies, OSHA does not necessarily believe such an
adjustment of significance levels to be appropriate, based upon the
testimony of Mr. Park of NIOSH, nor is it typically performed in the
occupational epidemiology literature (Document ID 3579, Tr. 151-152).
Similarly, the ACC stated that the confidence intervals are overly
narrow because they ignore model uncertainty, and that multiple
imputation of uncertain exposure values should have been performed
(Document ID 2307, Attachment A, p. 75). OSHA rejects this assertion on
the grounds that the authors used detailed exposure estimates that the
ACC recognized raised the credibility of the study; the ACC wrote,
regarding the study, "it involved a very large cohort and was of
higher quality in terms of design, conduct, and detail of exposure
measurements" (Document ID 2307, Attachment A, p. 73). Lastly, the ACC
argued that an exposure threshold should have been examined (Document
ID 2307, Attachment A, p. 75). OSHA discusses at length this issue of
thresholds, and the difficulty in ruling them in or out at low
exposures, in Section V.I, Comments and Responses Concerning Thresholds
for Silica-Related Diseases.
In summary, OSHA notes that the ACC has not provided any non-
speculative evidence to support its claims that the risk estimates
derived from the Miller and MacCalman (2009) study are biased upwards.
As stated in the Review of Health Effects Literature and Preliminary
QRA, and acknowledged by the ACC (Document ID 2307, p. 73), OSHA
believes these risk estimates to be very credible, as the study was
based on well-defined union membership rolls with good reporting, had
over 17,000 participants with nearly 30 years of follow-up, and had
detailed exposure measurements of both dust and quartz, as well as
smoking histories (Document ID 1711, pp. 288-289).
c. Steenland (2001a) and ToxaChemica (2004)
OSHA also received several comments on the ToxaChemica (2004,
Document ID 0469) analysis, which was based on the Steenland et al.
(2001a, Document ID 0452) pooled analysis. First, the ACC claimed that
there is significant heterogeneity in the exposure-response
coefficients, derived from the individual studies. Because the risk
estimates based on these coefficients differ by almost two orders of
magnitude, the ACC suggested that these models are misspecified for the
data (Document ID 2307, Attachment A, pp. 75-76). Essentially, the ACC
claimed that the exposure-response coefficients differ too much among
the individual studies, and asserted that it is therefore inappropriate
to use the pooled models. Dr. Cox wrote: "Steenland et al. did not
address the heterogeneity, but artificially suppressed it by
unjustifiably applying a log transformation. This is not a valid
statistical approach for exposure estimates with substantial estimation
errors" (Document ID 2307, Attachment 4, p. 75). During the public
hearing, however, Dr. Steenland explained to OSHA's satisfaction how
the data in his study was transformed, using accepted statistical
methods. Specifically, referring to his use of a log transformation to
address the heterogeneity, Dr. Steenland testified:
[I]t reduces the effect of the very highest exposures being able
to drive an exposure-response curve because those exposures are
often [skewed] way out--skewed to the right, because occupational
exposure data is often log normal. With some very high exposures,
they are sort of extreme, and that can drive your exposure-response
curve. And you take the log, it pulls them in, and so therefore
gives less influence to those high data points. And I think those
high data points are often measured with more error (Document ID
3580, Tr. 1265-1266).
OSHA finds this testimony to be persuasive and, therefore, believes
that Dr. Steenland's use of a log transformation to address the
heterogeneity was appropriate. The log transformation also permits a
better model fit when attenuation of the response is observed at high
cumulative exposures.
Dr. Morfeld commented that Steenland et al. did not take into
account smoking, which could explain the observed excess lung cancer of
20 percent (SMR = 1.2). Dr. Morfeld stated, "Thus, lung cancer excess
risks were demonstrated only under rather high occupational exposures
to RCS dust, and, even then, an upward bias due to smoking and a
necessary intermediate role for silicosis could not be ruled out"
(Document ID 2307, Attachment 2, p. 10). Dr. Steenland addressed the
concern about a potential smoking bias during his testimony:
We concluded that this positive exposure response was not likely
due to different smoking habits between high exposed and low exposed
workers. And the reason we did that was twofold. First, workers tend
to smoke similar amounts regardless of their exposure level in
general. We often worry about comparing workers to the general
population because workers tend to smoke more than the general
population. But, in internal analyses, we don't have this problem
very often. When we have smoking data, we see that it is not related
to exposure, so a priori we don't think it is likely to be a strong
confounder in internal analyses. Secondly, a number of the studies
we used in our pool[ed] cohort had smoking data, either for the
whole cohort or partially. And when they took that into account,
their results did not change. In fact, they also found that smoking
was not related to exposure in their studies, which means that it
won't affect the exposure-disease relationship because if it is
going to do that, it has to differ between the high exposed and the
low exposed, and it generally did not (Document ID 3580, Tr. 1227-
1228).
In addition, Brown and Rushton (2009), in their review article
submitted to the rulemaking record by Dr. Morfeld, appeared to agree
with Dr. Steenland, stating, "This [Steenland et al.] internal
analysis removed the possibility of confounding by smoking" (Document
ID 3573, Attachment 5, p. 150). Thus, OSHA rejects Dr. Morfeld's
assessment that the risk estimates may be biased upwards due to
smoking.
The ACC also commented that exposure misclassification due to
uncertain exposure estimates in Steenland's pooled cohort could have
created the appearance of a monotonic relationship, in which the
response increases with the exposure, even if the true response was not
monotonic (Document ID 2307, Attachment A, p. 76). The ACC, along with
Dr. Borak (representing the U.S. Chamber of Commerce) and others,
likewise cited OSHA's statement from the Review of Health Effects
Literature and Preliminary QRA, in which the Agency acknowledged that
uncertainty in the exposure estimates that underlie each of the 10
studies in the pooled analysis was likely to represent one of the most
important sources of uncertainty in the risk estimates (Document ID
1711, p. 292; 2376, p. 16). Dr. Borak also quoted Mannetje et al.
(2002), who developed quantitative exposure data for the pooled
analysis, as stating, "While some measurement error certainly occurred
in our estimates, a categorical analysis based on broad exposure groups
should not be much affected by the resulting level of
misclassification" (Document ID 2376, p. 17, quoting 1090, p. 84).
From this statement, Dr. Borak concluded that the researchers
themselves believed the data were only adequate for "categorical
analyses which might lead to qualitative conclusions" (Document ID
2376, p. 17).
OSHA disagrees with Dr. Borak's interpretation of the Mannetje et
al. statement, as categorical analyses are typically quantitative in
nature, with the data being used to draw quantitative conclusions.
However, OSHA recognized the possibility for uncertainty in the
exposure estimates, and it is for this reason that OSHA commissioned a
quantitative analysis of uncertainty in Steenland's pooled study
(ToxaChemica, 2004, Document ID 0469). This analysis suggested that
exposure misclassification had little effect on the pooled exposure
coefficient (and the variance around that estimate) for the lung cancer
risk model (Document ID 1711, pp. 313-314). Given this analysis, OSHA
also disagrees with the ACC's statement that "it is virtually certain
that substantial exposure estimation error infused the pooled analysis,
resulting in exposure misclassification that would create a false
appearance of a monotonically increasing exposure-response even where
none exists" (Document ID 2307, Attachment A, p. 78). OSHA notes that
this statement is not supported with any evidence from the Steenland et
al. (2001) study. In addition, as discussed at length in Section V.K,
Comments and Responses Concerning Exposure Estimation Error and
ToxaChemica's Uncertainty Analysis, exposure estimation error can also
bias results towards the null (weaken or obscure the exposure-response
relationship) (Document ID 3580, Tr. 1266-67; 3576, Tr. 358-359; 3574,
p. 21). Other criticisms from the ACC concerning alleged modeling
errors and biases in the Steenland study and the alleged threshold for
the health effects of silica exposure are discussed generally in
Section V.J, Comments and Responses Concerning Biases in Key Studies,
and Section V.I, Comments and Responses Concerning Thresholds for
Silica-Related Diseases. Dr. Cox's and Dr. Morfeld's criticisms of the
uncertainty analysis performed by Toxachemica are addressed in Section
V.K, Comments and Responses Concerning Exposure Estimation Error and
ToxaChemica's Uncertainty Analysis. For the reasons stated in those
sections, OSHA is unpersuaded by these criticisms.
The ACC concluded:
For all these reasons, the pooled analysis by Steenland et al.
(2001) does not yield credible or reliable estimates of silica-
related lung cancer risk. But, even if risk estimates based on
Steenland et al. (2001) were not so problematic, that study would
not demonstrate that reducing the PEL from 0.1 mg/m\3\ [100
[micro]g/m\3\] to 0.05 mg/m\3\ [50 [micro]g/m\3\] will result in a
substantial reduction in the risk of lung cancer (Document ID 2307,
Attachment A, p. 81).
The ACC then discussed the ToxaChemica report (2004), which the ACC
claimed shows that "under the spline model (which the authors prefer
over the log cumulative model because of biological plausibility)"
reducing the PEL from 100 [micro]g/m\3\ to 50 [micro]g/m\3\ would
negligibly reduce the excess risk of lung cancer mortality from 0.017
(17/1,000) to 0.016 (16/1,000), "risk values that are
indistinguishable given the overlapping confidence limits of the two
estimates" (Document ID 2307, Attachment A, p. 81). In addition, the
ACC noted that the excess risk at 150 [micro]g/m\3\ and 250 [micro]g/
m\3\ in the spline model is the same as the excess risk at 50 [micro]g/
m\3\, while that at 200 [micro]g/m\3\ is lower. "Estimates of lung
cancer risk in the neighborhood of the current general industry PEL are
hugely uncertain--with the data suggesting that a greater reduction in
lung cancer risk could be achieved by doubling the PEL to 200 [micro]g/
m\3\ than by cutting it in half to a level of 50 [micro]g/m\3\"
(Document ID 2307, Attachment A, pp. 81-82).
OSHA notes that these risk estimates cited by the ACC were the
original estimates for the spline model provided to OSHA by ToxaChemica
in its 2004 report (Document ID 0469). These are not the risk estimates
used by OSHA. Instead, to estimate the risks published in this final
rule, the Agency used the exposure-response coefficients from the study
in an updated life table analysis using background all-cause mortality
and lung cancer mortality rates from 2006 and 2011, respectively. The
risk estimates using the 2011 background data are the most updated
numbers with which to make the comparisons ACC has suggested. With the
2011 background data, the estimated excess risk is 20 deaths per 1,000
workers at 100 [micro]g/m\3\, and 16 deaths per 1,000 workers at 50
[micro]g/m\3\, a reduction of 4 deaths. OSHA's estimated excess risk at
250 [micro]g/m\3\ is 24 deaths per 1,000 workers, an increase in 8
deaths when compared to 50 [micro]g/m\3\. Thus it is not the case, as
ACC suggested, that increasing the PEL would cause a reduction in lung
cancer mortality risk.
In addition, the linear spline model employed by Steenland et al.
(2001) was only one of three models used by OSHA to estimate
quantitative risks from the pooled analysis. OSHA also used the log-
linear model with log cumulative exposure as well as the linear model
with log cumulative exposure (see Section VI, Final Quantitative Risk
Assessment and Significance of Risk). OSHA notes that all three models
indicated a reduction in risk when comparing an exposure level of 100
[micro]g/m\3\ to 50 [micro]g/m\3\.
In summary, OSHA disagrees with the ACC's assertion that the
Steenland et al. pooled analysis does not yield credible risk estimates
for lung cancer mortality. Dr. Morfeld's assertion that the risk
estimates were biased upwards due to smoking is quite unlikely to be
true, given that the study was an internal (worker to worker) analysis.
The ACC's claim that exposure estimation error resulted in false
exposure-response relationships was not supported by any actual data;
as discussed in Section V.K, Comments and Responses Concerning Exposure
Estimation Error and ToxaChemica's Uncertainty Analysis, exposure
estimation error can also bias results towards the null (weaken or
obscure the exposure-response relationship) (Document ID 3580, Tr.
1266-67; 3576, Tr. 358-359; 3574, p. 21). For these reasons, OSHA
rejects the ACC's claims that the Steenland study of lung cancer
mortality does not yield credible risk estimates. Rather, based upon
its review, OSHA believes this pooled analysis to be of high quality.
As Dr. Steenland testified during the informal public hearings, this
pooled analysis, with its more than 60,000 workers and 1,000 lung
cancer deaths, involved "a rich dataset with high statistical power to
see anything, if there was anything to see" (Document ID 3580, Tr.
1227). In fact, OSHA believes the Steenland et al. (2001a) study to be
among the best available studies in the peer-reviewed literature on the
topic of silica exposure and its relationship to lung cancer mortality.
d. Rice et al. (2001)
The ACC also commented on the Rice et al. (2001, Document ID 1118)
study of diatomaceous earth workers, which found a significant risk of
lung cancer mortality that increased with cumulative silica exposure in
a cohort of diatomaceous earth workers. The ACC claimed that it had a
high likelihood of exposure misclassification. Dr. Cox contended that
the practice of "[a]ssigning each worker a single estimated cumulative
exposure based on estimated mean values produces biased results and
artificially narrow confidence intervals (and hence excess false-
positive associations)" (Document ID 2307, Attachment 4, p. 76). OSHA
notes that Rice et al. (2001) described the exposure estimation
procedure in their paper. There were more than 6,000 measurements of
dust exposure taken from 1948-1988; particle count data were converted
to gravimetric data using linear regression modeling. Cumulative
exposures to respirable crystalline silica were then estimated for each
worker using detailed employment records (Document ID 1118, p. 39).
OSHA concludes it is highly unlikely that the exposure estimates are
biased to such an extent, as Dr. Cox suggests, that they would produce
false-positive associations.
The ACC also noted that the mean crystalline silica exposure in the
diatomaceous earth worker cohort was 290 [mu]g/m\3\, approximately
three times the former PEL for general industry (Document ID 2307,
Attachment A, p. 83). OSHA, however, believes that the cumulative
respirable crystalline silica dust concentration is the metric of
concern here, as that is what was used in the regression models. The
mean cumulative respirable crystalline silica dust concentration in the
study was 2.16 mg/m\3\-yrs, which is a very realistic cumulative
exposure for many workers (Document ID 1118, p. 39).
The ACC also stated that the results of the Rice study were
confounded by smoking and possibly asbestos exposure (Document ID 2307,
Attachment A, p. 83). OSHA previously addressed the possible
confounding in this cohort in its Review of Health Effects Literature
and Preliminary QRA (Document ID 1711, pp. 139-143). Rice et al. (2001)
used the same cohort originally reported on by Checkoway et al. (1993,
Document ID 0324; 1996, 0325; 1997, 0326). The Rice study discussed the
smoking confounding analysis performed by Checkoway et al. (1997), in
which the Axelson method (1978) was used to make a worst case estimate
(assuming 20 times greater lung cancer risk in smokers compared to non-
smokers) and indirectly adjust the relative risk (RR) estimates for
lung cancer for differences in smoking rates (Document ID 1118, pp. 40-
41). With exposures in the Checkoway study lagged 15 years to account
for the latency period, the worst case effect was to reduce the RR for
lung cancer in the highest exposure group from 2.15 to 1.67. Checkoway
et al. concluded that the association between respirable silica
exposure and lung cancer was unlikely to be confounded by cigarette
exposure (Document ID 0326, pp. 684, 687). Regarding confounding by
asbestos exposure, Rice et al. (2001) stated:
Checkoway et al. found no evidence that exposure to asbestos
accounted for the observed association between mortality from lung
cancer and cumulative exposure to silica. Our analyses of their data
also found no evidence of confounding by asbestos in the Poisson
regression or Cox's proportional hazards models regardless of lag
period; therefore, exposure to asbestos was not included in the
models presented in this paper (Document ID 1118, p. 41).
Based upon these analyses, OSHA rejects the ACC's unsupported
assertion that the results of Rice et al. (2001) were confounded by
smoking and asbestos exposure.
Lastly, Dr. Cox asserted that there were several biases in Rice et
al. (2001), including multiple-testing bias from testing multiple lag
periods, exposure groupings, and model forms; model specification bias;
and a lack of model diagnostics (Document ID 2307, Attachment 4, pp.
63-64, 77). OSHA addressed these issues generally in Section V.J,
Comments and Responses Concerning Biases in Key Studies, and rejects
these assertions for the same reasons. OSHA also discussed regression
diagnostics at length in the same section. In summary, despite the
criticisms directed at the Rice et al. study by the ACC, OSHA continues
to believe that the quantitative exposure-response analysis by Rice et
al. (2001) is of high quality and appropriate for inclusion in the QRA
(Document ID 1711, p. 143).
e. Hughes et al. (2001)
The ACC, through the comments of Dr. Cox, presented a similar
critique of the study of North American industrial sand workers by
Hughes et al. (2001, Document ID 1060). This study found a
statistically significant association (increased odds ratios) between
lung cancer mortality and cumulative silica exposure as well as average
silica concentration (Document ID 1060). In this study, according to
Dr. Cox, "The selected model form guarantees a monotonic exposure-
response relation, independent of the data. Model uncertainty and
errors in exposure estimates have both been ignored, so the slope
estimate from Hughes et al. (2001), as well as the resulting excess
risk estimates, are likely to be biased and erroneous" (Document ID
2307, Attachment 4, p. 85). The ACC also noted that this cohort had
incomplete smoking information, with the proportion of "ever smokers"
significantly higher in cases than in controls. In addition, the ACC
asserted that asbestos exposure may have also occurred, as three death
certificates listed mesothelioma as the cause of death (Document ID
2307, Attachment A, pp. 85-86).
OSHA discussed the Hughes et al. (2001, Document ID 1060) study in
its Review of Health Effects Literature and Preliminary QRA,
highlighting as strengths the individual job, exposure, and smoking
histories that were available (Document ID 1711, p. 285). Exposure
levels over time were estimated via a job exposure matrix constructed
by Rando et al. (2001, Document ID 0415) utilizing substantial exposure
data, including 14,249 respirable dust and silica samples taken from
1974 to 1998 in nine plants (Document ID 1711, pp. 88, 124-128; 1060,
202). Smoking data were collected from medical records supplemented by
information from next of kin or living subjects for 91 percent of cases
and controls (Document ID 1060, p. 202). OSHA believes these smoking
histories allowed the authors to adequately control for confounding by
smoking in their analyses. Regarding the three death certificates
listing mesothelioma, McDonald et al. (2001) explained that two were
for workers not included in the case/control study because they were
hired at or after age 40 with less than 10 years of work time; the
third was for a worker hired at age 19 who then accumulated 32 years of
experience in maintenance jobs (Document ID 1091, p. 195). As such,
OSHA does not believe it likely that asbestos exposure was a large
source of confounding in typical industrial sand operations in this
study. OSHA also notes that the positive findings of this study were
consistent with those of other studies of workers in this cohort,
including Steenland and Sanderson (2001, Document ID 0455) and McDonald
et al. (2005, Document ID 1092).
The ACC also noted that there was no consistent correlation in
Hughes et al. (2001) between employment duration and lung cancer risk
(Document ID 2307, Attachment A, p. 86), with Dr. Cox suggesting that
model specification error was to blame (Document ID 2307, Attachment 4, p. 86).
OSHA believes that cumulative exposure is a more appropriate metric
for determining risk than is duration of exposure because the
cumulative exposure metric considers both the duration and intensity
of exposure. For example, some workers may have been employed for a
very long duration with low exposures, whereas others may have
been employed for a short duration but with high exposures;
both groups could have similar cumulative exposures.
In summary, OSHA considers the Hughes et al. (2001) study to be of
high enough quality to provide risk estimates for excess lung cancer
from silica exposure, as the study is unlikely to be substantially
confounded. For these reasons, the Agency finds the assertion that the
risk estimates based on this study are erroneous to be unconvincing.
Overall, regarding all of the studies upon which OSHA relied in its
Preliminary QRA, the ACC concluded, "In sum, none of the studies on
which OSHA relies is inconsistent with a concentration threshold above
100 [mu]g/m\3\ for any risk of silica-related lung cancer; none
demonstrates an increased lung cancer risk in the absence of silicosis;
and none provides a sound basis for estimating lung cancer risks at RCS
[respirable crystalline silica] exposure levels of 100 [mu]g/m\3\ and
below" (Document ID 2307, Attachment A, p. 87).
OSHA is not persuaded that the evidence presented by the ACC
supports these conclusions. On the contrary, as OSHA discussed in the
Section V.I, Comments and Responses Concerning Thresholds for Silica-
Related Diseases, demonstrating the absence of a threshold is not a
feasible scientific pursuit, and some models produce threshold
estimates well below the PELs. Similarly, the ACC has not put forward
any study that has proven that silicosis must be a precursor for lung
cancer and, as discussed in Section V.H, Mechanisms of Silica-Induced
Adverse Health Effects, some studies have shown genotoxic mechanisms by
which exposure to crystalline silica may lead to lung cancer. The
strong epidemiological evidence for carcinogenicity, supported by
evidence from experimental animal and mechanistic studies, allowed IARC
to conclude on multiple occasions that respirable crystalline silica is
a Group I carcinogen. OSHA places great weight on this conclusion given
IARC's authority and standing in the international scientific
community. In addition, all of the lung cancer studies relied upon by
OSHA used models that allow for the estimation of lung cancer risks at
crystalline silica exposure levels of 100 [mu]g/m\3\ and below. OSHA
believes these studies (Steenland et al., 2001a, Document ID 0452, as
re-analyzed in ToxaChemica, 2004, 0469; Rice et al., 2001, 1118;
Attfield and Costello, 2004, 0284; Hughes et al., 2001, 1060; and
Miller and MacCalman, 2009, 1306) are of high quality and contain well-
supported findings. Thus, OSHA continues to rely upon these studies for
deriving quantitative risk estimates in its QRA and continues to
believe that workers exposed to respirable crystalline silica at levels
at or near the previous and new PELs are faced with a significant risk
of dying from lung cancer. As such, the Agency believes it would be
irresponsible as a scientific matter, and inconsistent with its
statutory obligations to issue standards based on the best available
evidence after conducting an extensive rulemaking, to retain the
regulatory status quo.
G. Comments and Responses Concerning Renal Disease Mortality
OSHA estimated quantitative risks for renal disease mortality
(Document ID 1711, pp. 314-316) using data from a pooled analysis of
renal disease, conducted by Steenland et al. (2002a, Document ID 0448).
As illustrated in Table VI-1, the lifetime renal disease mortality risk
estimate for 45 years of exposure to the previous general industry PEL
(100 [mu]g/m\3\ respirable crystalline silica) is 39 deaths per 1,000
workers. However, for the final PEL (50 [mu]g/m\3\), it is 32 deaths
per 1,000 workers. Although OSHA acknowledges that there are
considerably less data for renal disease mortality, and thus the risk
findings based on them are less robust than those for silicosis, lung
cancer, and non-malignant respiratory disease (NMRD) mortality, the
Agency believes the renal disease risk findings are based on credible
data. Indeed, the Steenland et al. pooled analysis had a large number
of workers from three cohorts with sufficient exposure data, and
exposure matrices for the three cohorts had been used in previous
studies that showed positive exposure-response trends for silicosis
morbidity or mortality, thus tending to validate the underlying
exposure and work history data (see Document ID 1711, pp. 215-216).
Nevertheless, OSHA received comments that were critical of its risk
estimates for renal disease mortality. Based upon its review of the
best available evidence, OSHA finds that these comments do not alter
its overall conclusions on renal disease mortality. In addition, OSHA
notes that even if the risk of renal disease mortality is discounted,
there would remain clearly significant risks of lung cancer mortality,
silicosis and NMRD mortality, and silicosis morbidity, with more robust
risk estimates based upon a larger amount of data from numerous studies
(see Table VI-1).
OSHA received several comments from the ACC regarding the Agency's
quantitative risk estimates for renal disease mortality. Specifically,
the ACC argued that: (1) The pooled study (Steenland et al., 2002a,
Document ID 0448) that OSHA relied upon did not provide sufficient data
to estimate quantitative risks; (2) the individual studies included in
the pooled study had several limitations; and (3) most epidemiological
studies have not demonstrated a statistically significant association
between silica exposure and renal disease mortality (Document ID 2307,
Attachment A, pp. 139-157; 4209, pp. 92-96). As explained below, and as
stated above, although the Agency acknowledges there is greater
uncertainty in the risk estimates related to renal disease than other
silica-related diseases, the best available evidence is of sufficient
quality to quantify the risk of renal disease in the final risk
assessment.
1. Pooled Study
Some commenters expressed concern about the Steenland et al.
(2002a, Document ID 0448) pooled study of renal disease mortality,
which OSHA and its contractor, ToxaChemica, used to calculate
quantitative risk estimates. Specifically, the ACC questioned why the
analysis only used three studies (Homestake, North Dakota gold miners,
Steenland and Brown, 1995a, Document ID 0450; U.S. industrial sand
workers, Steenland et al., 2001b, Document ID 0456; Vermont granite
workers, Costello and Graham, 1988, Document ID 0991) out of the ten
originally used in the pooled study of lung cancer mortality (Steenland
et al., 2001a, Document ID 0452). Peter Morfeld, Dr. rer. medic.,
representing the ACC, wrote in his written testimony that although
Steenland et al. (2002a, Document ID 0448) indicated that the three
studies were selected because they were the only ones to have
information on multiple cause mortality, all 10 studies had information
on renal disease as an underlying cause of death (Document ID 2308,
Attachment 4, pp. 24-25). Since ToxaChemica focused on underlying cause
results in their discussion, Dr. Morfeld argued that not having used
all 10 studies in the pooled analysis "raises a suspicion of study
selection bias" (Document ID 2308, Attachment 4, pp. 24-25).
OSHA finds this assertion of study selection bias by the ACC and
Dr. Morfeld to be unpersuasive because Steenland et al.'s explanation
(2002a) for including only three studies in the pooled analysis was
sound. The authors reported in their pooled study that both underlying
cause and multiple cause mortality were available for only three
cohorts of silica-exposed workers, and "multiple cause (any mention on
the death certificate) was of particular interest because renal disease
is often listed on death certificates without being the underlying
cause" (Document ID 0448, p. 5). The authors likewise cited a study
(Steenland et al., 1992), indicating that the ratio of chronic renal
disease mortality shown anywhere on a U.S. death certificate versus
being shown as an underlying cause is 4.75 (Document ID 0453, Table 2,
pp. 860-861). Indeed, in their pooled analysis of renal disease
mortality, Steenland et al. noted that there were 51 renal disease
deaths when using underlying cause, but 204 when using multiple cause
mortality (Document ID 0448, p. 5). As renal disease is a serious
disabling disease, the use of multiple cause mortality gives a much
better sense of the burden of excess disease than does the use of
underlying cause of death as an endpoint. As such, Steenland et al.
calculated odds ratios by quartile of cumulative silica exposure for
renal disease in a nested case-control analysis that considered any
mention of renal disease on the death certificate as well as underlying
cause. For multiple-cause mortality, the exposure-response trend was
statistically significant for both cumulative exposure (p = 0.004) and
log cumulative exposure (p = 0.0002); whereas for underlying cause
mortality, the trend was statistically significant only for log
cumulative exposure (p = 0.03) (Document ID 1711, p. 315). Thus, OSHA
believes that Steenland et al. (2002a, Document ID 0448) were justified
in including only the three cohorts with all-cause mortality in their
pooled analysis.
Concern was also expressed about the model selection in the pooled
analysis. Dr. Morfeld noted that a statistically significant
association between exposure to crystalline silica and renal disease
mortality was only found in the underlying cause analysis in which the
model was logged (p = 0.03) (Document ID 2308, Attachment 4, p. 25).
Dr. Morfeld commented, "The authors stated that the log-model fit
better, but evidence was not given (e.g., information criteria), and it
is unclear whether the results are robust to other transformations"
(Document ID 2308, Attachment 4, p. 25).
OSHA disagrees with this criticism because a log transformation of
the cumulative exposure metric is reasonable, given that exposure
variables are often lognormally distributed in epidemiological studies,
as discussed in Section V.J, Comments and Responses Concerning Biases
in Key Studies. Also, while it is true that Steenland et al. (2002a)
only found a statistically significant association in the continuous
underlying cause analysis when the cumulative exposure metric was
logged (p = 0.03), OSHA notes that the authors also found a
statistically significant association in the highest quartile of
unlogged cumulative silica exposure (1.67 + mg/m\3\-yr) in the
categorical underlying cause analysis (95% confidence interval: 1.31-
11.76) (Document ID 0448, Table 2, p. 7). Thus, for the highest
cumulative exposures, there was a significant association with renal
disease mortality even without a log transformation of the exposure
metric. Dr. Morfeld also failed to mention that Steenland et al.
(2002a) found statistically significant associations in the continuous
analyses (for both untransformed and log-transformed cumulative
exposure) using any mention of renal disease on the death certificate,
which adds weight to the study's findings that exposure to respirable
crystalline silica is associated with renal disease mortality (Document
ID 0448, Table 2, p. 7). In light of this, OSHA concludes that Dr.
Morfeld's criticism of the pooled analysis is without merit.
The ACC also noted that the authors of this study, Drs. Kyle
Steenland and Scott Bartell, acknowledged the limitations of the data
in their 2004 ToxaChemica report to OSHA. Specifically, in reference to
the 51 renal deaths (underlying cause) and 23 renal cases in the pooled
study, Drs. Steenland and Bartell wrote, "This amount of data is
insufficient to provide robust estimates of risk" (Document ID 2307,
Attachment A, p. 139, citing 0469, p. 27). Given this acknowledgement,
the ACC concluded that OSHA's inclusion of the renal disease mortality
risk estimates in the significant risk determination and calculation of
expected benefits was speculative (Document ID 2307, Attachment A, pp.
139-140). During the hearing, Dr. Steenland further explained, "I
think there is pretty good evidence that silica causes renal disease. I
just think that there is not as big a database as there is for lung
cancer and silicosis. And so there is more uncertainty" (Document ID
3580, Tr. 1245). OSHA agrees with Dr. Steenland and acknowledges, as it
did in its Review of Health Effects Literature and Preliminary QRA
(Document ID 1711, p. 357), that its quantitative risk estimates for
renal disease mortality have more uncertainty and are less robust than
those for the other health effects examined (i.e., lung cancer
mortality, silicosis and NMRD mortality, and silicosis morbidity).
However, OSHA disagrees with the ACC's suggestion that the Agency's
renal disease risk estimates are "rank speculation" (Document ID
4209, pp. 95-96), as these estimates are based on the best available
evidence in the form of a published, peer-reviewed pooled analysis
(Steenland et al. 2002a, Document ID 0448) that uses sound
epidemiological and statistical methods. Thus, OSHA believes that it is
appropriate to present the risk estimates along with the associated
uncertainty estimate (e.g., 95% confidence intervals) (see Document ID
1711, p. 316).
2. Individual Studies in the Pooled Study
The ACC also identified limitations in each of the three
epidemiological studies included in the Steenland et al. (2002a,
Document ID 0448) pooled study. First, with respect to the Steenland
and Brown (1995a, Document ID 0450) study of North Dakota gold miners,
the ACC noted there was a significantly elevated standardized mortality
ratio (SMR) for chronic renal disease only in the men hired prior to
1930. It noted that there were no silica exposure measurement data
available for this early time period, such that Steenland and Brown
(1995a, Document ID 0450) instead estimated a median exposure (150
[mu]g/m\3\) that was seven times higher for men hired prior to 1930,
versus men hired after 1950 (20 [mu]g/m\3\) (Document ID 2307,
Attachment A, p. 147). The ACC maintained that these exposure estimates
were likely to be understated and not credible, while also suggesting
"the existence of an average exposure threshold >=150 [mu]g/m\3\ for
any risk of silica-related renal disease mortality" (Document ID 2307,
Attachment A, p. 147).
OSHA finds the ACC's suggestion of a threshold to be unpersuasive,
as the ACC provided no analysis to indicate a threshold in this study.
OSHA addresses the Steenland and Brown (1995a, Document ID 0450)
exposure assessment in Section V.D, Comments and Responses Concerning
Silicosis and Non-Malignant Respiratory Disease Mortality and
Morbidity. The ACC also ignored the alternative explanation, that
elevated chronic renal disease mortality may have only been seen in
the workers hired prior to 1930 because they had a higher cumulative
exposure than workers hired later, not because there was necessarily a
threshold.
The ACC had a similar criticism of the Steenland et al. (2001b,
Document ID 0456) study of North American industrial sand workers. The
ACC posited that the exposure estimates were highly uncertain and
likely to be understated (Document ID 2307, Attachment A, p. 149). The
ACC noted that these exposure estimates, developed by Sanderson et al.
(2000, Document ID 0429), were considerably lower than those developed
by Rando et al. (2001, Document ID 0415) for another study of North
American industrial sand workers (Document ID 2307, Attachment A, p.
149). After discussing several differences between these two exposure
assessments, the ACC pointed to OSHA's discussion in the lung cancer
section of the preamble to the Proposed Rule (78 FR at 56302) in which
the Agency acknowledged that McDonald et al. (2001, Document ID 1091),
Hughes et al. (2001, Document ID 1060) and Rando et al. (2001, Document
ID 0415) had access to smoking histories, plant records, and exposure
measurements that allowed for the development of a job exposure matrix,
while Steenland and Sanderson (2001, Document ID 0455) had limited
access to plant facilities, less detailed historic exposure data, and
used MSHA enforcement records for estimates of recent exposure
(Document ID 2307, Attachment A, pp. 149-151). The ACC then noted that
the McDonald et al. study (2005, Document ID 1092), using the Rando et
al. (2001, Document ID 0415) exposure assessment, found no association
between end-stage renal disease or renal cancer and cumulative silica
exposure (Document ID 2307, Attachment A, pp. 149, 152).
The ACC also noted that, based on underlying cause of death, the
SMR for acute renal death in the Steenland et al. (2001b, Document ID
0456) study was not significant (95% confidence interval: 0.70-9.86),
and the SMR for chronic renal disease was barely significant (95%
confidence interval: 1.06-4.08) (Document ID 2307, Attachment A, p.
151). In light of this, the ACC maintained that Steenland et al. based
their exposure-response analyses on multiple-cause mortality data,
using all deaths with any mention of renal disease on the death
certificate even if it was not listed as the underlying cause. The ACC
asserted that "only the underlying cause data involve actual deaths
from renal disease" (Document ID 2307, Attachment A, p. 152).
OSHA does not find this criticism persuasive. For regulatory
purposes, multiple-cause mortality data is, if anything, more relevant
because renal disease constitutes the type of material impairment of
health that the Agency is authorized to protect against through
regulation regardless of whether it is determined to be the underlying
cause of a worker's death. Moreover, the discrepancy in the renal
disease mortality findings is a moot point, as only the model in the
pooled study with renal disease as an underlying cause was used to
estimate risks in the Preliminary QRA (Document ID 1711, p. 316). In
any event, OSHA notes an important difference between the Steenland et
al. study (2001b, Document ID 0456) and the McDonald study (2005,
Document ID 1092): They did not look at the same cohort of North
American industrial sand workers. Steenland et al. (2001b) examined a
cohort of 4,626 workers from 18 plants; the average year of first
employment was 1967, with follow-up through 1996 (Document ID 0456, pp.
406-408). McDonald et al. (2005) examined a cohort of 2,452 workers
employed between 1940 and 1979 at eight plants, with follow-up through
2000 (Document ID 1092, p. 368). Although there was overlap of about
six plants in the studies (Document ID 1711, p. 127), these were
clearly two fairly different cohorts of industrial sand workers. These
differences in the cohorts might explain the discrepancy in the
studies' results. In addition, OSHA notes that McDonald et al. (2005,
Document ID 1092) observed statistically significant excess mortality
from nephritis/nephrosis in their study that was not explained by the
findings of their silica exposure-response analyses (Document ID 1092,
p. 369).
The ACC further argued that the Steenland et al. (2002a, Document
ID 0448) pooled study is inferior to the Vacek et al. (2011, Document
ID 2340) study of Vermont granite workers, which found no association
between cumulative silica exposure and mortality from either kidney
cancer or non-malignant kidney disease and which it contended has
better mortality and exposure data (Document ID 2307, Attachment A, p.
154) (citing Vacek et al. (2011, Document ID 2340). In particular, it
argued that the Vacek et al. study is more reliable for this purpose
than the unpublished Attfield and Costello data (2004, Document ID
0285) on Vermont granite workers, which Steenland et al. relied on in
finding an association between silica exposure and renal disease.
OSHA notes that Steenland et al. acknowledged in their pooled study
that that unpublished data had not undergone peer review (Document ID
0448, p. 5). Despite this limitation, OSHA is also unpersuaded that the
Vacek et al. study, although it observed no increased kidney disease
mortality (Document ID 2340, Table 3, p. 315), negates Steenland et
al.'s overall conclusions. OSHA discussed several substantial
differences between these two studies in Section V.F, Comments and
Responses Concerning Lung Cancer Mortality.
3. Additional Studies
The ACC also submitted to the record several additional studies
that did not show a statistically significant association between
exposure to crystalline silica and renal disease mortality. These
included the aforementioned studies by McDonald et al. (2005, Document
ID 1092) and Vacek et al. (2011, Document ID 2340), as well as studies
by Davis et al. (1983, Document ID 0999), Koskela et al. (1987,
Document ID 0363), Cherry et al. (2012, article included in Document ID
2340), Birk et al. (2009, Document ID 1468), Mundt et al. (2011,
Document ID 1478), Steenland et al. (2002b, Document ID 0454), Rosenman
et al. (2000, Document ID 1120), and Calvert et al. (2003, Document ID
0309) (Document ID 2307, Attachment A, pp. 140-145). In light of its
assertions on the limitations of the three studies in the pooled
analysis, and because the three studies "run counter to a larger
number of studies in which a causal association between silica exposure
and renal disease was not found," the ACC concluded that "the three
studies relied on by OSHA do not provide a reliable or supportable
basis for projecting any risk of renal disease mortality from silica
exposure" (Document ID 4209, p. 94). Similarly, the AFS argued that
renal disease was only "found in a couple of selected studies and not
observed in most others," including no foundry studies (Document ID
2379, Attachment 1, pp. 1-3).
In light of the analysis contained in the Review of Health Effects
Literature and Preliminary QRA, and OSHA's confirmation of its
preliminary findings through examination of the record, OSHA finds
these claims to be lacking in merit (Document ID 1711, pp. 211-229). In
the Review of Health Effects Literature and Preliminary QRA, OSHA
presented a comprehensive analysis of several studies that showed an
association between crystalline silica and renal disease, as well
as discussing other studies that did not (Document ID 1711, pp. 211-229).
Based upon its overall analysis of the literature, including
the negative studies, OSHA concluded that there was substantial
evidence suggesting an association between exposure to crystalline
silica and increased risks of renal disease. This conclusion
was supported by a number of case reports and epidemiological
studies that found statistically significant associations
between occupational exposure to silica dust and chronic renal
disease (Calvert et al., 1997, Document ID 0976), subclinical
renal changes (Ng et al., 1992c, Document ID 0386), end-stage renal
disease morbidity (Steenland et al., 1990, Document ID 1125), end-stage
renal disease incidence (Steenland et al. 2001b, Document ID 0456),
chronic renal disease mortality (Steenland et al., 2002a, 0448), and
granulomatosis with polyangitis (Nuyts et al., 1995, Document ID 0397).
In other findings, silica-exposed individuals, both with and without
silicosis, had an increased prevalence of abnormal renal function (Hotz
et al., 1995, Document ID 0361), and renal effects were reported to
persist after cessation of silica exposure (Ng et al., 1992c, Document
ID 0386). While the mechanism of causation is presently unknown,
possible mechanisms suggested for silica-induced renal disease included
a direct toxic effect on the kidney, deposition in the kidney of immune
complexes (IgA) following silica-related pulmonary inflammation, or an
autoimmune mechanism (Calvert et al., 1997, Document ID 0976; Gregorini
et al., 1993, 1032).
From this review of the studies on renal disease, OSHA concluded
that there were considerably less data, and thus the findings based on
them were less robust, than the data available for silicosis and NMRD
mortality, lung cancer mortality, or silicosis morbidity. Nevertheless,
OSHA concluded that the Steenland et al. (2002a, Document ID 0448)
pooled study had a large number of workers and validated exposure
information, such that it was sufficient to provide useful estimates of
risk of renal disease mortality. With regard to the additional negative
studies presented by the ACC, OSHA notes that it discussed the Birk et
al. (2009, Document ID 1468) and Mundt et al. (2011, Document ID 1478)
studies in the Supplemental Literature Review of the Review of Health
Effects Literature and Preliminary QRA, noting the short follow-up
period as a limitation, which makes it unlikely to observe the presence
of renal disease (Document ID 1711, Supplement, pp. 6-12). OSHA
likewise discussed the Vacek et al. (2011, Document ID 2340) study
earlier in this section, and notes that Cherry et al. reported a
statistically significant excess of non-malignant renal disease
mortality in the cohort for the period 1985-2008, with an unexplained
cause (2012, p. 151, article included in Document ID 2340). Although
these latter two studies did not find a significant association between
silica exposure and renal disease mortality, OSHA does not believe that
they substantially change its conclusions on renal disease mortality
from the Preliminary QRA, given the number of positive studies
presented and the limitations of those two studies.
Thus, OSHA recognizes that the renal risk estimates are less robust
and have more uncertainty than those for the other health endpoints for
which there is a stronger case for causality (i.e., lung cancer
mortality, silicosis and NMRD mortality, and silicosis morbidity). But,
for the reasons stated above, OSHA believes that the evidence
supporting causality regarding renal risk outweighs the evidence
casting doubt on that conclusion. Scientific certainty is not the legal
standard under which OSHA acts. OSHA is setting the standard based upon
the clearly significant risks of lung cancer mortality, silicosis and
NMRD mortality, silicosis morbidity, and renal disease mortality at the
previous PELs; even if the risk of renal disease mortality is
discounted, the conclusion would not change that regulation is needed
to reduce the significant risk of material impairment of health (see
Society of the Plastics Industry, Inc. v. OSHA, 509 F.2d 1301, 1308 (2d
Cir. 1975)).
H. Mechanisms of Silica-Induced Adverse Health Effects
In this section, OSHA describes the mechanisms by which silica
exposure may cause silica-related health effects, and responds to
comments criticizing the Agency's analysis on this topic. In the
proposal as well as this final rule, OSHA relied principally on
epidemiological studies to establish the adverse health effects of
silica exposure. The Agency also, however, reviewed animal studies (in
vivo and in vitro) as well as in vitro human studies that provide
information about the mechanisms by which respirable crystalline silica
causes such effects, particularly silicosis and lung cancer. OSHA's
review of this material can be found in the Review of Health Effects
Literature and Preliminary Quantitative Risk Assessment (QRA), which
provided background and support for the proposed rule (Document ID
1711, pp. 229-261).
As described in the Review of Health Effects Literature, OSHA
performed an extensive evaluation of the scientific literature
pertaining to inhalation of respirable crystalline silica (Document ID
1711, pp. 7-265). Due to the lack of evidence of health hazards from
dermal or oral exposure, the Agency focused solely on the studies
addressing the inhalation hazards of respirable crystalline silica.
OSHA determined, based on the best available scientific information,
that several cellular events, such as cytotoxicity (i.e., cellular
damage), oxidative stress, genotoxicity (i.e., damage to cellular DNA),
cellular proliferation, and inflammation can contribute to a range of
neoplastic (i.e., tumor-forming) and non-neoplastic health effects in
the lung. While the exact mechanisms have yet to be fully elucidated,
they are likely initiated by damage to lung cells from interaction
directly with the silica particle itself or through silica particle
activation of alveolar macrophages following phagocytosis (i.e.,
engulfing particulate matter in the lung for the purpose of removing or
destroying foreign particles). The crystalline structure and unusually
reactive surface properties of the silica particle appear to cause the
early cellular effects. Silicosis and lung cancer share common features
that arise from these early cellular interactions but OSHA, in its
Review of Health Effects Literature and Preliminary QRA,
"preliminarily conclude[d] that available animal and in vitro studies
have not conclusively demonstrated that silicosis is a prerequisite for
lung cancer in silica-exposed individuals" (Document ID 1711, p. 259).
Although the health effects associated with inhalation of respirable
crystalline silica are seen primarily in the lung, other observed
health effects include kidney and immune dysfunctions.
Below, OSHA reviews the record evidence and responds to comments it
received on the mechanisms underlying respirable crystalline silica-
induced lung cancer and silicosis. The Agency also addresses comments
regarding the use of animal studies to characterize adverse health
effects in humans caused by exposure to respirable crystalline silica.
1. Mechanisms for Silica-Related Health Effects
In 2012, IARC reevaluated the available scientific information
regarding respirable crystalline silica and lung cancer and reaffirmed
that crystalline silica is carcinogenic to humans,
i.e., a Group 1 carcinogen (Document ID 1473, p. 396). OSHA's
review of all the evidence now in the rulemaking record, including the
results of IARC's reevaluation, indicates that silica may lead to
increased risk of lung cancer in humans by a multistage process that
involves a combination of genotoxic (i.e., causing damage to cellular
DNA) and non-genotoxic (i.e., not involving damage to DNA) mechanisms.
Respirable crystalline silica may cause genotoxicity as a result of
reactive oxygen species (ROS) produced by activated alveolar
macrophages and other lung cells exposed to crystalline silica
particles during phagocytosis. ROS have been shown to damage DNA in
human lung cells in vitro (see Document ID 1711, pp. 236-239). This
genotoxic mechanism is believed to contribute to neoplastic
transformation and silica-induced carcinogenesis. ROS is not only
produced during the early cellular interaction with crystalline silica
but also produced by PMNs (polymorphonuclear leukocytes) and
lymphocytes recruited during the inflammatory response to crystalline
silica. In addition to genotoxicity contributed by ROS, it is also
plausible that reactive molecules on the surface of crystalline silica
itself may bind directly to DNA and result in genotoxicity (Document ID
1711, p. 236). It should be noted that the mechanistic evidence
summarized above suggests that crystalline silica may cause early
genotoxic events that are independent of the advanced chronic
inflammatory response and silicosis (Document ID 1473, pp. 391-392).
Non-genotoxic mechanisms are also believed to contribute to the
lung cancer caused by respirable crystalline silica. Phagocytic
activation as well as silica-induced cytotoxicity trigger release of
the aforementioned ROS, cytokines (e.g., TNF[alpha]), and growth
factors (see Document ID 1711, pp. 233-235). These agents are able to
cause cellular proliferation, loss of cell cycle regulation, activation
of oncogenes (genes that have the potential to cause cancer), and
inhibition of tumor suppressor genes, all of which are non-genotoxic
mechanisms known to promote the carcinogenic process. It is plausible
that these mechanisms may be involved in silica-induced tumorigenesis.
The biopersistence and cytotoxic nature of crystalline silica leads to
a cycle of cell death (i.e., cytotoxicity), activation of alveolar
macrophages, recruitment of inflammatory cells (e.g., PMNs,
leukocytes), and continual release of the non-genotoxic mediators
(i.e., ROS, cytokines) able to promote carcinogenesis. The non-
genotoxic mechanisms caused by early cellular responses (e.g.,
phagocytic activation, cytotoxicity) are regarded, along with
genotoxicity, as important potential pathways that lead to the
development of tumors (Document ID 1711, pp. 232-239; 1473, pp. 394-
396).
The same non-genotoxic processes that may cause lung cancer from
respirable crystalline silica exposure are also believed to lead to
chronic inflammation, lung scarring, fibrotic lesions, and eventually
silicosis. This would occur when inflammatory cells move from the
alveolar space through the interstitium of the lung as part of the
clearance process. In the interstitium, respirable crystalline silica-
laden cells--macrophages and neutrophils--release ROS and TNF-[alpha],
as well as other cytokines, stimulating the proliferation of
fibroblasts (i.e., the major lung cell type in silicosis).
Proliferating fibroblasts deposit collagen and connective tissue,
inducing the typical scarring that is observed with silicosis.
Alternatively, alveolar epithelial cells containing respirable
crystalline silica die and may be replaced by fibroblasts due to
necrosis of the epithelium. This allows for uninhibited growth of
fibroblasts and formation of connective tissue where scarring
proliferates (i.e., silicosis). As scarring increases, there is a
reduction in lung elasticity concomitant with a reduction of the lung
surface area capable of gas exchange, thus reducing pulmonary function
and making breathing more difficult (Document ID 0314; 0315). It should
be noted that silicosis involves many of the same mechanisms that occur
during the early cellular interaction with crystalline silica.
Therefore, it is plausible that development of silicosis may also
potentially contribute to silica-induced lung cancer. However, the
relative contributions of silicosis-dependent and silicosis-independent
pathways are not known.
Although it is clear that exposure to respirable crystalline silica
increases the risk of lung cancer in exposed workers (see Section VI,
Final Quantitative Risk Assessment and Significance of Risk), some
commenters claimed that such exposure cannot cause lung cancer
independently of silicosis (i.e., only those workers who already have
silicosis can get lung cancer) (Document ID 2307, Attachment A, p. 53).
This claim is inconsistent with the credible scientific evidence
presented above that genotoxic and non-genotoxic mechanisms triggered
by early cellular responses to crystalline silica prior to development
of silicosis may contribute to crystalline silica-induced
carcinogenesis. OSHA finds, based on its review of all the evidence in
the rulemaking record, that workers without silicosis, as well as those
with silicosis, are at risk of lung cancer if regularly exposed to
respirable crystalline silica at levels permitted under the previous
and new PELs. The Agency also emphasizes that, regardless of the
mechanism by which respirable crystalline silica exposure increases
lung cancer risk, the fact remains that workers exposed to respirable
crystalline silica continue to be diagnosed with lung cancer at a
higher rate than the general population. Therefore, as discussed in
section VI, Final Quantitative Risk Assessment and Significance of
Risk, OSHA has met its burden of proving that workers exposed to
previously allowed levels of respirable crystalline silica are at
significant risk, by one or more of these mechanisms, of serious and
life-threatening health effects, including both silicosis and lung
cancer.
2. Relevance of Animal Models to Humans
Animal data has been used for decades to evaluate hazards and make
inferences regarding causal relationships between human health effects
and exposure to toxic substances. The National Academies of Science has
endorsed the use of well-conducted animal studies to support hazard
evaluation in the risk assessment process (Document ID 4052, p. 81) and
OSHA's policy has been to rely on such studies when regulating
carcinogens. In the case of respirable crystalline silica, OSHA has
used evidence from animal studies, along with human epidemiology and
other relevant information, to establish that occupational exposure is
associated with silicosis, lung cancer, and other non-malignant
respiratory diseases, as well as renal and autoimmune effects (Document
ID 1711, pp. 261-266). Exposure to various forms of respirable
crystalline silica by inhalation and intratracheal instillation has
consistently caused lung cancer in rats (IARC, 1997, Document ID 1062,
pp. 150-163). These results led IARC and NTP to conclude that there is
sufficient evidence in experimental animals to demonstrate the
carcinogenicity of crystalline silica in the form of quartz dust. IARC
also concluded that there is sufficient evidence in human studies for
the carcinogenicity of crystalline silica in the form of quartz or
cristobalite.
In its pre-hearing comments and post-hearing brief, the ACC noted
that increased lung cancer risks from exposure to respirable
crystalline silica have not been found in animal species other than
rats, and questioned the relevance of the rat model for evaluating
potential lung carcinogenicity in humans (Document ID 2307, Attachment
A, p. 30; 4209, p. 32). Specifically, the ACC highlighted studies by
Holland (1995) and Saffiotti et al. (1996) indicating that bioassays in
respirable crystalline silica-exposed mice, guinea pigs, and Syrian
hamsters have not found increased lung cancer (Document ID 2307,
Attachment A, p. 30, f. 51).
The ACC proposed that the increased lung cancer risk in respirable
crystalline silica-exposed rats is due to a particle overload
phenomenon, in which lung clearance of nonfibrous durable particles
initiates a non-specific response that results in intrapulmonary lung
tumors (Document ID 2307, Attachment A, p. 30, n. 51). Dr. Cox, on
behalf of the ACC, citing Mauderly (1997, included in Document ID
3600), Oberdorster (1996, Document ID 3969), and Nikula et al. (1997,
included in Document ID 3600), likewise commented that rats are
"uniquely sensitive to particulate pollution, for species-specific
reasons that do not generalize to other rodents or mammals, including
humans" (Document ID 2307, Attachment 4, p. 83). OSHA reviewed the
three studies referenced by Dr. Cox and notes that two actually appear
to support the use of the rat model and the third does not reject it.
Mauderly (1997) noted that the rat model was the only one to correctly
predict carcinogenicity after inhalation exposure to several types of
asbestos, and highlighted the shortcomings of other models, such as
those using hamsters, which are highly insensitive to particle-induced
lung cancers (article included in Document ID 3600, pp. 1339-1343).
While Mauderly (1997) advised caution when using the rat because it is
the most sensitive rodent species for lung cancer, he concluded that
"there is evidence supporting continued use of rats in exploration of
carcinogenic hazards of inhaled particles," and that the other test
species are problematic because they provide too many false negatives
to be predictive (article included in Document ID 3600, p. 1343).
Similarly, Oberdorster (1996), in discussing particle parameters used
in the evaluation of exposure-dose-relationships of inhaled particles,
stated that "the rat model should not be dismissed prematurely"
(Document ID 3969, p. 73). Oberdorster (1996) postulated that humans
and rats have very similar responses to particle-induced effects when
analyzing the exposure-response relationship using particle surface
area, rather than particle mass, as the exposure metric. Oberdorster
concluded that there simply was not enough known regarding exact
mechanisms to reject the model outright (Document ID 3969, pp. 85-87).
The remaining paper cited by Dr. Cox, Nikula et al. (1997), evaluated
the anatomical differences between primate and rodent responses to
inhaled particulate matter and the role of clearance patterns and
physiological responses to inhaled toxicants. The study noted that the
differences between primate clearance patterns and rat clearance
patterns may play a role in the pathogenesis from inhaled poorly
soluble particles but did not dismiss the rat model as irrelevant to
humans (Nikula, 1997, included in Document ID 3600, pp. 83, 93, 97).
Thus, OSHA finds that the Mauderly (1997) and Oberdorster (1996)
articles generally support the rat as an appropriate model for
qualitatively assessing the hazards associated with particle
inhalation. OSHA likewise notes that the rat model is a common and
well-accepted toxicological model used to assess human health effects
from toxicant inhalation (ILSI, 2000, Document ID 3906, pp. 2-9). OSHA
evaluated the available studies in the record, both positive and non-
positive, and believes that it is appropriate to regard positive
findings in experimental studies using rats as supportive evidence for
the carcinogenicity of crystalline silica. This determination is
consistent with that of IARC (Document ID 1473, p. 388) and NTP
(Document ID 1164, p. 1), which also regarded the significant increases
in incidence of malignant lung tumors in rats from multiple studies by
both inhalation and intratracheal instillation of crystalline silica to
be sufficient evidence of carcinogenicity in experimental animals and,
therefore, to contribute to the evidence for carcinogenicity in humans.
3. Hypothesis That Lung Cancer Is Dependent on Silicosis
The ACC asserted in its comments that "if it exists at all,
silica-related carcinogenicity most likely arises through a silicosis
pathway or some other inflammation-mediated mechanism, rather than by
means of a direct genotoxic effect" (Document ID 2307, Attachment A,
p. 52; 4209, p. 51; 2343, Attachment 1, pp. 40-44). It explained that
the "silicosis pathway" means that lung cancer stems from chronic
inflammatory lung damage, which in turn, "implies that there is a
threshold for any causal association between silica exposure and risk
of lung cancer" (Document ID 2307, Attachment A, pp. 52-53). The ACC
went on to state that a mechanism that involves ROS, growth factors,
and inflammatory cytokines from alveolar macrophages is "most
consistent" with development of advanced chronic inflammation (e.g.,
epithelial hyperplasia, lung tissue damage, fibrosis, and silicosis).
According to this hypothesis, silica-related lung cancer is restricted
to people who have silicosis (Document ID 2307, Attachment 2, p. 7).
Regarding this hypothesis, the ACC concluded, "[t]his view of the
likely mechanism for silica-related lung cancer is widely accepted in
the scientific community, including by OSHA's primary source of silica-
related health risk estimates, Dr. Kyle Steenland. OSHA appears to
share this view as well" (Document ID 2307, Attachment A, p. 54).
The ACC statement regarding acceptance by OSHA and the scientific
community is inaccurate. It implies scientific consensus, as well as
OSHA's concurrence, that the chronic inflammation from silicosis is the
only mechanism by which crystalline silica exposure results in lung
cancer. The ACC has over-simplified and neglected the findings of the
mechanistic studies that show activation of phagocytic and epithelial
cells to be an early cellular response to crystalline silica prior to
chronic inflammation (see Document ID 1711, pp. 234-238). As discussed
previously, alveolar macrophage activation leads to initial production
of ROS and release of cytokine growth factors that could contribute to
silica-induced carcinogenicity through both genotoxic and non-genotoxic
mechanisms. The early cellular response does not require chronic
inflammation and silicosis to be present, as postulated by the ACC. It
is possible that the early mechanistic influences that increase cancer
risk may be amplified by a later severe chronic inflammation or
silicosis, if such a condition develops. However, as Brian Miller,
Ph.D., stated "this issue of silicosis being a precursor for lung
cancer is unanswerable, given that we cannot investigate for early
fibrotic lesions in the living, but must rely on radiographs."
(Document ID 3574, Tr. 31).
In pre-hearing comments the ACC commented, as proof of silicosis
being linked to lung cancer, that fibrosis was linked to
adenocarcinomas (Document ID 2307, Attachment A, p. 61). This statement
is misleading. As explained earlier, silicosis results from stimulation
of fibroblast cells that cause lung fibrosis. Adenocarcinomas,
a hallmark tumor type in respirable crystalline silica-induced lung cancer,
are tumors that arise not from fibroblasts, but exclusively from lung
epithelial cells (IARC, 2012, Document ID 1473, pp. 381-389, 392).
These tumors may be linked to the genotoxic and non-genotoxic mechanisms
that occur prior to fibrosis, not secondary to the fibrotic process itself.
OSHA also received some comments that questioned the existence of a
direct genotoxic mechanism. Jonathan Borak, M.D., on behalf of the U.S.
Chamber of Commerce, commented, "there is no direct evidence that
silica causes cancer by means of a directly DNA-reactive mechanism"
(Document ID 2376, p. 21). Dr. Peter Morfeld, on behalf of the ACC, as
well as Peter Valberg, Ph.D., and Christopher M. Long, Sc.D., of
Gradient Corporation, on behalf of the U.S. Chamber of Commerce, cited
a scientific article by Borm et al. (2011, included in Document ID
3573) which reported finding evidence against a genotoxic mechanism and
in favor of a mechanism secondary to chronic inflammation (Document ID
3458, pp. 5-7; 4016, pp. 5-6; 4209, p. 51). Borm et al. (2011, included
in Document ID 3573) analyzed 245 published studies from 1996 to 2008
identified using the search terms "quartz" and `toxicity" in
conjunction with "surface," "inflammation," "fibrosis," and
"genotoxicity." The authors then estimated the lowest dose (in units
of micrograms per cell surface area) to consistently induce DNA damage
or induce markers of inflammation (e.g., IL-8 upregulation) in in vitro
studies. They adjusted the in vitro doses for the lung surface area
encountered in vivo and found the crystalline silica dose that produced
primary genotoxicity was 60-120 times higher than the dose that
produced inflammatory cytokines (Borm et al., 2011, included in
Document ID 3573, p. 762). Drs. Valberg and Long concluded that Borm et
al. demonstrated that genotoxicity was a secondary response to chronic
inflammation, except at very high exposures at which genotoxicity
independent of inflammation might occur. They also maintained that lung
cancer as a secondary response to chronic inflammation is considered to
have a threshold (Document ID 4016, p. 6).
OSHA reviewed the Borm et al. study (2011, Document ID 3889), and
notes several limitations. The authors examined the findings from
various genotoxic assays (comet assay, 8-OH-dG, micronucleus test)
(Borm et al., 2011, 3889, p. 758). They reported that 40 [mu]g/cm\2\
was the lowest dose in vitro to produce significant direct DNA damage
from crystalline silica. This genotoxic dose appears to be principally
obtained from a study of a specific quartz sample (i.e., DQ12) in a
single human alveolar epithelial cell line (i.e., A549 cells), even
though Appendix Table 3 cited in vitro studies using other cells (e.g.,
fibroblasts) and other types of quartz (e.g., MinUsil) that produced
direct genotoxic effects at lower doses (Borm et al., 2011, Document ID
3889, pp. 760, 769-770). This is especially pertinent since Borm et al.
state that in vitro systems utilizing single-cell cultures are
generally much less sensitive than in vivo systems, especially if
attempting to determine oxidative stress-induced effects, since many
cell culture systems use reagents that can scavenge ROS (Borm et al.
2011, Document ID 3889, p. 760). There was no indication that the
authors accounted for this deficiency. They go on to conclude that
their work shows a large-scale variation in hazard across different
forms of quartz with regard to effects such as DNA breakage (e.g.,
genotoxicity) and inflammation (Borm et al. 2011, Document ID 3889, p.
762).
The extreme variation in response along with reliance on an
insensitive genotoxicity test system could overestimate the appropriate
genotoxic dose in human lung cells in vivo. In addition, Borm et al.
used the dose sufficient to initiate production of an inflammatory
cytokine (i.e., IL-8) in the A549 cell-line as the threshold for
inflammation. It is not clear that an early cellular response, such as
IL-8 production necessarily reflects a sustained inflammatory response.
In summary, OSHA finds inconsistencies in this analysis, leaving some
questions regarding the study's conclusion that silica induces
genotoxicity only as a secondary response to an inflammation-driven
mechanism. While the in vitro dose comparisons in this study fail to
demonstrate that genotoxicity is secondary to the inflammatory
response, the study findings do indicate that cellular responses to
crystalline silica that drive inflammation may also lead to
tumorigenesis through both genotoxic and non-genotoxic mechanisms.
Dr. Morfeld, in his hearing testimony on behalf of the ACC,
referred to the paper by Borm et al. (2011) as reaching the conclusion
that the mechanism of silica-related lung cancer is secondary
inflammation-driven genotoxicity. As summarized by the ACC in post-
hearing comments, he observed that "there are no crystalline silica
particles found in the nucleus of the cells. There is nothing going on
with particles in the epithelial cells inside the lung" (Document ID
4209, p. 52). In hearing testimony, however, Dr. Morfeld acknowledged
that the Borm paper had limitations on extrapolating from in vitro to
in vivo and cited a study by Donaldson et al. (2009), which discussed
some of the limitations and the need for caution in extrapolating from
in vitro to in vivo (Document ID 3582, Tr. 2076-2077; 3894, pp. 1-2).
In considering this testimony, OSHA notes that the Donaldson et al.
(2009) study, which includes the same authors as the Borm et al. (2011)
study, acknowledged that direct interaction between respirable
crystalline silica and epithelial cellular membranes induces
intracellular oxidative stress which is capable of being genotoxic
(Document ID 3894, p. 3). This is consistent with the OSHA position as
well as the most recent IARC reevaluation of the cancer hazard from
crystalline silica dust. As IARC stated in its most recent evaluation
of the carcinogenicity of respirable crystalline silica under a section
on direct genotoxicity and cell transformation (Document ID 1473,
section 4.2.2, pp. 391-393):
Reactive oxygen species are generated not only at the particle
surface of crystalline silica, but also by phagocytic and epithelial
cells exposed to quartz particles....Oxidants generated by
silica particles and by the respiratory burst of silica-activated
phagocytic cells may cause cellular and lung injury, including DNA
damage (Document ID 1473, p. 391).
Given the IARC determination as well as the animal and in vitro
studies reviewed herein, OSHA finds that there is no conclusive
evidence that silica-related lung cancer only occurs as a secondary
response to chronic inflammation, or that silicosis is a necessary
prerequisite for lung cancer. Instead, OSHA finds support in the
scientific literature for a conclusion that tumors may form through
genotoxic as well as non-genotoxic mechanisms that result from
respirable crystalline silica interaction with alveolar macrophages and
other lung cells prior to onset of silicosis.
4. Hypothesis That Crystalline Silica-Induced Lung Disease Exhibits a
Threshold
It is well established that silicosis arises from an advanced
chronic inflammation of the lung. As noted above, a common hypothesis
is that pathological conditions that depend on chronic inflammation may
have a threshold. The exposure level at which silica-induced health
effects might begin to appear, however, is poorly characterized in the
literature (see Section V.I, Comments and Responses Concerning Thresholds for
Silica-Related Diseases). The threshold exposure level required for a
sustained inflammatory response is dependent upon multiple pro- and
anti-inflammatory factors that can be quite variable from individual to
individual and from species to species (Document ID 3896).
Discounting or overlooking the evidence that respirable crystalline
silica may be genotoxic in the absence of chronic inflammation, Drs.
Valberg and Long commented that crystalline silica follows a threshold
paradigm for poorly soluble particles (PSPs). PSPs are defined
generally as nonfibrous particles of low acute toxicity, which are not
directly genotoxic (ILSI, 2000, Document ID 3906, p. 1). Specifically,
Drs. Valberg and Long stated:
Mechanisms whereby lung cells respond to retention of a wide
variety of PSPs, including crystalline silica, follow a generally
accepted threshold paradigm, where the initiation of a chronic
inflammatory response is a necessary step in the disease process,
and the inflammatory response does not become persistent until
particle retention loads become sufficient to overwhelm lung defense
mechanisms. This overall progression from increased but controlled
pulmonary inflammation across a threshold exposure that leads to
lung damage has been described by a number of investigators
(Mauderly and McCunney, 1995; ILSI, 2000; Boobis et al., 2009;
Porter et al. 2004) (Document ID 2330, p. 19).
Similarly, Dr. Cox, in his post-hearing comments, discussed his
2011 article describing a quantifiable exposure-response threshold for
lung diseases induced by inhalation of respirable crystalline silica
(Document ID 4027, p. 29). Dr. Cox hypothesized the existence of an
exposure threshold such that exposures to PSPs, which he described as
including titanium dioxide, carbon black, and crystalline silica, must
be intense enough and last long enough to disrupt normal homeostasis
(i.e., normal cellular functions) and overwhelm normal repair
processes. Under the scenario he described, a persistent state of
chronic, unresolved inflammation results in a disruption of macrophage
and neutrophil ability to clear silica and other foreign particles from
the lung (Document ID 1470, pp. 1548-1551, 1555-1556).
OSHA disagrees with these characterizations about exposure
thresholds because, among other reasons, respirable crystalline silica
is not generally considered to be in the class of substances defined as
PSPs.\7\ Specifically, regarding the comments of Drs. Valberg and Long,
OSHA notes that the two cited documents (Mauderly and McCunney, 1995,
and ILSI, 2000) summarizing workshops on PSPs did not include
crystalline silica in the definition of PSP and the lung "overload"
concept, instead highlighting silica's cytotoxic and genotoxic
mechanisms. Mauderly and McCunney (1995) stated, "[i]t is generally
accepted that the term `overload' should be used in reference to
particles having low cytotoxicity, which overload clearance
[mechanisms] by virtue of the mass, volume, or surface area of the
deposited material (Morrow, 1992)" (p. 3, article cited in Document ID
2330, p. 19). Mauderly specifically cited quartz as a cytotoxic
particle that may fall outside this definition (p. 24, article cited in
Document ID 2330, p. 19). The International Life Science Institute's
(ILSI) Workshop Report (2000) intended only to address particles of
"low acute toxicity," such as carbon black, coal dust, soot, and
titanium dioxide (Document ID 3906, p. 1). OSHA believes that the
cytotoxic nature of crystalline silica would exclude it from the class
of rather nonreactive, non-toxic particles mentioned above. Therefore,
the Agency concludes that most scientific experts would not include
crystalline silica in the class of substances known as PSPs, nor intend
for findings regarding PSPs to be extrapolated to crystalline silica.
---------------------------------------------------------------------------
\7\ OSHA notes that crystalline silica has many mechanistic
features in common with asbestos. They are both durable,
biopersistent mineral forms where there is sufficient evidence of an
association with lung cancer (i.e., IARC Group 1 carcinogens),
chronic lung inflammation, and severe pulmonary fibrosis (i.e.,
silicosis and asbestosis) in humans. Like crystalline silica,
asbestos has reactive surfaces or other physiochemical properties
able to hinder phagocytosis and activate macrophages to release
reactive oxygen species, cytokines, and growth factors that lead to
DNA damage, cytotoxicity, cell proliferation and an inflammatory
response responsible for the disease outcomes mentioned above (see
IARC 2012, Document ID 1473, pp. 283-290). Crystalline silica and
asbestos can trigger phagocytic activation well below the high mass
burdens required to "overload" the lung and impair pulmonary
clearance that is typical of carbon black and other low acute-
toxicity PSPs.
---------------------------------------------------------------------------
During the public hearing, OSHA questioned Dr. Morfeld about the
relevance of the rat overload response and whether he considered
crystalline silica to be like other PSPs such as carbon black. Dr.
Morfeld replied that he was well aware of the literature and indicated
that crystalline silica was not considered one of the PSPs
(specifically not like carbon black) that these reports reviewed
(Document ID 3582, Tr. 2072-2074). OSHA also notes a report of the
European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC),
which was cited by the ACC (Document ID 4209, p. 32) and stated that
"particles exhibiting significant surface related (cyto)toxicity like
crystalline silica (quartz) and/or other specific toxic properties do
not fall under this definition [of PSPs]" (Document ID 3897, p. 5).
Respirable crystalline silica differs from PSPs because it does not
require particle overload to induce the same response typical of PSPs.
"Overload" refers to the consequence of exposure that results in a
retained lung burden of particles that is greater than the steady-state
burden predicted from deposition rates and clearance kinetics (Document
ID 4174, p. 20). This is a result of a volumetric over-exposure of dust
in the lung, which overwhelms macrophage function. Respirable
crystalline silica does not operate on this mechanism since macrophage
function is inhibited by the cytotoxic nature of respirable crystalline
silica rather than a volumetric overload (Oberdorster, 1996, Document
ID 3969). Therefore, respirable crystalline silica does not require
particle overload to induce the same response. Studies have found that
the respirable crystalline silica exposure levels required to induce
tumor formation in some animal studies are similar to those observed in
human studies, whereas studies involving PSPs tend to show responses at
much higher levels of exposure (Muhle et al., 1991, Document ID 1284;
Muhle et al., 1995, 0378; Saffiotti and Ahmed, 1995, 1121).
A study by Porter et al. (2004) demonstrated that pulmonary
fibrosis induction does not require silica particle overload (Document
ID 0410, p. 377). The ACC cited this study in its post-hearing brief,
stating, "Porter...noted that the response of the rat lung to
inhaled crystalline silica particles is biphasic, with a below-
threshold phase characterized by increased but controlled pulmonary
inflammation" (Document ID 4209, p. 52). OSHA notes that this biphasic
response is due in part to the cytotoxic nature of crystalline silica,
which disrupts macrophage clearance of silica particles leading to a
chronic inflammatory response at less than overload conditions. While
there are some mechanistic similarities, OSHA believes that the
argument that crystalline silica operates on the basis of lung overload
is erroneous and based on false assumptions that ignore toxicological
properties unique to crystalline silica, such as cytotoxicity and the
generation of intracellular ROS (Porter et al., 2002, Document ID 1114;
Porter et al., 2004, 0410). As previously discussed, the generation of
ROS could potentially damage cellular DNA by a genotoxic mechanism that
may not exhibit a threshold.
OSHA thoroughly reviewed Dr. Cox's 2011 article (Document ID 1470),
in which he proposed a threshold for crystalline silica, in its
Supplemental Literature Review (Document ID 1711, Attachment 1, pp. 37-
39). OSHA concluded that the evidence used to support Cox's assertion
that the OSHA PEL was below a threshold for lung disease in humans was
not supported by the evidence presented (Document ID 1470, p. 1543;
1711, Attachment 1). Specifically, Cox (2011) modelled a threshold
level for respirable crystalline silica using animal studies of PSPs.
This approach, according to the ILSI report (2000) and ECETOC report
(2013), is clearly not appropriate since the cytotoxic nature of
crystalline silica is not consistent with the low-toxicity PSPs
(Document ID 3906, p. 1; 3897, p. 5). Dr. Cox (2011) categorized
crystalline silica incorrectly as a PSP and ignored the evidence for
cytotoxicity and genotoxicity associated with crystalline silica. He
further failed to consider or include studies indicating a tumor
response at exposure levels below that leading to an excessive chronic
inflammatory response, such as Porter et al. (2002) and Muhle et al.
(1995) (Document ID 1114; 0378). Thus, OSHA considers the threshold
model designed by Dr. Cox (2011, Document ID 1470) and referenced by
Drs. Valberg and Long (Document ID 2330) to be contradicted by the best
available evidence regarding the toxicological properties of respirable
crystalline silica. Although OSHA acknowledges the possible existence
of a threshold for an inflammatory response, the Agency believes that
the threshold is likely much lower than that advocated by industry
representatives such as the ACC and the Chamber of Commerce (see
Section V.I, Comments and Responses Concerning Thresholds for Silica-
Related Diseases).
OSHA concludes that a better estimate of a threshold effect for
inflammation and carcinogenesis was done by Kuempel et al. (2001,
Document ID 1082). These researchers studied the minimum human
exposures necessary to achieve adverse functional and pathological
evidence of inflammation. They employed a physiologically-based lung
dosimetry model, included more relevant studies, and considered a
genotoxic effect for lung cancer (Kuempel et al., 2001, Document ID
1082; see 1711, pp. 231-232). Briefly, Kuempel et al. evaluated both
linear and nonlinear (threshold) models and determined that the average
minimum critical quartz lung burden (Mcrit) in rats
associated with reduced pulmonary clearance and increased neutrophil
inflammation was 0.39 mg quartz/g lung tissue. Mcrit is
based on the lowest observed adverse effect level in a study in rats
(Kuempel, 2001, Document ID 1082, pp. 17-23). A human lung dosimetry
model, developed from respirable coal mine dust and quartz exposure and
lung burden data in UK coal miners (Tran and Buchanan, 2001, Document
ID 1126), was then used to estimate the human-equivalent working
lifetime exposure concentrations associated with lung doses. An 8-hour
time-weighted average (TWA) concentration of 0.036 mg/m\3\ (36 [mu]g/
m\3\) over a 45-year working lifetime was estimated to result in a
human-equivalent lung burden to the average Mcrit in rats
(Document ID 1082, pp. 24-26). OSHA peer reviewer Gary Ginsburg, Ph.D.,
summarized, "the Kuempel et al. (2001, 2001b) rat analysis of lung
threshold loading and extrapolation to human dosimetry leads to the
conclusion that in the median case this threshold is approximately 3
times below the current [now former] OSHA PEL" (Document ID 3574, pp.
23). This estimated threshold would be significantly below the final
PEL of 50 [mu]g/m\3\.
In pre-hearing comments, ACC stated that some health organizations
suggested a silicosis-dependent threshold exists for lung cancer (ACC,
Document ID 2307, Attachment A, pp. 60-62). Specifically, ACC cited
Environment and Health Canada as stating:
Although the mechanism of induction for the lung tumours has not
been fully elucidated, there is sufficient supportive mode of action
evidence from the data presented to demonstrate that a threshold
approach to risk assessment is appropriate based on an understanding
of the key events in the pathogenesis of crystalline silica induced
lung tumours (pp. 49-51 as cited by ACC, Document ID 2307, p. 62).
In addition to the statement submitted by ACC, Environment and
Health Canada also stated that:
While there is sufficient evidence to support key events in a
threshold mode of action approach for lung tumours, the molecular
mechanism is still not fully elucidated. Also, despite the fact that
the effects seen in rats parallel the effects observed in human
studies, additional mechanistic studies could further clarify why
lung tumours are not seen in all experimental animals...Thus,
the question of whether silica exposure, in the absence of silicotic
response, results in lung tumours remains unanswered." (pp. 51-52
as cited by ACC, Document ID 2307, pp. 59-61).
It should be noted that the Environment and Health Canada report
was to determine general population risk of exposure to respirable
crystalline silica as a fraction of PM10. Environment and
Health Canada found that levels 0.1-2.1 [mu]g/m\3\ respirable
crystalline silica were sufficiently protective for the general
population because they represented a margin of exposure (MOE) 23-500
times lower than the 50 [mu]g/m\3\ quartz concentration associated with
silicosis in humans (pp. 50-51 as cited by ACC, Document ID 2307, pp.
59-61).
A report by Mossman and Glenn (2013) reviewed the findings from
several international OEL setting panels (Document ID 4070). The report
cites findings from the European Commission's Scientific Committee on
Occupational Exposure Limits for respirable crystalline silica. The
findings "acknowledged a No Observed Adverse Exposure Level (NOAEL)
for respirable crystalline silica in the range below 0.020 mg/m\3\, but
stated that a clear threshold for silicosis could not be identified"
(Mossman and Glen, 2013; Document ID 4070, p. 655). The report went on
to state that SCOEL (2002) recommended that an OEL should lie below 50
[mu]g/m\3\ (Document ID 4070, p. 655). Therefore, even if silica-
induced lung cancer were limited only to a mechanism that involved an
inflammation-dependent threshold, OSHA concludes that exposure
threshold would likely be lower than the final PEL.
5. Renal Disease and Autoimmunity
While mechanistic data is limited, other observed health effects
from inhalation of respirable crystalline silica include kidney and
autoimmune effects. Translocation of particles through the lymphatic
system and filtration through the kidneys may induce effects in the
immune and renal systems similar to the types of changes observed in
the lung (Miller, 2000, Document ID 4174, pp. 40-45). A review of the
available literature indicates that respirable crystalline silica most
likely induces an oxidative stress response in the renal and immune
cells similar to that described above (Donaldson et al., 2009, Document
ID 3894).
6. Conclusion
OSHA has reviewed and responded to the comments received on the
mechanistic studies of respirable crystalline silica-induced lung
cancer and silicosis, as well as comments that the mechanistic data
imply the existence of an exposure threshold. OSHA concludes that: (1)
Lung cancer likely results from both genotoxic and non-genotoxic
mechanisms that arise during early cellular responses as well
as during chronic inflammation from exposure to crystalline silica; (2)
there is not convincing data to demonstrate that silicosis is a
prerequisite for lung cancer; (3) experimental studies in rats are
relevant to humans and provide supporting evidence for carcinogenicity;
(4) crystalline silica does not behave like PSPs such as titanium
dioxide; and (5) any threshold for an inflammatory response to
respirable crystalline silica is likely several times below the final
PEL of 50 [mu]g/m\3\. Thus, the best available evidence on this issue
supports OSHA's findings that respirable crystalline silica increases
the risk of lung cancer in humans, even in the absence of silicosis,
and that lung cancer risk can be increased by exposure to crystalline
silica at or below the new OSHA PEL of 50 [mu]g/m\3\.
I. Comments and Responses Concerning Thresholds for Silica-Related
Diseases
In this section, OSHA discusses comments focused on the issue of
exposure-response thresholds for silica exposure. In the comments
received by OSHA on this topic, an exposure-response "threshold" for
silica exposure typically refers to a level of exposure such that no
individual whose exposure is below that level would be expected to
develop an adverse health effect. Commenters referred to thresholds
both in terms of concentration and cumulative exposure (i.e., a level
of cumulative exposure below which an individual would not be expected
to develop adverse health effects). In addition to individual
thresholds, some commenters referred to a "population average
threshold," that is, the mean or median value of individual thresholds
across a population of workers. There is significant scientific
controversy over whether any such thresholds exist for silicosis and
lung cancer, as well as the cumulative exposure level or concentration
at which a threshold effect may occur and whether certain statistical
modeling approaches can be used to identify threshold effects.
OSHA has reviewed the evidence in the record pertaining to
thresholds, and has determined that the best available evidence
supports the Agency's use of non-threshold exposure-response models in
its risk assessments for silicosis and lung cancer. The voluminous
scientific record accrued by OSHA in this rulemaking supports lowering
the existing PEL to 50 [mu]g/m\3\. Rather than indicating a threshold
of risk that starts above the previous general industry PEL, the weight
of this evidence, including OSHA's own risk assessment models, supports
a conclusion that there continues to be significant, albeit reduced,
risk at the 50 [mu]g/m\3\ exposure limit. OSHA's evaluation of the best
available evidence on thresholds indicates that there is considerable
uncertainty about whether there is any threshold below which silica
exposure causes no adverse health effects; but, in any event, the
weight of evidence supports the view that, if there is a threshold of
exposure for the health effects caused by respirable crystalline
silica, it is likely lower than the new PEL of 50 [mu]g/m\3\.
Commenters have not provided convincing evidence of a population
threshold (e.g., an exposure level safe for all workers) above the
revised PEL. In addition, OSHA's final risk assessment demonstrates
that achieving this limit--which OSHA separately concludes is overall
the lowest feasible level for silica-generating operations--will result
in significant reductions in mortality and morbidity from occupational
exposure to respirable crystalline silica.
1. Thresholds--General
In the Preliminary Quantitative Risk Assessment (QRA) (Document ID
1711, pp. 275, 282-285), OSHA reviewed evidence on thresholds from a
lung dosimetry model developed by Kuempel et al. (2001, Document ID
1082) and from epidemiological analyses conducted by Steenland and
Deddens (2002, Document ID 1124). As discussed in the Preliminary QRA,
Kuempel et al. (2001) used kinetic lung models for both rats and humans
to relate lung burden of crystalline silica and estimate a minimum
critical lung burden (Mcrit) of quartz above which particle
clearance begins to decline and lung inflammation begins to increase
(early steps in the process of developing silica-related disease). The
Mcrit would be achieved by a human equivalent airborne
exposure to 36 [mu]g/m\3\ for 45 years, based on the authors' rat-to-
human lung model conversion. Exposures below this level would not lead
to an excess lung cancer risk in the average individual, if it were
assumed that cancer is strictly a secondary response to persistent
inflammation. OSHA notes, however, that if some of the silica-related
lung cancer risk occurs as a result of direct genotoxicity from early
cellular interaction with respirable silica particles, then this
threshold value may not be applicable. Since silicosis is caused by
persistent lung inflammation, this exposure level could be viewed as a
possible average threshold level for that disease as well (Document ID
1711, p. 284). As 36 [mu]g/m\3\ is well below the previous general
industry PEL of 100 [mu]g/m\3\ and below the final PEL of 50 [mu]g/
m\3\, the Kuempel et al. study showed no evidence of an exposure-
response threshold high enough to impact OSHA's choice of PEL.
Steenland and Deddens (2002, Document ID 1124) examined a pooled
lung cancer study originally conducted by Steenland et al. (2001a).
They found that a threshold model based on the log of cumulative dose
(15-year lag) fit better than a no-threshold model, with the best
threshold at 4.8 log mg/m\3\-days (representing an average exposure of
10 [mu]g/m\3\ over a 45-year working lifetime). OSHA preliminarily
concluded that, in the Kuempel et al. (2001) study and among the
studies evaluated by Steenland et al. (2001a) in the pooled analysis,
there was no empirical evidence of a threshold for lung cancer in the
exposure range represented by the previous and final PELs (i.e., at 50
[mu]g/m\3\ or higher) (Document ID 1711, pp. 275, 284). Thus, based on
these two studies, workers exposed at or below the new PEL of 50 [mu]g/
m\3\ over a working lifetime still face a risk of developing silicosis
and lung cancer because their exposure would be above the supposed
exposure threshold.
In its prehearing comments, the ACC argued that OSHA's examination
of the epidemiological evidence, along with animal studies and
mechanistic considerations, "has not shown that reducing exposures
below currently permitted exposure levels would create any additional
health benefits for workers. OSHA's analysis and the studies on which
it relies have not demonstrated the absence of an exposure threshold
above 100 [mu]g/m\3\ for the various adverse health effects considered
in the QRA" (Document ID 2307, Attachment A, p. 26; also 2348,
Attachment 1, p. 33). According to the ACC, an exposure threshold above
OSHA's previous general industry PEL of 100 [mu]g/m\3\ means that
workers exposed below that level will not get sick, negating the need
to lower the PEL (Document ID 2307, Attachment A, p. 91).
Members of OSHA's peer review panel for the Review of Health
Effects Literature and Preliminary Quantitative Risk Assessment
(Document ID 1711) rejected the ACC's comments as unsupportable. Peer
reviewer Mr. Bruce Allen stated: "it is essentially impossible to
distinguish between dose-response patterns that represent a threshold
and those that do not" in epidemiological data (Document ID 3574, p.
8). Peer reviewer Dr. Kenneth Crump similarly commented:
OSHA is on very solid ground in the [Preliminary QRA's]
statement that "available information cannot firmly establish a
threshold exposure for silica-related effects"...the hypothesis
that a particular dose response does not have a threshold is not
falsifiable. Similarly, the hypothesis that a particular dose response
does have a threshold is not falsifiable (Document ID 3574, p. 17).
Dr. Cox, representing the ACC, agreed with Dr. Crump that "it's
impossible to prove a negative, empirically...you could never rule
out that possibility" of a threshold at a low level of exposure
(Document ID 3576, Tr. 402). However, he contended that it is possible
to rule out a threshold in the higher-level range of observed exposures
based on observed illness: "I think that there are plenty of chemicals
for which the hypothesis of a threshold exist[ing] at or above current
standards could be ruled out because you see people getting sick at
current levels" (Document ID 3576, Tr. 403). Other commenters stated
their belief that workers recently diagnosed with silicosis must have
had exposures above the previous general industry PEL and, based on
this supposition, concluded that OSHA has not definitively proven risk
to workers exposed below the previous general industry PEL (Document ID
4224, pp. 2-5; Tr. 3582, pp. 1951-1963).
OSHA agrees with Dr. Cox that observation of workers "getting sick
at current levels" can rule out a threshold effect at those levels. As
is discussed below, there is evidence that workers exposed to silica at
cumulative or average exposure levels permitted under the previous PELs
have become ill and died as a result of their exposure. OSHA thus
strongly disagrees with any implication from commenters that the Agency
should postpone reducing a PEL until it has extensive documentation of
sick and dying workers to demonstrate that the current PEL is not
sufficiently protective (see Section II, Pertinent Legal Authority, and
Section VI, Final Quantitative Risk Assessment and Significance of
Risk).
The ACC's and Chamber's comments on this issue essentially argue
that the model OSHA used to assess risk was inadequate to assess
whether a threshold of risk exists and, if one does exist, at what
level (Document ID 2307, Attachment A, pp. 52-65; 2376, pp. 20-22;
2330, pp. 17-21). According to OSHA peer reviewer Dr. Crump, however,
the analytical approach taken by OSHA in the Preliminary QRA was
appropriate. Considering the inherent limitations of epidemiological
data:
an attempt to distinguish between threshold and non-threshold dose
responses is not even a scientific exercise...The best that can
be done is to attempt to place bounds on the amount of risk at
particular exposures consistent with the available data, which is
what OSHA had done in their risk assessment (Document ID 3574, p.
17).
A further source of uncertainty in investigating thresholds was
highlighted by Dr. Mirer, on behalf of the AFL-CIO (Document ID 3578,
Tr. 988-989) and by peer reviewer Dr. Andrew Salmon, who stated:
[m]any of the so-called thresholds seen in epidemiological studies
represent thresholds of observability rather than thresholds of
disease incidence...studies (and anecdotal observations) with
less statistical power and shorter post-exposure followup (or none)
will necessarily fail to see the less frequent and later-appearing
responses at lower doses. This creates an apparent threshold which
is higher in these studies than the apparent threshold implied by
studies with greater statistical power and longer follow-up
(Document ID 3574, p. 37).
Peer reviewer Dr. Gary Ginsberg suggested that, recognizing these
inherent limitations, OSHA should characterize the body of evidence and
argument surrounding thresholds by discussing the following factors
related to whether a threshold for silica-related health effects exists
at exposure levels above the previous general industry PEL:
the choices relative to the threshold concept for the silica dose
response...[including] specific dose response datasets that are
consistent with a linear or a threshold-type model, if a threshold
seems likely, where was it seen relative to the current and proposed
PEL, and a general discussion of mechanism of action, measurement
error and population variability as concepts that can help us
understand silica dose response for cancer and non-cancer endpoints
(Document ID 3574, p. 24).
Following Dr. Ginsberg's suggestion, OSHA has, in its final health
and risk analysis, considered the epidemiological evidence relevant to
possible threshold effects for silicosis and lung cancer. As discussed
below, first in "Thresholds--Silicosis and NMRD" and then in
"Thresholds--Lung Cancer," OSHA has carefully considered comments
about statistical methods, exposure measurement uncertainty, and
variability as they pertain to threshold effects. The discussion
addresses the epidemiological evidence with respect to both cumulative
and concentration thresholds. For reference, a working lifetime (45
years) of exposure to silica at the previous general industry PEL (100
[mu]g/m\3\) and the final PEL (50 [mu]g/m\3\) yield cumulative
exposures of 4.5 mg/m\3\-yrs and 2.25 mg/m\3\-yrs, respectively. Other
sections with detailed discussions pertinent to threshold issues
include Section V.H, Mechanisms of Silica-Induced Adverse Health
Effects, and Section V.K, Comments and Responses Concerning Exposure
Estimation Error and ToxaChemica's Uncertainty Analysis.
2. Thresholds--Silicosis and NMRD
OSHA has determined that the studies most relevant to the threshold
issue in this rulemaking are those of workers who have cumulative
exposures or average exposure concentrations below the levels
associated with the previous general industry PEL (100 [mu]g/m\3\, or
cumulative exposure of 4.5 mg/m\3\-yrs). Contrary to comments that OSHA
only relied on studies involving exposures far above the levels of
interest to OSHA in this rulemaking, and then extrapolated exposure-
response relationships down to relevant levels (e.g., Document ID 2307,
Attachment A, pp. 94-95; 4226, p. 2), a number of silicosis studies
included workers who were exposed at levels close to or below the
previous OSHA PEL for general industry. For example, four of the six
cohorts of workers in the pooled silicosis mortality risk analysis
conducted by Mannetje et al. (2002) had median cumulative exposures
below 2.25 mg/m\3\-yrs., and three had median silica concentrations
below 100 [mu]g/m\3\ (Mannetje et al., 2002, Document ID 1089, p. 724).
Other silicosis studies with significant numbers of relatively low-
exposed workers include analyses of German pottery workers (Birk et
al., 2009, Document ID 4002, Attachment 2; Mundt et al., 2011, 1478;
Morfeld et al., 2013, 3843), Vermont granite workers (Attfield and
Costello, 2004, Document ID 0285; Vacek et al., 2011, 1486), and
industrial sand workers (McDonald et al., 2001, Document ID 1091;
Hughes et al., 2001, 1060; McDonald et al., 2005, 1092). In this
section, OSHA will discuss each of them in relationship to whether they
suggest the existence of a threshold above 100 [mu]g/m\3\, the previous
PEL for general industry.
a. Mannetje et al. Pooled Study and Related Analyses
Mannetje et al. (2002b, Document ID 1089) estimated excess lifetime
risk of silicosis based on six of the ten cohorts that were part of the
IARC multi-center exposure-response study (Steenland et al., 2001a,
Document ID 0452). The six cohorts were U.S. diatomaceous earth (DE)
workers, Finnish granite workers, U.S. granite workers, U.S. industrial
sand workers, U.S. gold miners, and Australian gold miners. Together,
the cohorts included 18,634 subjects and 170 silicosis deaths. All
cohorts except the Finnish granite workers and Australian gold miners
had significant numbers of workers with median cumulative and/or
average exposures below the levels associated with OSHA's previous
general industry PEL. Checking for nonlinearities in their
exposure-response model, Mannetje et al. found that a five-knot
cubic spline model (which allows for deviations, such as thresholds,
from a linear relationship) did not fit the data better than the linear
model used in their main analysis. The result of this attempt to check
for nonlinearities suggests that there is no threshold effect in the
relationship between cumulative silica exposure and silicosis risk in
the study. Significantly, NIOSH stated that the results of Mannetje et
al.'s analysis "suggest the absence of threshold at the lowest
[cumulative] exposure analyzed...in fact, the trend for silicosis
mortality risk extends down almost linearly to the lowest cumulative
exposure stratum", in which "the average cumulative exposure is the
equivalent of 45 years of exposure at 11.1 [mu]g/m\3\ silica"
(Document ID 4233, pp. 34-35). This level is significantly below the
new OSHA PEL of 50 [mu]g/m\3\.
As discussed in Section V.K, Comments and Responses Concerning
Exposure Estimation Error and ToxaChemica's Uncertainty Analysis, OSHA
commissioned Drs. Kyle Steenland and Scott Bartell to examine the
potential effects of exposure measurement error on the mortality risk
estimates derived from the pooled studies of lung cancer (Steenland et
al., 2001, Document ID 0452) and silicosis (Mannetje et al., 2002b,
Document ID 1089). Their analysis of the pooled data, using a variety
of standard statistical techniques (e.g., regression analysis), also
found the data either consistent with the absence of a threshold or
inconsistent with the existence of a threshold \8\ (Document ID 0469).
Thus, neither Mannetje et al. nor Steenland and Bartell's analyses of
the pooled cohorts suggested the existence of a cumulative exposure
threshold effect; in fact, they suggested the absence of a threshold.
Given the predominance in these studies of cohorts where at least half
of the workers had cumulative exposures below 4.5 mg/m\3\-yrs, OSHA
believes these results constitute strong evidence against an exposure
threshold above the level of cumulative exposure resulting from long-
term exposure at the previous PEL of 100 [mu]g/m\3\.
---------------------------------------------------------------------------
\8\ This analysis included a log-cumulative logistic regression
model, as well as a categorical analysis and five-knot restricted
cubic spline analysis using log-cumulative exposure. Had the spline
analysis shown a better-fitting model with a flat exposure-response
at low cumulative exposure levels, it might have suggested a
threshold effect for cumulative exposure. However, no significant
difference was observed between the parametric model and the two
other models, which had greater flexibility in the shape of the
exposure-response (Document ID 0469, p. 50, Figure 5).
---------------------------------------------------------------------------
b. Vermont Granite Workers
As discussed in the Supplemental Literature Review of
Epidemiological Studies, Vacek et al. (2011, Document ID 1486) examined
exposures from 1950 to 1999 for a group of 7,052 workers in the Vermont
granite industry (Document ID 1711, Attachment 1, pp. 2-5). The
exposure samples show relatively low exposures for the worker
population. For the period 1950 to 2004, Verma et al. (2012), who
developed the job exposure matrix used by Vacek et al., estimated that
average exposure concentrations in 21 of 22 jobs were below 100 [mu]g/
m\3\, and 11 of the 22 job classes were at 50 [mu]g/m\3\ or below. The
remaining job category, laborer, had an estimated average exposure
concentration of exactly 100 [mu]g/m\3\ (Verma et al., 2011, Document
ID 1487, p. 75).
Six of the 5,338 cohort members hired in or after 1940, when
Vermont's dust control program was in effect, were identified as having
died of silicosis by the end of the follow-up period (Vacek et al.,
Document ID 1486, p. 314). The frequency of observed silicosis
mortality in the population is significant by OSHA standards (1.1 per
1,000 workers), and may be underestimated due to under-reporting of
silicosis as a cause of death (see Section V.E, Comments and Responses
Concerning Surveillance Data on Silicosis Morbidity and Mortality).
This observed silicosis mortality shows that deaths from silicosis
occurred among workers hired after silica concentrations were reduced
below OSHA's previous general industry PEL. It therefore demonstrates
that a threshold for silicosis above 100 [mu]g/m\3\ is unlikely.
In terms of morbidity, Graham et al.'s study of radiographic
evidence of silicosis among retired Vermont granite workers found
silicosis in 5.7 percent of workers hired after 1940 (equivalent to 57/
1,000 workers) (Graham et al., 2004, Document ID 1031, p. 465). OSHA
concludes that these studies of low-exposed workers in the Vermont
granite industry show significant risk of silicosis--both mortality and
morbidity--at concentrations below the previous PELs. These studies
also indicate that a threshold at an exposure concentration
significantly above the previous PEL for general industry, as posited
by industry representatives, is unlikely.
c. U.S. Industrial Sand Workers
In an exposure-response study of 4,027 workers in 18 U.S.
industrial sand plants, Steenland and Sanderson (2001) reported that
approximately three-quarters of the workers with complete work
histories had cumulative exposures below 1.28 mg/m\3\-yrs, well below
the cumulative exposure of 2.25 mg/m\3\-yrs associated with a working
lifetime of exposure at the final PEL of 50 [mu]g/m\3\ (Document ID
0455, p. 700). The study identified fourteen deaths from silicosis and
unspecified pneumoconiosis (~3.5 per 1,000 workers) (Document ID 0455,
p. 700), of which seven occurred among workers with cumulative
exposures below 1.28 mg/m\3\-yrs. As with other reports of silicosis
mortality, this figure may underestimate the true rate of silicosis
mortality in this worker population.
Hughes et al. (2001) reported 32 cases of silicosis mortality in a
cohort of 2,670 workers at nine North American industrial sand plants
(~12 per 1,000) (Document ID 1060, p. 203). The authors developed a
job-exposure matrix based on exposure samples collected by the
companies and by MSHA between 1973 and 1994, along with the 1946
exposure survey used by Steenland and Sanderson (2001, Document ID
0455; 2307, Attachment 7, p. 6). Job histories were available for 29
workers who died of silicosis. Of these, fourteen had estimated
cumulative exposure less than or equal to 5 mg/m\3\-yrs, and seven had
cumulative exposures less than or equal to 1.5 mg/m\3\-yrs (Document ID
1060, p. 204). Both studies clearly showed silicosis risk among workers
whose cumulative exposures were comparable to those that workers could
experience under the final PEL (Document ID 0455, p. 700; 1060, p.
204), indicating that a threshold above this level of cumulative
exposure is unlikely.
d. German Porcelain Workers
A series of papers by Birk et al. (2009, Document ID 4002,
Attachment 2; 2010, Document ID 1467), Mundt et al. (2011, Document ID
1478), and Morfeld et al. (2013, Document ID 3843) examined silicosis
mortality and morbidity in a population of over 17,000 workers in the
German porcelain industry. Cohort members' annual average
concentrations of respirable quartz dust were reconstructed from
detailed work histories and dust measurements collected in the industry
from 1951 onward (Birk et al., 2009, Document ID 4002, Attachment 2,
pp. 374-375). Morfeld et al. observed 40 silicosis morbidity cases (ILO
profusion category 1/1 or greater), and noted that additional
follow-up of the cohort might be necessary due to the long latency
period of silicosis (2013, Document ID 3843, p. 1032).
Follow-up time is a critical factor for detection of silicosis,
which has a typical latency of 20-30 years (see Morfeld et al., 2013,
Document ID 3843, p. 1028). As stated in Section V.C, Summary of the
Review of Health Effects Literature and Preliminary QRA, the disease
latency for silicosis can extend to around 30 years. Follow-up was
extremely limited in the German porcelain workers silicosis morbidity
analysis, with a mean of 7.5 years of follow up for the study
population (Document ID 3843). Despite the limited follow-up time, the
cohort showed evidence of silicosis morbidity among low-exposed
workers: 17.5 percent of cases occurred among workers whose highest
average silica exposure in any year ("highest annual") was estimated
by the authors to be less than 250 [mu]g/m\3\, and 12.5 percent of
cases occurred among workers whose highest annual silica exposure was
estimated at less than 100 [mu]g/m\3\ (Document ID 3843).
The lead author of the study, Dr. Peter Morfeld, testified at the
public hearings on behalf of the ACC Crystalline Silica Panel. In his
post-hearing comments, Dr. Morfeld stated that "[m]echanistic
considerations imply that we should not expect to see a threshold for
cumulative exposure" in silicosis, but that the question of whether a
threshold concentration level may exist remains (Document ID 4003, p.
3). The study by Morfeld et al. "focused on the statistical estimation
of a concentration threshold...[and] simultaneously took into
account the cumulative exposure to respirable crystalline silica dust
as a driving force of the disease" (Document ID 4003, p. 3). Morfeld
et al. applied a technique developed by Ulm et al. (1989, 1991) to
estimate a concentration threshold. In this method a series of
candidate exposure concentration values are subtracted from the
estimated annual mean concentration data. Using the recalculated
exposure estimates for the study population, regression analyses for
each candidate are run to identify the best fitting model, using the
Akaike Information Criterion (AIC) to evaluate model fit (Document ID
3843, p. 1029). According to Morfeld, the best fitting model in their
study estimated a threshold concentration of 250 [mu]g/m\3\ (AIC =
488.3) with a 95 percent confidence interval of 160 to 300 [mu]g/m\3\.
A second model with very similar fit (AIC = 488.8) estimated a
threshold concentration of 200 [mu]g/m\3\ with a 95 percent confidence
interval of 57 [mu]g/m\3\ to 270 [mu]g/m\3\. A third model with a
poorer fit (AIC=490.6) estimated a threshold concentration of 80 [mu]g/
m\3\ with a 95 percent confidence interval of 0.2 [mu]g/m\3\ to 210
[mu]g/m\3\ (Document ID 3843, Table 3, p. 1031).
In the Final Peer Review Report, Dr. Crump stated that Morfeld et
al.'s modeling approach, like "all such attempts statistically to
estimate a threshold," is "not reliable because the threshold
estimates so obtained are highly unstable" (Document ID 3574, p. 17).
Dr. Morfeld's co-author, Dr. Mundt, stated in the public hearings:
I'll be the first one to tell you there is a lot of imprecision
and, therefore, say confidence intervals or uncertainty should be
respected, and that the--I'm hesitant to just focus on a single
point number like the .25 [250 [mu]g/m\3\], and prefer that you
encompass the broader range that was reported in the Morfeld, on
which I was an author and consistently brought this point to the
table (Document ID 3577, Tr. 645).
NIOSH submitted post-hearing comments on the analysis in Morfeld et
al. (2013). NIOSH pointed out that the exposure measurements in the
analysis were based on German dust samplers, which for pottery have
been shown to collect approximately twice as much dust as U.S.
samplers. Therefore, "when Dr. Morfeld cited 0.15 mg/m\3\ (150 [mu]g/
m\3\) as the lower 95% confidence limit for the threshold, that would
convert to 0.075 mg/m\3\ (75 [mu]g/m\3\) in terms of equivalent
measurements made with a U.S. sampler" (Document ID 4233, p. 21).
Similarly, the U.S. equivalent of each of the other threshold estimates
and confidence limits presented in Morfeld et al.'s analysis would be
about half the reported exposure levels. NIOSH also commented that
Morfeld et al.'s analysis appears to be consistent with both threshold
and non-threshold models (Document ID 4233, p. 55). Furthermore, NIOSH
observed that Morfeld et al. did not account for uncertainty in the
values of one of their model parameters ([egr]); therefore their
reported threshold confidence limits of 0.16-0.30 are too narrow
(Document ID 4233, p. 56). More generally, NIOSH noted that Morfeld et
al. did not quantitatively evaluate how uncertainty in exposure
estimates may have impacted the results of the analysis; Morfeld agreed
that he had not performed a "formal uncertainty analysis" (Document
ID 4233, p. 58; 3582, Tr. 2078-2079). NIOSH concluded, "it is our firm
recommendation to discount results based on the model specified in
[Morfeld et al. Eq. 3]...including all results related to a
threshold" (Document ID 4233, p. 58). OSHA has evaluated NIOSH's
comments on the analysis and agrees that the issues raised by NIOSH
raise serious questions about Morfeld et al.'s conclusions regarding a
silica threshold.
OSHA's greater concern with Dr. Morfeld's estimate of 250 [mu]g/
m\3\ as a threshold concentration for silicosis is the fact that a
substantial proportion of workers with silicosis in Dr. Morfeld's study
had no estimated exposure above the threshold suggested by the authors;
this threshold was characterized by commenters, including the Chamber
of Commerce (Chamber), as a concentration "below which the lung
responses did not progress to silicosis" (Document ID 4224, Attachment
1, p. 3). This point was emphasized by Dr. Brian Miller in the Final
Peer Review Report (Document ID 3574, p. 57) and by NIOSH (Document ID
4233, p. 57). In the study, 17.5 percent of workers with silicosis were
classified as having no exposure above Morfeld et al.'s estimated
threshold of 250 [mu]g/m\3\, (Document ID 3843, p. 1031) and 12.5
percent of these workers were classified as having no exposure above
100 [mu]g/m\3\. OSHA believes the presence of these low-exposed workers
with silicosis clearly contradicts the authors' estimate of 250 [mu]g/
m\3\ as a level of exposure below which no worker will develop
silicosis (see Document ID 4233, p. 57).
In a post-hearing comment, Dr. Morfeld offered a different
interpretation of his results, describing his threshold estimate as a
"population average" which would not be expected to characterize risk
for all individuals in a population. Rather, according to Dr. Morfeld
"we expect to see differences in response thresholds among subjects"
(Document ID 4003, p. 5). OSHA agrees with this interpretation, which
was similarly expressed in several comments from OSHA's peer reviewers
on the subject of thresholds (e.g., Document ID 3574, pp. 13, 21-22).
Consistent with its peer reviewers' opinions, OSHA draws the conclusion
from the data and discussion concerning population averages that these
"differences in response thresholds among subjects" support setting
the PEL at 50 [mu]g/m\3\ in order to protect the majority of workers in
the population of employees exposed to respirable crystalline silica.
OSHA's review of the Morfeld et al. data on German porcelain workers
thus reinforces its view that reducing exposures to this level will
benefit the many workers who would develop silicosis at exposure levels
below that of the "average" worker.
Dr. Morfeld's discussion of his estimate as a "population
average" among workers with different individual responses to silica
exposure echoes several comments from OSHA's peer reviewers on the subject of
thresholds. In the Final Peer Review Report, Dr. Ginsberg observed that
a linear exposure-response model may reflect a distribution of
individual "thresholds," such that "the population can be
characterized as having a distribution of vulnerability. This
distribution may be due to differences in levels of host defenses that
come with differences in age, co-exposure to other chemicals, the
presence of interacting background disease processes, non-chemical
stressors, and a variety of other host factors" (Document ID 3574, p.
21). Given the number of factors that may influence vulnerability to
certain diseases in a population of workers, Dr. Ginsberg continued:
it is logical for OSHA to strongly consider inter-subject
variability...as the reason for linearly-appearing regression
slopes in silica-related non-cancer and cancer studies. This
explanation does not imply an artifact [that is, a false appearance
of linear exposure-response] but that the linear (or log linear)
regression coefficient extending down to low dose reflects the
inherent variability in susceptibility such that the effect of
concern...may occur in some individuals at doses well below what
might be a threshold in others (Document ID 3574, pp. 21-22).
Peer reviewer Mr. Bruce Allen agreed that "[i]t makes no sense to
discuss a single threshold value...Given, then, that thresholds
must be envisioned as a distribution in the population, then there is
substantial population-level risk even at the mean threshold value, and
unacceptably high risk levels at exposures far below the mean
threshold." He further stated:
It is NOT, therefore, inappropriate to model the population-
level observations using a non-threshold model...In fact, I
would claim that it is inappropriate to include ANY threshold models
(i.e., those that assume a single threshold value) when modeling
epidemiological data. A non-threshold model for characterizing the
population dose-response behavior is theoretically and practically
the optimal approach (Document ID 3574, p. 13).
OSHA concludes that this German porcelain workers cohort shows
evidence of silicosis among workers exposed at levels below the
previous PELs, and that continued follow-up of this cohort would be
likely to show greater silicosis risk among low-exposed workers due to
the short follow-up time. Furthermore, the Chamber's characterization
of Dr. Morfeld's result as "a threshold concentration of 250 [mu]g/
m\3\ below which the lung responses did not progress to silicosis"
(Document ID 4224, p. 3) is plainly inaccurate, as the estimated
exposures of a substantial proportion of the workers with silicosis in
the data set did not exceed this level.
e. Park et al. (2002)
The ACC submitted comments on the Park et al. (2002, Document ID
0405) study which examined silicosis and lung disease other than cancer
(i.e., NMRD) in a cohort of diatomaceous earth workers. The ACC's
comments on this study are discussed in detail in Section V.D, Comments
and Responses Concerning Silicosis and Non-Malignant Respiratory
Disease Mortality and Morbidity, including comments relating to
exposure-response thresholds in this study. Briefly, the ACC claimed
that the Park et al. (2002) study is "fully consistent" with
Morfeld's estimate of a threshold above the 100 [mu]g/m\3\
concentration for NMRD, including silicosis, mortality (Document ID
2307, Attachment A, p. 107). However, NIOSH explained in its post-
hearing brief that categorical analysis for NMRD indicated no threshold
existed at or above a cumulative exposure corresponding to 25 [mu]g/
m\3\ over 40 years of exposure, which is below the cumulative exposure
equivalent to the new PEL over 45 years (Document ID 4233, p. 27). Park
et al. did not attempt to estimate a threshold below that level because
the data lacked the power needed to discern a threshold (Document ID
4233, p. 27). OSHA agrees with NIOSH's assessment, which indicates
that, if there is a cumulative exposure threshold for NMRD, including
silicosis, it is significantly below the final PEL of 50 [mu]g/m\3\.
f. Conclusion--Silicosis and NMRD
OSHA concludes that the body of epidemiological literature clearly
demonstrates risk of silicosis and NMRD morbidity and mortality among
workers who have been exposed to cumulative exposures or average
exposure concentrations at or below the levels associated with the
previous general industry PEL (100 [mu]g/m\3\, or cumulative exposure
of 4.5 mg/m\3\-yrs). Thus, OSHA does not agree with commenters who have
stated that the previous general industry PEL is fully protective and
that reducing it will yield no health benefits to silica-exposed
workers (e.g., Document ID 4224, p. 2-5; Tr. 3582, pp. 1951-1963).
Instead, the Agency finds that the evidence is at least as consistent
with a finding that no threshold is discernible as it is with a finding
that a threshold exists at some minimal level of exposure. The best
available evidence also demonstrates silicosis morbidity and mortality
below the previous PEL of 100 [mu]g/m\3\, indicating that any threshold
for silicosis (understood as an exposure level below which no one would
develop disease), if one exists, is below that level. Even if the
conclusion reached by Dr. Morfeld that a population average threshold
exists above the level of the previous PEL is accurate, there will
still be a substantial portion of the population who will develop
silicosis from exposures below the identified "threshold." These
findings support OSHA's action in lowering the PEL to 50 [mu]g/m\3\.
3. Thresholds--Lung Cancer
OSHA's Preliminary QRA and supplemental literature review included
several studies that provide information on possible threshold effects
for lung cancer. OSHA has determined that the epidemiological studies
most relevant to the threshold issue are those with workers who have
cumulative exposures or average exposure concentrations below the
levels associated with the previous general industry PEL (100 [mu]g/
m\3\, or cumulative exposure of 4.5 mg/m\3\-yrs). As with the silicosis
studies previously discussed, contrary to comments that OSHA only
relied on studies involving exposures far above the levels of interest
to OSHA in this rulemaking (e.g., Document ID 2307, Attachment A, pp.
94-95; 4226, p. 2), a number of lung cancer studies included workers
who were exposed at levels close to or below the previous general
industry PEL. Five of the 10 cohorts of workers in the pooled lung
cancer risk analysis conducted by Steenland et al. (2001a) had median
cumulative exposures below 4.5 mg/m\3\-yrs (the cumulative level
associated with a working lifetime of exposure at the previous general
industry PEL); four were also below 2.25 mg/m\3\-yrs (the cumulative
level associated with a working lifetime of exposure at the revised
PEL) and three had median silica concentrations below 100 [mu]g/m\3\
(Document ID 0452, p. 775). Other lung cancer studies with significant
numbers of relatively low-exposed workers include analyses of the
Vermont granite workers (Attfield and Costello, 2004, Document ID 0285;
Vacek et al., 2011, 1486) and industrial sand workers (McDonald et al.,
2001, Document ID 1091; Hughes et al., 2001, 1060; McDonald et al.,
2005, 1092) described in the previous discussion on silicosis. In
addition to the epidemiological studies discussed here, in Section V.H,
Mechanisms of Silica-Induced Adverse Health Effects, OSHA discussed
studies that have shown direct genotoxic mechanisms by which exposure
to crystalline silica at any level, with no threshold effect, may lead
to lung cancer.
a. Steenland et al. Pooled Lung Cancer Study and Related Analyse
Steenland et al. (2001a) estimated excess lifetime risk of lung
cancer based on a 10-cohort pooled study, which included several
cohorts with significant numbers of workers with median cumulative and
average exposures below those allowed by the previous general industry
PEL (Document ID 0452). Results indicated that 45 years of exposure at
0.1 mg/m\3\ (100 [mu]g/m\3\) would result in a lifetime risk of 28
excess lung cancer deaths per 1,000 workers (95% confidence interval
(CI) 13-46 per 1,000). An alternative (non-linear) model yielded a
lower risk estimate of 17 per 1,000 (95% CI 2-36 per 1,000).
A follow-up letter by Steenland and Deddens (2002, Document ID
1124) addressed the possibility of an exposure threshold effect in the
pooled lung cancer analysis conducted by Steenland et al. in 2001.
According to Dr. Steenland, "We further investigated whether there was
a level below which there was no increase in risk, the so-called
threshold. So we fit models that had a threshold versus those that
didn't, and we explored various thresholds that might apply" (Document
ID 3580, Tr. 1229). Threshold models using average exposure and
cumulative exposure failed to show a statistically significant
improvement in fit over models without a threshold. However, the
authors found that when they used the log of cumulative exposure (a
transformation commonly used to reduce the influence of high exposure
points on a model), a threshold model with a 15-year lag fit better
than a no-threshold model. The authors reported the best threshold
estimate at 4.8 log mg/m\3\-days (Document ID 1124, p. 781), or an
average exposure of approximately 10 [mu]g/m\3\ over a 45-year working
lifetime, one-fifth of the final PEL. Dr. Steenland explained what his
analysis indicated regarding a cumulative exposure threshold for lung
cancer: "we found, in fact, that there was a threshold model that fit
better than a no-threshold model, not enormously better but better
statistically, but that threshold was extremely low...far below the
...silica standard proposed by OSHA" (Document ID 3580, Tr. 1229).
In response to comments from ACC Panel members Dr. Valberg and Dr.
Long that the analysis presented by Steenland et al. showed a clear
threshold at a level of cumulative exposure high enough to bear on
OSHA's choice of PEL (Document ID 2330, p. 20), Dr. Steenland explained
that their conclusion was based on a misreading of an illustration in
his study:
[I]f you look at the figure, you see that the curve of the
spline [a flexible, nonlinear exposure-response model] starts to go
up around four on the log scale of microgram per meter cubed days.
And if you transform that from the log to the regular scale, that is
quite consistent with the threshold we got when we did a formal
analysis using the log transform model [discussed above] (Document
ID 3580, Tr. 1255).
The ACC representatives' comments do appear to be based on a
misunderstanding of the figure in question, due to an error in Dr.
Steenland's 2001 publication in which the axis of the figure under
discussion was incorrectly labeled. This error was later corrected in
an erratum (Document ID 3580, Tr. 1257; Steenland et al., 2002,
Erratum. Cancer Causes Control, 13:777).
In addition, at OSHA's request, Drs. Steenland and Bartell
(ToxaChemica, 2004, Document ID 0469) conducted a quantitative
uncertainty analysis to examine the effects of possible exposure
measurement error on the pooled lung cancer study results (see Section
V.K, Comments and Responses Concerning Exposure Estimation Error and
ToxaChemica's Uncertainty Analysis). These analyses showed no evidence
of a threshold effect for lung cancer at the final or previous PELs.
Based on Dr. Steenland's work, therefore, OSHA believes that no-
threshold models are appropriate for evaluating the exposure-response
relationship between silica exposure and lung cancer. Even if
commenters are correct that threshold models are preferable, the
threshold is likely at a level of cumulative exposure significantly
below what a worker would accumulate in 45 years of exposure at the
final PEL, and is therefore immaterial to this rulemaking (see Document
ID 1124, p. 781).
b. Vermont Granite Workers
In the Preliminary QRA and supplemental literature review, OSHA
reviewed several studies on lung cancer among silica-exposed workers in
the Vermont granite industry, whose exposures were reduced to
relatively low levels due to a program for dust control initiated in
1938-1940 by the Vermont Division of Industrial Hygiene (Document ID
1711, pp. 97-102; 1711, Attachment 1, pp. 2-5; 1487, p. 73). As
discussed above, Verma et al. (2012) reported that all jobs in the
industry had average exposure concentrations at or below 100 [mu]g/
m\3\--most of them well below this level--in the time period 1950-2004
after implementation of exposure controls (Document ID 1487, Table IV,
p. 75).
Attfield and Costello (2004) examined a cohort of 5,414 Vermont
granite workers, including 201 workers who died of lung cancer
(Document ID 0285, pp. 130, 134). In this study, cancer risk was
elevated at cumulative exposure levels below 4.5 mg/m\3\-yrs, the
amount of exposure that would result from a 45-year working lifetime of
exposure at the previous PEL. The authors reported elevated lung cancer
in all exposure groups, observing statistically significant elevation
among workers with cumulative exposures between 0.5 and 1 mg/m\3\-yrs
(p < 0.05), cumulative exposures between 2 and 3 mg/m\3\-yrs (p <
0.01), and cumulative exposures between 3 and 6 mg/m\3\-yrs (p < 0.05)
(Document ID 0285, p. 135). These findings indicate that a threshold in
exposure-response for lung cancer is unlikely at cumulative exposure
levels associated with 45 years of exposure at the previous PEL and
below.
Vacek et al. (2011) examined a group of 7,052 men, overlapping with
the Attfield and Costello cohort, who worked in the Vermont granite
industry at any time between January 1, 1947 and December 31, 1998
(Document ID 1486). Like Attfield and Costello, Vacek et al. reported
significantly elevated lung cancer (p < 0.01) (Document ID 1486, p.
315). Most of the lung cancer cases in Vacek et al. (305/356) had
cumulative exposures less than or equal to 4.1 mg/m\3\-yrs (Document ID
1486, p. 316), below the cumulative exposure level of 4.5 mg/m\3\-yrs
associated with 45 years of exposure at the previous PEL and below.
However, unlike Attfield and Costello, Vacek et al. did not find a
statistically significant relationship of increasing lung cancer risk
with increasing silica exposure, leading Vacek et al. to conclude that
increased lung cancer mortality in the cohort may not have been due to
silica exposure (Document ID 1486, p. 312).
The strengths and weaknesses of both studies and the differences
between them that could account for their conflicting conclusions were
discussed in great detail in Section V.F, Comments and Responses
Concerning Lung Cancer Mortality. For the purpose of evaluating the
effects of low concentrations of silica exposure, as well as whether a
threshold exposure exists, OSHA believes the Attfield and Costello
study may merit greater weight than Vacek et al. As discussed in
Section V.F, Comments and Responses Concerning Lung Cancer Mortality,
OSHA believes Attfield and Costello's choice to exclude the highest
exposure group from their analysis likely improved their study's
estimate of the exposure-response relationship at lower exposures; by
making this choice, they limited the influence of highly uncertain
exposure estimates at higher levels and helped to reduce the impact of
the healthy worker survivor effect. The Agency acknowledges the
strengths of the Vacek et al. analysis as well, including longer
follow-up of workers.
In conclusion, OSHA does not find compelling evidence in these
studies of Vermont granite workers of a cumulative exposure threshold
for lung cancer in the exposure range below the previous general
industry PEL. This conclusion is based on the statistically significant
elevations in lung cancer reported in both cohorts described above,
which were composed primarily of workers whose cumulative exposures
were below the level associated with a working lifetime of exposure.
However, OSHA acknowledges that a strong conclusion regarding a
threshold is difficult to draw from these studies, due to the
disagreement between Attfield and Costello and Vacek et al. regarding
the likelihood that excess lung cancer among Vermont granite workers
was due to their silica exposures.
c. Industrial Sand Workers
OSHA's Preliminary QRA (Document ID 1711, pp. 285-287) evaluated a
2001 case-control analysis of industrial sand workers including 2,640
men employed before 1980 for at least three years in one of nine North
American sand-producing plants. One of the sites was a large associated
office complex where workers' exposures were lower than those typically
experienced by production workers (Hughes et al., 2001, Document ID
1060). A later update by McDonald et al. (2005, Document ID 1091)
eliminated one plant, following 2,452 men from the 8 remaining U.S.
plants. Both cohorts overlapped with an earlier industrial sand cohort,
including 4,626 workers at 18 plants, which was included in Steenland
et al.'s pooled analysis (2001a, Document ID 0452). OSHA noted that
these studies (Hughes et al., 2001, Document ID 1060; McDonald et al.,
2005, 1092; Steenland and Sanderson, 2001, 0455) showed similar
exposure-response patterns of increased lung cancer mortality with
increased exposure.
In the Final Peer Review Report, Dr. Ginsberg commented on the
relevance of the industrial sand cohort studies, which included low-
exposed workers with exceptionally well-characterized exposures, for
threshold issues:
With respect to the body of silica epidemiology literature,
perhaps the case with the least amount of measurement error is of US
industrial sand workers wherein many measurements were made with
filter samples and SRD determination of crystalline silica and in
which there was very careful estimation of historical exposure for
both silica and smoking (MacDonald et al. 2005; Steenland and
Sanderson 2001; Hughes et al. 2001) (Document ID 3574, pp. 22-23).
OSHA agrees with Dr. Ginsberg's assessment of these studies and has
found them to be particularly high quality. Thus, the Agency was
especially interested in the studies' findings, which showed that
cancer risk was elevated at cumulative exposure levels below 4.5 mg/
m\3\-yrs, the amount of exposure that would result from a 45-year
working lifetime of exposure at the previous PEL. OSHA believes these
results provide strong evidence against a threshold in cumulative
exposure at any level high enough to impact OSHA's choice of PEL. Dr.
Ginsberg agrees with OSHA's conclusion (Document ID 3574, p. 23).
d. Other Studies
Comments submitted by the ACC briefly mentioned several
epidemiological studies that, they claim, "suggest the existence of a
threshold for any increased risk of silica-related lung cancer,"
including studies by Sogl et al. (2012), Mundt et al. (2011), Pukkala
et al. (2005), Calvert et al. (2003), Checkoway et al. (1997), and
Steenland et al. (2001a). OSHA previously reviewed several of these
studies in the Review of Health Effects Literature and Preliminary
Quantitative Risk Assessment, and the Supplemental Literature Review,
though not with specific attention to their implications for exposure-
response thresholds (Document ID 1711, pp. 139-155; 1711, Attachment 1,
pp. 6-12). The studies cited by ACC are discussed below, with the
exception of Steenland et al. (2001a), which was previously reviewed in
this section.
e. German Porcelain Workers
OSHA reviewed Mundt et al. (2011, Document ID 1478) in its
Supplemental Literature Review (Document ID 1711, Attachment 1, pp. 6-
12). As discussed there, Mundt et al. examined the risks of silicosis
morbidity and lung cancer mortality in a cohort of 17,644 German
porcelain manufacturing workers who had participated in medical
surveillance programs for silicosis between 1985 and 1987. This cohort
was also examined in a previous paper by Birk et al. (2009, Document ID
4002, Attachment 2).
Quantitative exposure estimates for this cohort showed an average
annual exposure of 110 [mu]g/m\3\ for workers hired prior to 1960 and
an average of 30 [mu]g/m\3\ for workers hired after 1960. More than 40
percent of the cohort had cumulative exposures less than 0.5 mg/m\3\-
yrs at the end of follow-up, and nearly 70 percent of the cohort had
average annual exposures less than 50 [mu]g/m\3\ (Mundt et al., 2011,
Document ID 1478, pp. 283-284).
The lung cancer mortality hazard ratios (HRs) associated with
average annual exposure were statistically significant in two of the
four average annual exposure groups: 2.1 (95% CI 1.1-4.0) for average
annual exposure group >50-100 [mu]g/m\3\ and 2.4 (95% CI 1.1-5.2) for
average annual exposure group >150-200 [mu]g/m\3\, controlling for age,
smoking, and duration of employment. In contrast, the HRs for lung
cancer mortality associated with cumulative exposure were not
statistically elevated after controlling for age and smoking.
The authors suggested the possibility of a threshold for lung
cancer mortality. However, no formal threshold analysis for lung cancer
was conducted in this study or in the follow-up threshold analysis
conducted on this population by Morfeld et al. for silicosis (2013,
Document ID 4175). Having reviewed this study carefully, OSHA believes
it is inconclusive on the issue of thresholds due to the elevated risk
of lung cancer seen among low-exposed workers (for example, those with
average exposures of 50-100 [mu]g/m\3\), which is inconsistent with the
ACC's claim that a threshold exists at or above the previous PEL of 100
[mu]g/m\3\, and due to several limitations which may preclude detection
of a relationship between cumulative exposure and lung cancer in this
cohort. As discussed in the Preliminary QRA, these include: (1) A
strong healthy worker effect observed for lung cancer; (2) Mundt et al.
did not follow the typical convention of considering lagged exposures
to account for disease latency; and (3) the relatively young age of
this cohort (median age 56 years old at time of silicosis
determination) (Document ID 1478, p. 288) and limited follow-up period
(average of 19 years per subject) (Birk et al. 2009, Document ID 4002,
Attachment 2, p. 377). Only 9.2 percent of the cohort was deceased by
the end of the follow up period. Mundt et al. (2011) acknowledged this
limitation, stating that the lack of increased risk of lung cancer was
a preliminary finding (Document ID 1478, p. 288).
f. German Uranium Miners
In pre-hearing comments, Dr. Morfeld described a study of 58,677
German uranium miners by Sogl et al. (2012, Document ID 3842; 2307, Attachment 2, p. 11).
Dr. Morfeld noted that the study was based on a detailed exposure
assessment of respirable crystalline silica (RCS) dust. According to
Dr. Morfeld, Sogl et al. "showed that no lung cancer excess risk was
observed at RCS dust exposure levels below 10 mg/m\3\-years"
(Document ID 2307, Attachment 2, p. 11). OSHA's review of this publication
confirmed that the authors reported a spline function with a single
knot at 10 mg/m\3\-yrs, which Morfeld interprets to suggest a threshold
for lung cancer of approximately 250 [mu]g/m\3\ average exposure concentration
for workers exposed over the course of 40 years. However, the authors also noted
that an increase in risk below this level could not be ruled out due to
strong confounding with radon, resulting in possible over-adjustment
(Sogl et al., Document ID 3842, p. 9). That is, because workers with
high exposures to silica would also have had high exposures to the lung
carcinogen radon, the models used by Sogl et al. may have been unable
to detect a relationship between silica and lung cancer in the presence
of radon. As described previously, excess lung cancer has been observed
among workers with lower cumulative exposures than the Sogl et al.
"threshold" in other studies which do not suffer from confounding
from potent lung carcinogens other than silica (for example, industrial
sand workers), and which are, therefore, likely to provide more
reliable evidence on the issue of thresholds. OSHA concludes that the
Sogl et al. study does not provide convincing evidence of a cumulative
exposure threshold for lung cancer.
g. U.S. Diatomaceous Earth Workers
Checkoway et al. (1997) investigated the risk of lung cancer among
diatomaceous earth (DE) workers exposed to respirable cristobalite (a
type of silica found in DE) (Document ID 0326; 1711, pp. 139-143).
Exposure samples were collected primarily at one of the two plants in
the study by plant industrial hygienists over a 40-year timeframe from
1948 to 1988 and used to estimate exposure for each individual in the
cohort (Seixas et al., 1997, Document ID 0431, p. 593). Based on 77
deaths from cancer of the trachea, lung, and bronchus, the standardized
mortality ratios (SMR) were 129 (95% CI 101-161) and 144 (95% CI 114-
180) based on rates for U.S. and local county males, respectively
(Document ID 0326, pp. 683-684). The authors found a positive, but not
monotonic, exposure-response trend for lung cancer. The risk ratios for
lung cancer with increasing quintiles of respirable crystalline silica
exposure were 1.00, 0.96, 0.77, 1.26 and 2.15 with a 15-year exposure
lag. Lung cancer mortality was thus elevated for workers with
cumulative exposures greater than 2.1 mg/m\3\-yrs, but was only
statistically significantly elevated for the highest exposure category
(RR = 2.15; 95% CI 1.08-4.28) (Document ID 0326, p. 686). OSHA notes
that this highest exposure category includes cumulative exposures only
slightly higher than 4.5 mg/m\3\-yrs, the level of cumulative exposure
resulting from a 45-year working lifetime at the previous PEL of 100
[mu]g/m\3\. OSHA does not believe that the appearance of a
statistically significantly elevated lung cancer risk in the highest
category should be interpreted as evidence of an exposure-response
threshold, especially in light of the somewhat elevated risk seen at
lower exposure levels. OSHA believes it is more likely to reflect
limited power to detect excess risk at lower exposure levels, a common
issue in epidemiological studies which was emphasized by peer reviewer
Dr. Andrew Salmon in relation to purported thresholds (Document ID
3574, p. 37).
h. Finnish Nationwide Job Exposure Matrix
OSHA reviewed Pukkala et al. (2005, Document ID 0412) in the Review
of Health Effects Literature and Preliminary Quantitative Risk
Assessment (Document ID 1711, pp. 153-154). As discussed there, Pukkala
et al. (2005) evaluated the occupational silica exposure among all
Finns born between 1906 and 1945 who participated in a national
population census on December 31, 1970. Follow-up of the cohort was
through 1995. Between 1970 and 1995, there were 30,137 cases of
incident lung cancer among men and 3,527 among women. Exposure data
from 1972 to 2000 was collected by the Finnish Institute of
Occupational Health (FIOH). Cumulative exposure categories for
respirable quartz were defined as: <1.0 mg/m\3\-yrs (low), 1.0-9.9 mg/
m\3\-yrs (medium) and >10 mg/m\3\-yrs (high). For men, over 18 percent
of the 30,137 lung cancer cases worked in occupations with potential
exposure to silica dust. The cohort showed statistically significantly
increased lung cancer among men in the lowest occupationally exposed
group (those with less than 1.0 mg/m\3\-yrs cumulative silica
exposure), as well as for men with exposures in the two higher groups
(1.0-9.9 mg/m\3\-yrs and >10 mg/m\3\-yrs). For women, the cohort showed
statistically significantly increased lung cancer among women with at
least 1.0 mg/m\3\-yrs cumulative silica exposure. Given these results,
it is unclear why ACC stated that Pukkula's results suggest that
"excess risk of lung cancer is mainly attributable to...cumulative
exposure exceeding 10 mg/m\3\-years" (Document ID 4209, p. 54).
Indeed, Pukkula's analysis appears to show excess risk of lung cancer
among men with any level of occupational exposure and among women whose
cumulative exposures were quite low (at least equivalent to about 25
[mu]g/m\3\ over 45 years). It does not support the ACC's contention
that lung cancer is seen primarily in workers with exposures greater
than 200 [mu]g/m\3\ (Document ID 4209, p. 54), but rather suggests that
any threshold for lung cancer risk would likely be well below 100
[mu]g/m\3\.
i. U.S. National (27 states) Case-Control Study
As discussed in the Review of Health Effects Literature and
Preliminary Quantitative Risk Assessment (Document ID 1711, pp. 152-
153), Calvert et al. (2003, Document ID 3890) conducted a case-control
study using 4.8 million death certificates from the National
Occupational Mortality Surveillance data set. Death certificates were
collected from 27 states covering the period from 1982 to 1995. Cases
were persons who had died from any of several diseases of interest:
Silicosis, tuberculosis, lung cancer, chronic obstructive pulmonary
disease (COPD), gastrointestinal cancers, autoimmune-related diseases,
or renal disease. Worker exposure to crystalline silica was categorized
as no/low, medium, high, or super-high based on their industry and
occupation. The authors acknowledged the potential for confounding by
higher smoking rates for cases compared to controls, and partially
controlled for this by eliminating white-collar workers from the
control group in the analysis. Following this adjustment, the authors
reported weak, but statistically significantly elevated, lung cancer
mortality odds ratios (OR) of 1.07 (95% CI 1.06-1.09) and 1.08 (95% CI
1.01-1.15) for the high- and super-high exposure groups, respectively
(Calvert et al., 2003, Document ID 3890, p. 126). Upon careful review
of this study, OSHA maintains its position that it should not be used
for quantitative risk analysis (including determination of threshold
effects) because it lacks an exposure characterization based on
sampling. Any determination regarding the existence or location of a
threshold based on Calvert et al. (2003) must, therefore, be considered
highly speculative.
j. Conclusion--Lung Cancer
In conclusion, OSHA has determined that the best available evidence
on the issue of a threshold for silica-related lung cancer does not
support the ACC's contention that an exposure-response threshold, below
which respirable crystalline silica exposure is not expected to cause
cancer, exists at or above the previous general industry PEL of 100
[mu]g/m3. While there are some studies that claim to point
to thresholds above the previous general industry PEL, multiple studies
contradict this evidence, most convincingly through evidence that
cohort members with low cumulative silica exposures suffered from lung
cancer as a result of their exposure. These studies indicate that there
is either no threshold for silica-related lung cancer, or that this
threshold is at such a low level that workers cumulatively exposed at
or below the level allowed by the new PEL of 50 [mu]g/m3
will still be at risk of developing lung cancer. Thus, OSHA does not
agree with commenters who have stated that the previous general
industry PEL is fully protective and that reducing it will yield no
health benefits to silica-exposed workers (e.g., Document ID 4224, p.
2-5; Tr. 3582, pp. 1951-1963).
4. Exposure Uncertainty and Thresholds
In his pre-hearing comments, Dr. Cox stated that the observation of
a positive and monotonic exposure-response relationship in
epidemiological studies "does not constitute valid evidence against
the hypothesis of a threshold," and that OSHA's findings of risk at
exposures below the previous PEL for general industry "could be due
simply to exposure misclassification" in studies of silica-related
health effects in exposed workers (Document ID 2307, Attachment 4, pp.
41-42). His statements closely followed his analyses from a 2011 paper,
in which Cox presented a series of simulation analyses designed to show
that common concerns in epidemiological analyses, such as uncontrolled
confounding, errors in exposure estimates, and model specification
errors, can obscure evidence of an exposure-response threshold, if such
a threshold exists (Document ID 3600, Attachment 7). Dr. Cox concluded
that the currently available epidemiological studies "do not provide
trustworthy information about the presence or absence of thresholds in
exposure-response relations" with respect to an exposure concentration
threshold for lung cancer (Document ID 3600, Attachment 7, p. 1548).
OSHA has reviewed Dr. Cox's comments and testimony, and concludes
that uncertainty about risk due to exposure estimation and confounding
cannot be resolved through the application of the statistical
procedures recommended by Dr. Cox. (Similar comments from Dr. Cox about
alleged biases in the studies relied upon are addressed in the next
section, where OSHA reaches similar conclusions). A reviewer on the
independent peer review panel, Dr. Ginsberg, commented that:
epidemiology studies will always have issues of exposure
misclassification or other types of error that may create
uncertainty when it comes to model specification. However, these
types of error will also bias correlations to the null such that if
they were sufficiently influential to obscure a threshold they may
also substantially weaken regression results and underestimate the
true risk (Document ID 3574, p. 23).
OSHA agrees with Dr. Ginsberg. As discussed in Section V.K,
Comments and Responses Concerning Exposure Estimation Error and
ToxaChemica's Uncertainty Analysis, a "gold standard" exposure sample
is not available for the epidemiological studies in the silica
literature, so it is not possible to determine the direction or
magnitude of the effects of exposure misclassification on OSHA's risk
estimates. The silica literature is not unique in this sense. As stated
by Mr. Robert Park of NIOSH, "modeling exposure uncertainty as
described by Dr. Cox...is infeasible in the vast majority of
retrospective observational studies. Nevertheless, mainstream
scientific thought holds that valid conclusions regarding disease
causality can still be drawn from such studies" (Document ID 4233, p.
32).
For the reasons discussed throughout this analysis of the
scientific literature, OSHA concludes that, even acknowledging a
variety of uncertainties in the studies relied upon, these
uncertainties are, for the most part, typical or inherent in these
types of studies. OSHA therefore finds that the weight of evidence in
these studies, representing the best available evidence on the health
effects of silica exposure, strongly supports the findings of
significant risk from silicosis, NMRD, lung cancer, and renal disease
discussed in this section and in the quantitative risk assessment that
follows in the next section (see Benzene, 448 U.S. at 656 ("OSHA is
not required to support its finding that a significant risk exists with
anything approaching scientific certainty. Although the Agency's
findings must be supported by substantial evidence, 29 U.S.C. 655(f),
6(b)(5) specifically allows the Secretary to regulate on the basis of
the `best available evidence.' ")).
5. Conclusion
In summary, OSHA acknowledges that common issues with
epidemiological studies limit the Agency's ability to determine whether
and where a threshold effect exists for silicosis and lung cancer.
However, as shown in the foregoing discussion, there is evidence in the
epidemiological literature that workers exposed to silica at
concentrations and cumulative levels allowable under the previous
general industry PEL not only develop silicosis, but face a risk of
silicosis high enough to be significant ( >1 per 1,000 exposed
workers). Although the evidence is less clear for lung cancer, studies
nevertheless show excess cases of lung cancer among workers with
cumulative exposures in the range of interest to OSHA. Furthermore, the
statistical model-based approaches proposed in public comments do not
demonstrate the existence or location of a "threshold" level of
silica exposure below which silica exposure is harmless to workers. The
above considerations lead the Agency to conclude that any possible
exposure threshold is likely to be at a low level, such that some
workers will continue to suffer the health effects of silica exposure
even at the new PEL of 50 [mu]g/m3.
There is a great deal of argument and analysis directed at the
question of thresholds in silica exposure-response relationships, but
nothing like a scientific consensus about the appropriate approach to
the question has emerged. If OSHA were to accept the ACC's claim that
exposure to 100 [mu]g/m3 silica is safe for all workers (due
to a threshold at or above an exposure concentration of 100 [mu]g/
m3) and set a PEL at 100 [mu]g/m3 for all
industry sectors, and if that claim is in fact erroneous, the
consequences of that error to silica-exposed workers would be grave. A
large population of workers would remain at significant risk of serious
occupational disease despite feasible options for exposure reduction.
J. Comments and Responses Concerning Biases in Key Studies
OSHA received numerous comments and testimony, particularly from
representatives of the ACC, regarding biases in the data that the
Agency relied upon to conduct its Preliminary Quantitative Risk
Assessment (Preliminary QRA). In this section, OSHA focuses on these
comments regarding biases, particularly with respect to how such biases
may have affected the data and findings from the key peer-reviewed,
published studies that OSHA relied upon in its Preliminary QRA.
The data utilized by OSHA to conduct its Preliminary QRA came from
published studies in the peer-reviewed scientific literature. When
developing health standards, OSHA is not required or expected to
conduct original research or wait for better data or new studies (see
29 U.S.C. 655(b)(5); e.g., United Steelworkers v. Marshall, 647 F.2d
1189, 1266 (D.C. Cir. 1980), cert. denied, 453 U.S. 913 (1981)).
Generally, OSHA bases its determinations of significant risk of
material impairment of health on the cumulative evidence found in a
number of studies, no one of which may be conclusive by itself (see
Public Citizen Health Research Group v. Tyson, 796 F.2d 1479, 1495
(D.C. Cir. 1986) (reviewing courts do not "seek a single dispositive
study that fully supports the Administrator's determination...
Rather, [OSHA's] decision may be fully supportable if it is based...
on the inconclusive but suggestive results of numerous studies.").
OSHA's critical reading and interpretation of scientific studies is
thus appropriately guided by the instructions of the Supreme Court's
Benzene decision that "so long as they are supported by a body of
reputable scientific thought, OSHA is free to use conservative
assumptions in interpreting the data with respect to carcinogens,
risking error on the side of overprotection rather than
underprotection" (Industrial Union Dep't v. American Petroleum Inst.,
448 U.S. 607, 656 (1980)).
Since OSHA is not a research agency, it draws from the best
available existing data in the scientific literature to conduct its
quantitative risk assessments. In most cases, with the exception of
certain risk and uncertainty analyses prepared for OSHA by its
contractor ToxaChemica, OSHA had no involvement in the data generation
or analyses reported in those studies. Thus, in calculating its risk
estimates, OSHA used published regression coefficients or equations
from key peer-reviewed, published studies, but had no control over the
actual published data; nor did the Agency have access to the raw data
from such studies.
As discussed throughout Section V of this preamble, the weight of
scientific opinion indicates that respirable crystalline silica is a
human carcinogen that causes serious, life-threatening disease at the
previously-permitted exposure levels. Under its statutory mandate, the
Agency can and does take into account the potential for statistical and
other biases to skew study results in either direction. However, the
potential biases of concern to the commenters are well known among
epidemiologists. OSHA therefore believes that the scientists who
conduct the studies and subject them to peer review before publication
have taken the potential for biases into account in evaluating the
quality of the data and analysis. As discussed further below, OSHA
heard testimony from David Goldsmith, Ph.D., describing how scientists
use "absolutely the best evidence they can lay their hands on" and
place higher value on studies that are the least confounded by other
factors that, if unaccounted for, could contribute to the effect (e.g.,
lung cancer mortality). (Document ID 3577, Tr. 894-895). Dr. Goldsmith
also testified that many of the assertions of biases put forth in the
rulemaking docket are speculative in nature, with no actual evidence
presented (Document ID 3577, Tr. 901). Thus, while taking seriously the
critiques of the "body of reputable scientific thought" OSHA has used
to support this final silica standard, the Agency finds no reason, as
discussed below, to consider discredited in any material way its key
conclusions regarding causation or significant risk of harm.
In his pre-hearing comments, Dr. Cox, on behalf of the ACC, claimed
that the Preliminary QRA did not address a number of sources of
potential bias:
The Preliminary QRA and the published articles that it relies on
do not correct for well-known biases in modeling statistical
associations between exposures and response. (These include study,
data, and model selection biases; model form specification and model
over-fitting biases; biases due to residual confounding, e.g.,
because age is positively correlated with both cumulative exposure
and risk of lung diseases within each age category (typically 5 or
more years long); and biases due to the effects of errors in
exposure estimates on shifting apparent thresholds to lower
concentrations). As a result, OSHA has not demonstrated that there
is any non-random association between crystalline silica exposure
and adverse health responses (e.g., lung cancer, non-malignant
respiratory disease, renal disease) at exposure levels at or below
100 [[micro]g/m\3\]. The reported findings of such an association,
e.g., based on significantly elevated relative risks or
statistically significant positive regression coefficients for
exposed compared to unexposed workers, are based on unverified
modeling assumptions and on ignoring uncertainty about those
assumptions (Document ID 2307, Attachment 4, pp. 1-2).
These biases, according to Dr. Cox, nearly always result in false
positives, i.e., finding that an exposure-response relationship exists
when there really is no such relationship (Document ID 3576, Tr. 380).
Although his comments appear to be directed to all published, peer-
reviewed studies relied upon by OSHA in estimating risks, Dr. Cox
admitted at the hearing that his statements about false positives were
based on his review of the Preliminary QRA with relation to lung cancer
only, and that he "[didn't] really know" whether the same allegations
of bias he directed at the lung cancer studies are relevant to the
studies of silica's other health risks (Document ID 3576, Tr. 426). In
his comments, Dr. Cox discussed each source of bias in detail; OSHA
will address them in turn. The concerns expressed by commenters,
including Dr. Cox, about exposure uncertainty--another potential source
of bias--are addressed in Section V.K, Comments and Responses
Concerning Exposure Estimation Error and ToxaChemica's Uncertainty
Analysis.
1. Model Specification Bias
Dr. Cox stated that model specification error occurs when the model
form, such as the linear absolute risk model, does not correctly
describe the data (Document ID 2307, Attachment 4, p. 21). Using a
simple linear regression example from Wikipedia, Dr. Cox asserted that
common indicators of goodness-of-fit, including sum of square residuals
and correlation coefficients, can be weak in identifying
"nonlinearities, outliers, influential single observations, and other
violations of modeling assumptions" (Document ID 2307, Attachment 4,
pp. 52-53). He advocated for the use of diagnostic tests to check that
a model is a valid and robust choice, stating, "[u]nfortunately,
OSHA's Preliminary QRA and the underlying papers and reports on which
it relies are not meticulous in reporting the results of such model
diagnostics, as good statistical and epidemiological practice
requires" (Document ID 2307, Attachment 4, p. 21). In his post-hearing
brief, Dr. Cox further described these diagnostic tests to include
plots of residuals, quantification of the effects of removing outliers
and influential observations, and comparisons of alternative model
forms using model cross-validation (Document ID 4027, p. 2). He also
suggested using Bayesian Model Averaging (BMA) or other model ensemble
methods to quantify the effects of model uncertainty (Document ID 4027,
p. 3).
OSHA believes that guidelines for which diagnostic procedures
should be performed, and whether and how they are reported in published
papers, are best determined by the scientific community through the
pre-publication peer review process. Many studies in the silica literature
did not report the results of diagnostic tests. For example, the Vacek et al.
(2009) study of lung cancer and silicosis mortality, which was
submitted to the rulemaking record by the ACC to support its position,
made no mention of the results of model diagnostic tests; rather, the
authors simply stated that models were fitted by maximum likelihood,
with the deviance used to examine model fitting
(Document ID 2307, Attachment 6, pp. 11-12). As illustrated by
this example, authors of epidemiological studies do not normally report
the results of diagnostic tests; nor do such authors publish their raw
data. Therefore, there is no data readily available to OSHA with which
it could perform the diagnostic analysis that Dr. Cox states is
necessary. If the suggestion is that no well-conducted epidemiological
study that failed to report a battery of diagnostic tests or disclose
what they showed should be relied upon for regulatory purposes, there
would be virtually no body of scientific study left for OSHA to
consider, raising the legal standard for issuing toxic substance
standards far above what the Benzene decision requires. Despite this,
OSHA maintains that, given the large number of peer-reviewed studies in
the published scientific literature on crystalline silica, subjecting
each model in each study to diagnostic testing along the lines
advocated by Dr. Cox would not fundamentally change the collective
conclusions when examining the literature base as a whole. Despite Dr.
Cox's criticisms, the scientific literature that OSHA reviewed to draw
its conclusions regarding material impairment of health and used in its
quantitative risk assessment, constitutes the best available evidence
upon which to base this toxic substance standard, in accordance with 29
U.S.C. 655(b) and the Benzene decision and subsequent case law.
Dr. Cox's other suggested approach to addressing model uncertainty,
BMA, can be used to construct a risk estimate based on multiple
exposure-response models. Unlike BMA, standard statistical practice in
the epidemiological literature is to evaluate multiple possible models,
identify the model that best represents the observations in the data
set, and use this model to estimate risk. In some cases, analysts may
report the results of two or more models, along with their respective
fit statistics and other information to aid model selection for risk
assessment and show the sensitivity of the results to modeling choices
(e.g., Rice et al., 2001, Document ID 1118). These standard approaches
were used in each of the studies relied on by OSHA in its Preliminary
QRA.
In contrast, BMA is a probabilistic approach designed to account
for uncertainty inherent in the model selection process. The analyst
begins with a set of possible models (Mi) and assigns each a
prior probability (Pr[Mi]) that reflects the analyst's
initial belief that model Mi represents the true exposure-
response relationship. Next, a data set is used to update the
probabilities assigned to the models, generating the posterior
probability for each model. Finally, the models are used in combination
to derive a risk estimate that is a composite of the risk estimates
from each model, weighted by each model's posterior probability (see
Viallefont et al., 2001, Document ID 3600, Attachment 34, pp. 3216-
3217). Thus, BMA combines multiple models, and uses quantitative
weights accounting for the analyst's belief about the plausibility of
each model, to generate a single weighted-average risk estimate. These
aspects of BMA are regarded by some analysts as improvements to the
standard approaches to exposure-response modeling.
However, Kyle Steenland, Ph.D., Professor, Department of
Environmental Health, Rollins School of Public Health, Emory
University, the principal author of a pooled study that OSHA heavily
relied upon, noted that BMA is not a standard method for risk
assessment. "[Bayesian] model averaging, to my knowledge, has not been
used in risk assessment ever. And so, sure, you could try that. You
could try a million things. But I think OSHA has correctly used
standard methods to do their risk assessment and [BMA] is not one of
those standard methods" (Document ID 3580, Tr. 1259).
Indeed, BMA is a relatively new method in risk analysis. Because of
its novelty, best practices for important steps in BMA, such as
defining the class of models to include in the analysis, and choosing
prior probabilities, have not been developed. Until best practices for
BMA are established, it would be difficult for OSHA to conduct and
properly evaluate the quality of BMA analyses. Evaluation of the
quality of available analyses is a key step in the Agency's
identification of the best available evidence on which to base its
significant risk determination and benefits analysis.
OSHA also emphasizes that, as noted by Dr. Steenland,
scientifically accepted and standard practices were used to estimate
risk from occupational exposure to crystalline silica (Document ID
3580, Tr. 1259). Thus OSHA has decided that it is not necessary to use
BMA in its QRA, and that the standard statistical methods used in the
studies it relies upon to estimate risk are appropriate as a basis for
risk estimation. OSHA notes that it is possible to incorporate risk
estimates based on more than one model in its risk assessment by
presenting ranges of risk, a strategy often used by OSHA when the best
available evidence includes more than one model, analytical approach,
or data set. In its Preliminary QRA, OSHA presented ranges of risks for
silica-related lung cancer and silicosis based on different data sets
and models, thus further lessening the utility of using more complex
techniques such as BMA. OSHA continued this practice in its final risk
assessment, presented in Section VI, Final Quantitative Risk Assessment
and Significance of Risk.
2. Study Selection Bias
Another bias described by Dr. Cox is study selection bias, which he
stated occurs when only studies that support a positive exposure-
response relationship are included in the risk assessment, and when
criteria for the inclusion and exclusion of studies are not clearly
specified in advance (Document ID 2307, Attachment 4, pp. 22-23). Dr.
Cox noted the criteria used by OSHA to select studies, as described in
the Supplemental Literature Review of Epidemiological Studies on Lung
Cancer Associated with Exposure to Respirable Crystalline Silica
(Supplemental Literature Review) (Document ID 1711, Attachment 1, p.
29). Dr. Cox, however, claimed that OSHA did not apply these criteria
consistently, in that there may still be exposure misclassification or
confounding present in the studies OSHA relied upon to estimate the
risk of the health effects evaluated by the Agency (Document ID 2307,
Attachment 4, pp. 24-25). Similarly, the American Foundry Society
(AFS), in its post-hearing brief, asserted that, "No formal process is
described for search criteria or study selection" and that OSHA's
approach of identifying studies based upon the IARC (1997) and NIOSH
(2002) evaluations of the literature "is a haphazard approach that is
not reproducible and is subject to bias. Moreover it appears to rely
primarily on information that is more than 10 years old" (Document ID
4229, p. 4).
OSHA disagrees with the arguments presented by Dr. Cox and the AFS,
as did some commenters. The American Public Health Association (APHA),
in its post-hearing brief, expressed strong support for OSHA's study
selection methods. Dr. Georges Benjamin, Executive Director, wrote,
"APHA recognizes that OSHA has thoroughly reviewed and evaluated the
peer-reviewed literature on the health effects associated with exposure
to respirable crystalline silica. OSHA's quantitative risk assessment is sound.
The agency has relied on the best available evidence and acted appropriately
in giving greater weight to those studies with the most robust designs and
statistical analyses" (Document ID 2178, Attachment 1, p. 1). Similarly,
Dr. Steenland testified that "OSHA has done a very capable job in
conducting the summary of the literature" (Document ID 3580, Tr.
1235).
In response to the criticisms by Dr. Cox and the AFS, OSHA notes
that the silica literature was exhaustively reviewed by IARC in 1997
and NIOSH in 2002 (Document ID 1062; 1110). As a result, there was no
need for OSHA to initiate a new review of the historical literature.
Instead, OSHA used the IARC and NIOSH reviews as a starting point for
its own review. As recognized by the APHA, OSHA evaluated and
summarized many of the studies referenced in the IARC and NIOSH
reviews, and then performed literature searches to identify new studies
published since the time of the IARC and NIOSH reviews. OSHA clearly
described this process in its Review of Health Effects Literature:
"OSHA has included in its review all published studies that the Agency
deems relevant to assessing the hazards associated with exposure to
respirable crystalline silica. These studies were identified from
numerous scientific reviews that have been published previously such as
the IARC (1997) and NIOSH (2002) evaluations of the scientific
literature as well as from literature searches and contact with experts
and stakeholders" (Document ID 1711, p. 8). For its Preliminary QRA,
OSHA relied heavily on the IARC pooled exposure-response analyses and
risk assessment for lung cancer in 10 cohorts of silica-exposed workers
(Steenland et al., 2001a, Document ID 0452) and multi-center study of
silicosis mortality (Mannetje et al., 2002b, Document ID 1089). As
stated in the Review of Health Effects Literature, these two studies
"relied on all available cohort data from previously published
epidemiological studies for which there were adequate quantitative data
on worker exposures to crystalline silica to derive pooled estimates of
disease risk" (Document ID 1711, p. 267).
In addition to relying on these two pooled IARC multi-center
studies, OSHA also identified single cohort studies with sufficient
quantitative information on exposures and disease incidence and
mortality rates. As pointed out by Dr. Cox, OSHA described the criteria
used for selection of the single cohort studies of lung cancer
mortality:
OSHA gave studies greater weight and consideration if they (1)
included a robust number of workers; (2) had adequate length of
follow-up; (3) had sufficient power to detect modest increases in
lung cancer incidence and mortality; (4) used quantitative exposure
data of sufficient quality to avoid exposure misclassification; (5)
evaluated exposure-response relationships between exposure to silica
and lung cancer; and (6) considered confounding factors including
smoking and exposure to other carcinogens (Document ID 1711,
Attachment 1, p. 29).
Using these criteria, OSHA identified four single-cohort studies of
lung cancer mortality that were suitable for quantitative risk
assessment; two of these cohorts (Attfield and Costello, 2004, Document
ID 0285; Rice et al., 2001, 1118) were included among the 10 used in
the IARC multi-center study and two appeared later (Hughes et al.,
2001, Document ID 1060; Miller and MacCalman, 2009, 1306) (Document ID
1711, p. 267). For NMRD mortality, in addition to the IARC multi-center
study (Mannetje et al., 2002b, Document ID 1089), OSHA relied on Park
et al. (2002) (Document ID 0405), who presented an exposure-response
analysis of NMRD mortality (including silicosis and other chronic
obstructive pulmonary diseases) among diatomaceous earth workers
(Document ID 1711, p. 267). For silicosis morbidity, several single-
cohort studies with exposure-response analyses were selected (Chen et
al., 2005, Document ID 0985; Hnizdo and Sluis-Cremer, 1993, 1052;
Steenland and Brown, 1995b, 0451; Miller et al., 1998, 0374; Buchanan
et al., 2003, 0306) (Document ID 1711, p. 267).
With respect to Dr. Cox's claim that OSHA did not apply its
criteria consistently, on the basis that there may still be exposure
misclassification or confounding present, OSHA notes that it selected
studies that best addressed the criteria; OSHA did not state that it
only selected studies that addressed all of the criteria. Given the
fact that some of the epidemiological studies concern exposures of
worker populations dating back to the 1930's, there is always some
potential for exposure misclassification or the absence of information
on smoking. When this was the case, OSHA discussed these limitations in
its Review of Health Effects Literature and Preliminary QRA (Document
ID 1711). For example, OSHA discussed the lack of smoking information
for cases and controls in the Steenland et al. (2001a, Document ID
0452) pooled lung cancer analysis (Document ID 1711, pp. 150-151).
With respect to the AFS's claim that OSHA relied on studies that
were more than 10 years old, OSHA again notes that it reviewed, in its
Review of Health Effects Literature and its Supplemental Literature
Review, the studies in the silica literature and selected the ones that
best met the criteria described above (Document ID 1711; 1711,
Attachment 1). It would be improper to only select the most recent
studies, particularly if the older studies are of higher quality based
on the criteria. Furthermore, the studies OSHA relied upon in its
Preliminary QRA were published between 1993 and 2009; the claim that
OSHA primarily relied on older studies is thus misleading, when the
studies were of relatively recent vintage and determined to be of high
quality based on the criteria described above. The AFS also suggested
that OSHA examine several additional foundry studies of lung cancer
(Document ID 2379, Attachment 2, p. 24); OSHA retrieved all of these
suggested studies, added them to the rulemaking docket following the
informal public hearings, and discusses them in Section V.F, Comments
and Responses Concerning Lung Cancer Mortality.
3. Data Selection Bias
A related bias presented by Dr. Cox is data selection bias, which
he stated occurs when only a subset of the data is used in the analysis
"to guarantee a finding of a positive" exposure-response relationship
(Document ID 2307, Attachment 4, p. 26). He provided an example, the
Attfield and Costello (2004, Document ID 0285) study of lung cancer
mortality, which excluded data as a result of attenuation observed in
the highest exposure group (Document ID 2307, Attachment 4, pp. 26-27).
Attenuation of response means the exposure-response relationship
leveled off or decreased in the highest exposure group. Referring to
another study of the same cohort, Vacek et al. (2009, Document ID 2307,
Attachment 6; 2011, 1486), Dr. Cox stated, "OSHA endorses the Attfield
and Costello findings, based on dropping cases that do not support the
hypothesis of an ER [exposure-response] relation for lung cancer, while
rejecting the Vacek et al. study that included more complete data (that
was not subjected to post hoc subset selection) but that did not find a
significant ER [exposure-response] relation"
(Document ID 2307, Attachment 4, pp. 26-27).
OSHA believes there are very valid reasons for the observance of
attenuation of response in the highest exposure group that would
justify the exclusion of data in Attfield and Costello (2004, Document
ID 0285) and other studies. This issue was discussed by Gary Ginsberg,
Ph.D., an OSHA peer reviewer from the Connecticut Department of Public
Health, in his post-hearing comments. Dr. Ginsberg noted that several
epidemiological studies have found an attenuation of response at higher
doses, with possible explanations including: (1) Measurement error,
which arises from the fact that the highest doses are associated with
the oldest datasets, which are most prone to measurement error; (2)
"intercurrent causes of mortality" from high dose exposures that
result in death to the subject prior to the completion of the long
latency period for cancer; and (3) the healthy worker survivor effect,
which occurs when workers with ill health leave the workforce early
(Document ID 3574, p. 24). As discussed in Section V.F, Comments and
Responses Concerning Lung Cancer Mortality, OSHA disagrees strongly
with Dr. Cox's assertion that data were excluded to ensure a positive
exposure-response relationship (Document ID 2307, Attachment 4, p. 26).
In addition, as detailed in Section VI, Final Quantitative Risk
Assessment and Significance of Risk, OSHA calculated quantitative risk
estimates for lung cancer mortality from several other studies that did
not rely on a subset of the data (Rice et al., 2001, Document ID 1118;
Hughes et al., 2001, 1060; Miller and MacCalman, 2009, 1306;
ToxaChemica, 2004, 0469; 1711, p. 351). These studies also demonstrated
positive exposure-response relationships.
4. Model Selection Bias
Another selection bias presented by Dr. Cox is model selection
bias, which he said occurs when many different combinations of models,
including alternative exposure metrics, different lags, alternative
model forms, and different subsets of data, are tried with respect to
their "ability to produce `significant'-looking regression
coefficients" (Document ID 2307, Attachment 4, p. 27). This is another
aspect of model specification error, as discussed above under model
averaging. Dr. Cox wrote:
This type of multiple testing of hypotheses and multiple
comparisons of alternative approaches, followed by selection of a
final choice based [on] the outcomes of these multiple attempts,
completely invalidates the claimed significance levels and
confidence intervals reported for the final ER [exposure-response]
associations. Trying in multiple ways to find a positive
association, and then selecting a combination that succeeds in doing
so and reporting it as `significant,' while leaving the nominal
(reported) statistical significance level of the final selection
unchanged (typically at p=0.05), is a well-known recipe for
producing false-positive associations (Document ID 2307, Attachment
4, p. 28).
Dr. Cox further stated that unless methods of significance level
reduction (i.e., reducing the nominal statistical significance level of
the final selection) are used, the study is biased towards false-
positive results (Document ID 2307, Attachment 4, p. 28).
During the informal public hearings, counsel for the ACC asked Mr.
Park of NIOSH's Risk Evaluation Branch about this issue, i.e., trying a
number of modeling choices, including exposure metrics, log-
transformations, lag periods, and model subsets (Document ID 3579, Tr.
149-150). Mr. Park's reply supports the use of multiple modeling
choices in the risk assessment as a form of sensitivity analysis:
Investigations like this look at a number of options. They come
into the study not totally na[iuml]ve. They, in fact, have some very
strong preference even before looking at the data based on prior
knowledge. So cumulative exposure, for example, is a generally very
high confidence choice in a metric. Trying different lags is
interesting. It helps validate the study because you know what it
ought to look like sort of. And in many cases, the choice does not
make a lot of difference. So it's kind of a robust test, and
similarly, the choice of the final model is not just coming in
na[iuml]ve. A linear exposure response has a lot of biological
support in many different contexts, but it could be not the best
choice (Document ID 3579, Tr. 150-151).
ACC counsel further asked, "And does one at the end of this
process, though, make any adjustment in what you consider to be the
statistically significant relationship in light of the fact that you've
looked at so many different models and arrangements?" (Document ID
3579, Tr. 151-152). Mr. Park replied, "No, I don't think that's a
legitimate application of a multiple comparison question" (Document ID
3579, Tr. 152). OSHA agrees with Mr. Park that significance level
reduction is not appropriate in the context of testing model forms for
risk estimation, and notes that, in the Agency's experience,
significance level reduction is not typically performed in the
occupational epidemiology literature. In addition, OSHA notes that, in
many of the key studies relied upon by the Agency to estimate
quantitative risks, the authors presented the results of multiple
models that showed statistically significant exposure-response
relationships. For example, Rice et al. (2001) presented the results of
six model forms, with all except one being significant (Table 1,
Document ID 1118, p. 41). Attfield and Costello (2004) presented the
results of their model with and without a 15-year lag and log
transformation, with many results being significant (Table VII,
Document ID 0285, p. 135). Thus, OSHA concludes that model selection
bias is not a problem in its quantitative risk assessment.
Furthermore, OSHA disagrees with Dr. Cox's assertion that modeling
choices are used to "produce `significant'-looking regression
coefficients" (Document ID 2307, Attachment 4, p. 27). OSHA believes
that the investigators of the studies it relied upon in its
Preliminary, and now final, QRA made knowledgeable modeling choices
based upon the exposure distribution and health outcome being examined.
For example, in long-term cohort studies, such as those of lung cancer
mortality relied upon by OSHA, most authors relied upon cumulative
exposure (mg/m\3\-yrs or mg/m\3\-days), i.e., the concentration of
crystalline silica exposure (mg/m\3\) multiplied by the duration of
exposure (years or days), as an exposure metric. Consistent with
standard statistical techniques used in epidemiology, the cumulative
exposure metric may then be log-transformed to account for an
asymmetric distribution with a long right tail, or attenuation, and the
metric may be lagged by several years to account for the long latency
period between the exposure and the development of lung cancer. When
investigators use subsets of the data, they typically explain the
rationale and the effect of using the subset in the analysis. These
choices all have important justifications and are not used purely to
produce the authors' desired results, as Dr. Cox suggested (Document ID
2307, Attachment 4, p. 27).
5. Model Uncertainty Bias
Related to model selection bias is Dr. Cox's assertion of model
uncertainty bias, which he said occurs when many different models are
examined and then one is selected on which to base risk calculations;
this approach "treats the finally selected model as if it were known
to be correct, for purposes of calculating confidence intervals and
significance levels. But, in reality, there remains great uncertainty
about what the true causal relation between exposure and response looks
like (if there is one)" (Document ID 2307, Attachment 4, pp. 28-29).
He further stated that ignoring this bias leads to artificially narrow
confidence intervals, which bias conclusions towards false-positive findings.
He then cited a paper (Piegorsch, 2013, included in Document ID 3600)
describing statistical methods for overcoming this bias by "including
multiple possible models in the calculation of results"
(Document ID 2307, Attachment 4, p. 29). OSHA concludes this bias is
really an extension of model specification error and model selection bias,
previously discussed, and maintains that best practices for model averaging
have not yet been established, making it difficult for the Agency to
conduct and properly evaluate the quality of BMA analyses.
6. Model Over-Fitting Bias
Next, Dr. Cox discussed model over-fitting bias, which he said
occurs when the same data set is used both to fit a model and to assess
the fit; this "leads to biased results: Estimated confidence intervals
are too narrow (and hence lower confidence limits on estimated ER
[exposure-response] slopes are too high); estimated significance levels
are too small (i.e., significance is exaggerated); and estimated
measures of goodness-of-fit overstate how well the model fits the
data" (Document ID 2307, Attachment 4, p. 39). He suggested using
appropriate statistical methods, such as "k-fold cross-validation,"
to overcome the bias (Document ID 2307, Attachment 4, p. 39).
OSHA does not agree that using the same data set to fit and assess
a model necessarily results in an over-fitting bias. The Agency
understands over-fitting to occur when a model is excessively complex
relative to the amount of data available such that there are a large
number of predictors relative to the total number of observations
available. For survival models, it is the number of events, i.e.,
deaths, that is relevant, rather than the size of the entire sample
(Babyak, 2004, included in Document ID 3600, p. 415). If the number of
predictors (e.g., exposure, age, gender) is small relative to the
number of events, then there should be no bias from over-fitting. In an
article cited and submitted to the rulemaking docket by Dr. Cox, Babyak
(2004) discussed a simulation study that found, for survival models, an
unacceptable bias when there were fewer than 10 to 15 events per
independent predictor (included in Document ID 3600, p. 415). In the
studies that OSHA relied on in its Preliminary QRA, there were
generally a large number of events relative to the small number of
predictors. For example, in the Miller and MacCalman (2009) study of
British coal miners, in the lung cancer model using both quartz and
coal dust exposures, there was a large number of events (973 lung
cancer deaths) relative to the few predictors in the model (quartz
exposure, coal dust exposure, cohort entry date, smoking habits at
entry, cohort effects, and differences in regional background cause-
specific rates) (Document ID 1306, pp. 6, 9). Thus, OSHA does not agree
the studies it relied upon were substantially influenced by over-
fitting bias. OSHA also notes that k-fold cross-validation, as
recommended by Dr. Cox, is not typically reported in published
occupational epidemiology studies, and that the studies the Agency
relied upon in the Preliminary QRA were published in peer-reviewed
journals and used statistical techniques typically used in the field of
occupational epidemiology and epidemiology generally.
7. Residual Confounding Bias
Dr. Cox also asserted a bias due to residual confounding by age.
Bias due to confounding occurs in an epidemiological study, in very
general terms, when the effect of an exposure is mixed together with
the effect of another variable (e.g., age) not accounted for in the
analysis. Residual confounding occurs when additional confounding
factors are not considered, control of confounding is not precise
enough (e.g., controlling for age by using groups with age spans that
are too wide), or subjects are misclassified with respect to
confounders (Document ID 3607, p. 1). Dr. Cox stated in his comments
that:
key studies relied on by OSHA, such as Park et al. (2002), do not
correct for biases in reported ER [exposure-response] relations due
to residual confounding by age (within age categories), i.e., the
fact that older workers may tend to have both higher lung cancer
risks and higher values of occupational exposure metrics, even if
one does not cause the other. This can induce a non-causal
association between the occupational exposure metrics and the risk
of cancer (Document ID 2307, Attachment 4, p. 29).
The Park et al. (2002) study of non-malignant respiratory disease
mortality, which Dr. Cox cited as not considering residual confounding
by age, used 13 five-year age groups (< 25, 25-29, 30-34, etc.) in the
models (Document ID 0405, p. 37). Regarding this issue in the Park et
al. (2002) study, in its post-hearing comments, NIOSH stated:
This is a non-issue. The five-year categorization was used only
for deriving the expected numbers of cases as an offset in the
Poisson analysis using national rates which typically are classified
in five-year intervals (on age and chronological time). The
cumulative exposures were calculated with a 10-day resolution over
follow-up and then averaged across observation time within 50
cumulative exposure levels cross-classified with the five-year age-
chronological time cells of the classification table. There would be
virtually no confounding between age and exposure [using this
approach] (Document ID 4233, p. 33).
OSHA agrees with this assessment, noting that it appears that age
groups were adequately constructed to prevent residual confounding.
OSHA thus rejects this assertion of residual confounding by age in the
Park et al. (2002) study.
8. Summary of Biases
In summary, OSHA received comments and heard testimony on potential
biases in the studies upon which it relied for its QRA. The ACC's Dr.
Cox, in particular, posited a long list of biases, including model form
specification bias, study selection bias, data selection bias, model
selection bias, model over-fitting bias, model uncertainty bias,
residual confounding bias, and bias as a result of exposure measurement
error. OSHA, in this section, has specifically addressed each of these
types of bias (except for bias due to exposure estimation error, which
is addressed in Section V.K, Comments and Responses Concerning Exposure
Estimation Error and ToxaChemica's Uncertainty Analysis).
In addition, OSHA heard testimony that countered the claims of
biases and their potential to cause false positive results. When asked
about the biases alleged by Dr. Cox and Dr. Long, Dr. Goldsmith
testified, "All of these other things, it seems to me, are smoke
screens for an inability to want to try and see what the body of
evidence really shows" (Document ID 3577, Tr. 895-896). Later in his
testimony, when asked about exposure misclassification, Dr. Goldsmith
similarly noted, "[a]nd for a lot of the arguments that are being put
forward by industry, they are speculating that there is the potential
for these biases, but they haven't gotten, [from] my perspective, the
actual evidence that this is the case" (Document ID 3577, Tr. 901).
Similarly, OSHA has reviewed the record evidence extensively and is not
aware of any specific, non-speculative evidence of biases in the
studies that it relied upon.
There also is a question of the extent to which Dr. Cox actually
reviewed all of the studies that he asserted to be biased. Upon
questioning from Anne Ryder, Attorney in the Office of the Solicitor,
Department of Labor, Dr. Cox admitted that he had not examined the
issue of silica and silicosis, and that his statements about false
positives were based on his review of the Preliminary QRA with relation
to lung cancer only:
MS. RYDER:...You talked a little bit earlier about the false
positives that are...present with a lot of the studies on lung
cancer. And, but I believe, in your comment you didn't say that
there are any of those same false positives with studies dealing
with silicosis and silica exposure. Is that correct?
DR. COX: I don't think I opined on that. So--and I really
haven't looked carefully at the question. I do take it as given that
silica at sufficiently high and prolonged exposures causes
silicosis. I've not really examined that literature.
MS. RYDER: So you don't think that those studies have the same
issues that some of the lung cancer studies have?
DR. COX: I don't really know (Document ID 3576, Tr. 426).
Dr. Cox further testified, regarding the likelihood that the
conclusions of the Preliminary QRA for silicosis are correct, "I
expect that the evidence is much stronger for silica and silicosis. But
I haven't reviewed it, so I can't testify to it" (Document ID 3576,
Tr. 427).
OSHA believes this testimony to be inconsistent with some of the
broad conclusions in Dr. Cox's pre-hearing written submission to the
rulemaking record, in which he claimed that all adverse outcomes in the
Preliminary QRA may have been affected by false positives. Dr. Cox
concluded in this submission that:
These multiple uncontrolled sources of false-positive bias can
generate findings of statistically "significant" positive ER
[exposure-response] associations even in random data, or in data for
which there is no true causal relation between exposure and risk of
adverse health responses. Because OSHA's Preliminary QRA and the
studies on which it relies did not apply appropriate technical
methods (which are readily available, as discussed in the
references) to diagnose, avoid, or correct for these sources of
false-positive conclusions, the reported findings of
"significantly" positive ER [exposure-response] associations
between crystalline silica exposures at and below the current PEL
and adverse outcomes (lung cancer, non-malignant lung disease, renal
disease) are not different from what might be expected in the
absence of any true ER [exposure-response] relations. They therefore
provide no evidence for (or against) the hypothesis that a true ER
[exposure-response] relation exists. Thus, OSHA has not established
that a non-random association exists between crystalline silica
exposures at or below the current PEL and the adverse health effects
on which it bases its determination of significant risk and
calculates supposed health effect benefits (Document ID 2307,
Attachment 4, pp. 29-30).
OSHA notes that "non-malignant lung disease" includes silicosis,
studies of which Dr. Cox subsequently testified that he did not
examine.
In conclusion, the studies relied upon by OSHA for its risk
assessment were peer-reviewed and used methods for epidemiology and
risk assessment that are commonly used. Dr. Cox provided no study-
specific evidence (e.g., data re-analysis) to support his comments that
the studies OSHA relied upon were adversely affected by numerous
different types of bias. As described above, OSHA recognizes that there
are uncertainties associated with the results of the studies relied on
for its risk assessment, as is typically the case for epidemiological
studies such as these. Nevertheless, as previously stated, OSHA
maintains that it has used a body of peer-reviewed scientific
literature that, as a whole, constitutes the best available evidence of
the relationship between respirable crystalline silica exposure and
silicosis, lung cancer, and the other health effects studied by the
Agency in promulgating this final rule.
K. Comments and Responses Concerning Exposure Estimation Error and
ToxaChemica's Uncertainty Analysis
Exposure estimation error, a typical feature of epidemiological
studies, occurs when the authors of an exposure-response study
construct estimates of the study subjects' exposures using uncertain or
incomplete exposure data. Prior to the publication of its Preliminary
Quantitative Risk Assessment (Preliminary QRA), the Agency commissioned
an uncertainty analysis conducted by Drs. Kyle Steenland and Scott
Bartell, through its contractor, ToxaChemica, Inc., to address exposure
estimation error in OSHA's risk assessment, and incorporated the
results into the Preliminary QRA. After reviewing comments submitted to
the record on the topic of exposure estimation error, OSHA maintains
that it has relied upon the best available evidence by: (1) Using high-
quality exposure-response studies and modeling approaches; (2)
performing an uncertainty analysis of the effect of exposure estimation
error on the risk assessment results; and (3) further submitting that
analysis to peer review. OSHA concludes from its uncertainty analysis
that exposure estimation error did not substantially affect the results
in the majority of studies examined (Document ID 1711, pp. 299-314).
Furthermore, having carefully considered the public comments
criticizing ToxaChemica's uncertainty analysis, OSHA has concluded that
it was not necessary to conduct additional analyses to modify the
approach adopted by Drs. Steenland and Bartell in the uncertainty
analysis. Nor was it necessary to incorporate additional sources of
uncertainty in the analysis. Also, given the evidence in the rulemaking
record that these estimation errors bias results towards
underestimating rather than overestimating the risks from exposure in
many circumstances, it is very unlikely that regression coefficients
and risk estimates from all of the different studies relied on in the
Preliminary QRA were biased upward. Accordingly, OSHA remains convinced
that the conclusions of the Agency's risk assessment are correct and
largely unaffected by potential error in exposure measurement.
OSHA received significant comments on the topic of exposure
estimation error in the studies it relied on in its Review of Health
Effects Literature and Preliminary QRA (Document ID 1711). A number of
commenters discussed the importance of accounting for exposure
estimation error. Dr. Cox, representing the ACC, described exposure
estimation error as perhaps the "most quantitatively important" issue
in the studies OSHA relied upon (Document ID 2307, Attachment 4, p.
40). Similarly, Christopher M. Long, Sc.D., Principal Scientist at
Gradient, representing the U.S. Chamber of Commerce (Chamber),
testified that exposure measurement error is a "common source of
uncertainty in most occupational and environmental epidemiologic
studies" (Document ID 3576, Tr. 298). According to Dr. Long, this type
of error can lead to inaccurate risk estimates by creating error in the
exposure-response curve derived from a data set and obscuring the
presence of a threshold (Document ID 3576, Tr. 300; see Section V.I,
Comments and Responses Concerning Thresholds for Silica-Related
Diseases, for further discussion on thresholds). Dr. Long further
stated that exposure measurement error can lead to over- or under-
estimation of risk: "the impact of exposure measurement error...
can bias either high or low. It can bias towards the null. It can be a
source of positive bias." (Document ID 3576, Tr. 358-359). A bias to
the null in an exposure-response model used in a quantitative risk
assessment is an underestimation of the relationship between exposure
level and the rate of the disease or health effect of interest, and
results in underestimation of risk.
OSHA agrees with the assessments of the ACC and the Chamber with
respect to the importance of exposure measurement error. Indeed, OSHA
peer reviewer, Dr. Gary Ginsberg, in his peer review comments
(Document ID 3574, p. 21), and OSHA's risk assessment contractor,
Dr. Steenland, in his hearing testimony (Document ID 3580, Tr. 1266-1267),
noted the potential for exposure measurement error to bias exposure-response
coefficients towards the null. Dr. Steenland explained: "misclassification
I would say in general tends to bias things to the null. It's harder to see
positive exposure-response trends in the face of misclassification. It depends
partly on the type of error....But, on the whole, I would say that
exposure measurement tends to bias things down rather than up"
(Document ID 3580, Tr. 1266-1267). Fewell et al., the authors of a
paper on residual confounding submitted by the ACC, wrote, "It is well
recognized that under certain conditions, nondifferential measurement
error in the exposure variable produces bias towards the null" (2007,
Document ID 3606, p. 646).
Several commenters representing the ACC challenged the methods used
in ToxaChemica's uncertainty analysis on the grounds that the analysis
failed to adequately address exposure estimation error. In spite of
their criticisms, critics were unable to supply better studies than
those OSHA used. Indeed, when asked during the hearing, Dr. Long was
unable to identify any studies that the Agency could use that
acceptably account for the impact of exposure measurement error on
exposure-response associations for crystalline silica (Document ID
3576, Tr. 356-357), and none was supplied following the hearings.
Taking into account the record evidence discussed above, OSHA
concludes that it is possible for exposure measurement error to lead to
either over- or under-estimation of risk and that this issue of
exposure measurement error is not specific to the silica literature. It
further concludes that industry representatives could not identify, and
failed to submit, any published epidemiological studies of occupational
disease that corrected for such bias to their satisfaction (Document ID
3576, Tr. 356-357).
Nevertheless, because OSHA agreed that an analysis of exposure
estimation error as a source of uncertainty is important, it
commissioned the uncertainty analysis discussed above to explore the
potential effects of exposure measurement error on the conclusions of
OSHA's risk assessment (Document ID 0469). The analysis examined the
potential effects of exposure measurement error on the mortality risk
estimates derived from the pooled studies of lung cancer (Steenland et
al. 2001a, Document ID 0452) and silicosis (Mannetje 2002b, Document ID
1089). This included the effects of estimation error on the detection
and location of a possible threshold effect in exposure-response
models.
The uncertainty analysis OSHA commissioned from Drs. Steenland and
Bartell (2004, Document ID 0469) addressed possible error in silica
exposure estimates from: (1) Random error in individual workers'
exposure estimates and (2) error in the conversion of dust measurements
(typically particle count concentrations) to gravimetric respirable
silica concentrations, which could have affected estimates of average
exposure for job categories in the job-exposure matrices used to
estimate workers' silica exposure. To address possible error in
individual workers' exposure estimates, the analysts performed a Monte
Carlo analysis, a type of simulation analysis which varies the values
of an uncertain input to an analysis (in this case, exposure estimates)
to explore the effects of different values on the outcome of the
analysis. The Monte Carlo analysis sampled new values for workers' job-
specific exposure levels from distributions they believed characterized
the exposures of individual workers in each job. In each run of the
Monte Carlo analysis, the sampled exposure values were used to
calculate new estimates of each worker's cumulative exposures, and the
resulting set was used to fit a new exposure-response model.
Similarly, the analysts performed a Monte Carlo analysis to address
the issue of uncertainty in conversion from dust to respirable silica
exposure, sampling new conversion factors from a normal distribution
with means equal to the original conversion factor, calculating new
estimates of workers' cumulative exposures, and re-fitting the
exposure-response model for each Monte Carlo run. To examine the
sensitivity of the model to the joint effects of both error types, the
analysts ran 50 Monte Carlo simulations using the sampling procedure
for both individual exposures and job-specific conversion factors. They
also examined the effects of systematic bias in conversion factors,
considering that these may have been consistently under-estimated or
over-estimated for any given cohort. They addressed possible biases in
either direction, conducting 20 simulations where the true silica
content was assumed to be either half or double the estimated silica
content of measured exposures.
The results of their analysis indicated that the conclusions of the
pooled lung cancer study conducted previously by Steenland et al.
(Document ID 0452) and included in OSHA's Preliminary QRA were unlikely
to be affected by the types of exposure estimation error examined by
Drs. Steenland and Bartell, whose analysis of the underlying data was
itself reviewed by OSHA's peer review panel. As explained below, after
reviewing comments critical of the uncertainty analysis, OSHA reaffirms
its conclusion that workers exposed to silica at the previous PELs are
at significant risk of disease from their exposure.
Drs. Long and Valberg, representing the Chamber, commented that
Drs. Steenland and Bartell's uncertainty analysis did not address all
potential sources of error and variability in exposure measurement,
such as possible instrument error; possible sampling error; random
variability in exposure levels; variability in exposure levels
resulting from changes in worker job functions during work shifts,
production process changes, or control system changes; variability in
sampler type used; variability in laboratory methods for determining
sampling results and laboratory errors; variability in duration of
exposure sampling; variability in sampling locations; variability in
reasons for sample data collection (e.g., compliance sampling, periodic
sampling, random survey sampling); variability in type of samples
collected (e.g., bulk samples, respirable dust samples); variation
among workers and over time in the size distribution, surface area,
recency of fracture, and other characteristics of the particles
inhaled; and extrapolation of exposure sampling data to time periods
for which sampling data are not available (Document ID 2330, pp. 4-5).
OSHA notes that these sources of potential error and variability are
common in occupational exposure estimation, and are sources of
uncertainty in most epidemiological studies, a point with which Drs.
Valberg and Long agree (Document ID 2330, p. 14).
OSHA has determined that its reliance on the best available
evidence provided it with a solid, scientifically sound foundation from
which to conclude that exposure to crystalline silica poses a
significant risk of harm, notwithstanding the various uncertainties
inherent in epidemiology generally or potentially affecting any given
study and that no studies exist entirely free from the types of data
limitations or error and variability Drs. Valberg and Long identified.
During the public hearing Dr. Long acknowledged that OSHA had not
overlooked studies that he believed adequately addressed the sources
of error cited in his comments. He was also unable to provide examples
of such analyses in the silica literature, or in any other area of
occupational epidemiology (Document ID 3576, Tr. 355-358; see also
Document ID 3577, Tr. 641, 648 (testimony of Dr. Kenneth Mundt)).
Additionally, Drs. Valberg and Long's critique of Drs.
Steenland and Bartell's uncertainty analysis ignores constraints on the
available data and reasonable limits on the analysts' ability to
investigate the full variety of possible errors and their potential
effects on OSHA's risk assessment.
OSHA additionally notes that Dr. Kenneth Crump, an OSHA peer
reviewer, in his examination of ToxaChemica's (Document ID 0469) study
of exposure uncertainty in the Steenland et al. pooled study, opined
that it was sound. He further observed that the "analysis of error
conducted by [ToxaChemica] is a very strong effort. The assumptions are
clearly described and the data upon [which] they are based appear to be
appropriate and appropriately applied." Dr. Crump was careful to note,
however, that "there are questions, as there will always be with such
an analysis...A major source of error that apparently was not
accounted for is in assuming that the average measure of exposure
assigned to a job is the true average" (Document ID 3574, pp. 161-
162). Dr. Cox referenced Dr. Crump's comment in his own pre-hearing
comments, in the context of a discussion on the importance of exposure
uncertainty in OSHA's risk analysis (Document ID 2307, p. 40). OSHA
addressed this particular criticism in the Review of Health Effects
Literature and Preliminary QRA. There, it stated that it is possible
that some job exposure estimates were above or below the true average
for a job; however, there was no "gold standard" measurement
available to appropriately test or adjust for this potential source of
error (Document ID 1711, p. xv). The Agency further stated that the
uncertainty, or sensitivity, analysis included potential error in job
averages, and found that most cohorts in the lung cancer and silicosis
mortality pooled studies were not highly sensitive to random or
systematic error in job-average exposure estimates (Document ID 1711,
pp. 303-314). In his final evaluation of OSHA's response to his
comments of 2009, Dr. Crump stated, "I believe that my comments have
been fairly taken into account in the current draft and I have no
further comments to make" (Document ID 3574, p. 17).
Similarly, Dr. Morfeld, representing the ACC, criticized Drs.
Steenland and Bartell for performing only 50 simulations of workplace
exposures as part of the uncertainty analysis (Document ID 2307,
Attachment 2, p. 10). Peer reviewer Mr. Bruce Allen also remarked that
this type of uncertainty analysis typically requires more than 50
simulations (Document ID 3574, p. 114). However, as stated by OSHA in
the response to peer review section of the Review of Health Effects
Literature and Preliminary QRA (Document ID 1711, pp. 379-400), the
results did not appear to change much with an increased number of
simulations. Thus, OSHA has concluded that the sensitivity findings
would not have changed substantially by running more simulations.
Indeed, in the final peer review report conveying his evaluation of
OSHA's response to his comments of 2009, Mr. Allen stated that OSHA
adequately addressed his comments in the updated risk assessment
(Document ID 3574, p. 5).
The overall salient conclusion that OSHA draws from this peer-
reviewed analysis is that even in those cohorts where exposure error
had some impact on exposure-response models for lung cancer or
silicosis, the resulting risk estimates at the previous and new PELs
remain clearly significant. Therefore, OSHA continues to rely on, and
have confidence in, the risk analysis it had performed. In particular,
OSHA concludes that Drs. Steenland and Bartell's modeling choices were
based on the best available data from a variety of industrial sources
and, through their uncertainty analysis, reached conclusions that
survive the ACC and Chamber criticisms of the study methodology. OSHA
further concludes that it is not necessary to conduct additional
analysis to modify the approach adopted by Drs. Steenland and Bartell
or to incorporate additional sources of exposure estimation uncertainty
in the analysis.
OSHA also disagrees with other specific criticisms that Drs. Long
and Valberg made concerning the uncertainty analysis. Dr. Long
testified that "there are no formal analyses conducted to determine
the error structures of the three sources of exposure measurement error
included in the sensitivity analyses; for example, without any formal
analysis, the OSHA assessment simply assumed a purely Berkson type
error structure from the assignment of job-specific average exposure
levels for individual exposures" (Document ID 3576, 304-305).\9\ Dr.
Cox expressed a similar concern that
---------------------------------------------------------------------------
\9\ The first component of ToxaChemica's analysis takes the
exposure level for each job in the job-exposure matrix as the mean
exposure level for workers in that job, with error (that results
from using the mean to estimate each individual worker's exposure)
varying randomly around the mean (Document ID 0469, P. 10). The
second type of error examined by ToxaChemica, resulting from the
assignment of a single conversion factor to represent quartz
percentage in dust samples for multiple jobs, similarly might be
expected to vary randomly around a mean equal to the recorded
conversion factor. Errors resulting from the assignment of job-
specific mean exposures (or conversion factors) to individual
workers or jobs results in a type of error known as Berkson error,
in which the true exposure level is assumed to vary randomly around
the assigned or "observed" exposure level for the job (Snedecor
and Cochran, 1989).
OSHA has not developed an appropriate error model specifically
for the exposure estimates in the crystalline silica studies and has
not validated (e.g., using a validation subset) that any of the ad
hoc error models that they discuss describes the real exposure
estimate errors of concern. They have also provided no justification
for ToxaChemica's assumption of a log-normal distribution without
outliers or mixtures of different distributions...and have
provided no rationale for the assumption that a=0.8*p (Document ID
---------------------------------------------------------------------------
2307, Attachment 4, p. 45).
OSHA disagrees with Dr. Long's and Dr. Cox's characterizations,
which implies that Drs. Steenland and Bartell did not adequately
investigate the patterns of error in the data available to them. As
noted in their 2004 report and by Dr. Steenland during the public
hearings, ToxaChemica did not have the internal validation data (true
exposures for a subset of the data set) that would be required to
conduct formal analyses or validation of the error structure within
each cohort of the pooled analysis (Document ID 0469, p. 16; 3580, pp.
1229-1231). Such data are not often available to analysts. However,
Drs. Steenland and Bartell researched and reviewed worker exposure and
dust composition data from several worksites to inform the error
structures used in their analyses. For example, their analysis of
individual workers' exposure data from the pooled analyses' industrial
sand cohort formed the basis of the equation used for the exposure
error simulation, which Dr. Cox represented as an assumption lacking
any rationale. Drs. Steenland and Bartell also reviewed a number of
studies characterizing the distribution of conversion factors across
and within jobs at different worksites. OSHA concludes that Drs.
Steenland and Bartell made a strong effort to collect data to inform
their modeling choices, and that their choices were based on the
best available information on error structure.
Dr. Long stated that "another limitation of the [ToxaChemica
uncertainty] assessment was its assumption of log-linear...types of
models, including log linear models with log-transformed exposure
variables, and it focused on cumulative measures of silica exposure
that obscure both within-person and between-person variability in
exposure rates" (Document ID 3576 pp. 305-306). Dr. Long's assertion
regarding the choice of exposure models is incorrect, as the
sensitivity analysis was not limited to log-linear models. It included
models with flexibility to capture nonlinearities in exposure-response,
including spline analyses and categorical analyses, and log-
transformation of the exposure variable was used only in the lung
cancer analysis where it was shown in the original pooled analysis to
better fit the data and address issues of heterogeneity between cohorts
(Document ID 0469). Drs. Steenland and Bartell found only slight
differences between the adjusted exposure-response estimates for each
type of model.
Drs. Long and Valberg also contended that the cumulative exposure
metric used in the Steenland and Bartell pooled study did not
sufficiently allow for examination of the effects of exposure
measurement uncertainty on the results of OSHA's risk assessment,
because other exposure metrics could be more relevant. OSHA disagrees.
As discussed in Section V.M, Comments and Responses Concerning Working
Life, Life Tables, and Dose Metric, cumulative exposure is widely
acknowledged by health experts as a driver of chronic diseases such as
silicosis and lung cancer, has been found to fit the exposure-response
data well in many studies of silicosis and lung cancer in the silica
literature, and best fit the exposure-response data in the underlying
pooled data sets to which Drs. Steenland and Bartell applied their
subsequent uncertainty analyses. Thus, OSHA believes it was appropriate
for this investigation of exposure estimation error to focus on the
cumulative exposure metric, for reasons including data fit and general
scientific understanding of this disease.
Furthermore, Dr. Long's concern that the choice of cumulative
silica exposure might "obscure within-person variability in exposure
rates" is not well supported in the context of lung cancer and
silicosis mortality. Because death from these diseases typically occurs
many years after the exposure that caused it, and complete records of
past exposures do not typically exist, it is very difficult, using any
metric, to trace within-person exposure variability (that is, changes
in a person's exposure over time); these factors, not the choice of
cumulative exposure metric, make it difficult to address variability in
individuals' exposures over time and their effects on risk. OSHA notes
that some analysts have explored the use of other exposure metrics in
threshold analyses, submitting studies to the record which the Agency
has reviewed and discussed in Section V.I, Comments and Responses
Concerning Thresholds for Silica-Related Diseases.
Dr. Long also testified that "[t]here's very little discussion in
the OSHA report regarding the potential impacts of exposure measurement
error on identification of thresholds...[ToxaChemica's 2004 report]
noted that exposure-response threshold estimates are imprecise and
appear to be highly sensitive to measurement errors" (Document ID 3576
p. 306). Dr. Cox further noted that exposure misclassification can
"create the appearance of a smooth, monotonically increasing estimated
ER [exposure-response] relation" and shift thresholds to the left
(Document ID 2307, Attachment 4, pp. 41-42); that is, create the
appearance that a threshold effect occurs at a lower exposure level
than would be seen in a data set without exposure misclassification.
In their uncertainty analysis, Drs. Steenland and Bartell estimated
an exposure-response threshold for the pooled cohorts in each of the 50
runs conducted for their lung cancer analysis. They defined the
"threshold" as the highest cumulative exposure for which the
estimated odds ratio was less than or equal to 1.0, reporting a mean
value of 3.04 mg/m\3\-days and median of 33.5 mg/m\3\-days across the
50 runs (Document ID 0469, p. 15). The authors observed that "[t]hese
estimates are somewhat lower than the original estimate (Steenland and
Deddens 2002) of a threshold at 121 mg/m\3\-days (4.8 on the log
scale), which translates to about 0.01 mg/m\3\ [10 [micro]g/m\3\] over
a working 30-year lifetime (considering a 15-year lag), or 0.007
[7[micro]g/m\3\] over a 45-year lifetime without considering a 15-year
lag" (Document ID 0469, p. 15). These exposure levels are about one-
fifth the PEL of 50 [mu]g/m\3\ included in the final standard.
As noted by Dr. Long, the threshold estimates were highly variable
across the 50 iterations (SD of 1.64 on the log scale), in keeping with
other comments received by OSHA that estimates of exposure-response
thresholds based on epidemiological data tend to be highly sensitive to
sources of measurement error and other issues common to epidemiological
investigations (see Section V.I, Comments and Responses Concerning
Thresholds for Silica-Related Diseases). However, the Agency notes that
the results of the uncertainty analysis, suggesting a possible
cumulative exposure threshold at approximately one-fifth the final 50
[mu]g/m3 PEL, provide no cause to doubt OSHA's determination
that significant risk exists at both the previous and the revised PEL.
An additional concern raised by Dr. Cox was based on his
misunderstanding that the equation used to characterize the
relationship between true and observed exposure in Drs. Steenland and
Bartell's simulation, "Exposuretrue = Exposureobserved + E",
concerned cumulative exposure. Dr. Cox stated that the equation is
"inappropriate for cumulative exposures [because] both the mean and
the variance of actual cumulative exposure received typically increase
in direct proportion to duration" (Document ID 2307, Attachment 4, p.
45). That is, the longer period of time over which a cumulative
exposure is acquired, the higher variance is likely to be, because
cumulative exposure is the sum of the randomly varying exposures
received on different days. However, the exposures referred to in the
equation are the mean job-specific concentrations recorded in the job-
exposure matrix (Exposureobserved) and individuals' actual exposure
concentrations from each job worked (Exposuretrue), not their
cumulative exposures (Document ID 0469, p. 11). Therefore, Dr. Cox's
criticism is unfounded.
Dr. Cox additionally criticized the simulation analysis on the
basis that "[t]he usual starting point for inhalation exposures [is]
with the random number of particles inhaled per breath modeled as a
time-varying (non-homogenous) Poisson process...It is unclear why
ToxaChemica decided to assume (and why OSHA accepted the assumption) of
an underdispersed distribution...rather than assuming a Poisson
distribution" (Document ID 2307, Attachment 4, pp. 45-46). OSHA
believes this criticism also reflects a misunderstanding of Drs.
Steenland and Bartell's analysis. While it could be pertinent to an
analysis of workers' silica dose (the amount of silica that enters the
body), the analysis addresses the concentration of silica in the air
near a worker's breathing zone, not internal dose. The worker's
airborne concentration is the regulated exposure endpoint and the
exposure of interest for OSHA's risk assessment. Thus, the uncertainty
analysis does not need to account for the number of particles inhaled
per breath.
More broadly, Dr. Cox asserted that the Monte Carlo analysis "is
an inappropriate tool for analyzing the effects of exposure measurement
error on estimated exposure-response data," citing a paper by Gryparis
et al. (2009) (Document ID 2307, Attachment 4, p. 44). This paper
indicates that by randomly simulating exposure measurement error, the
Monte Carlo approach can introduce classical error (Document ID 3870,
p. 262). Peer reviewer Dr. Noah Seixas similarly commented that "[t]he
typical Monte Carlo simulation, which is what appears to have been
done, would introduce classical error," that is, error which is
independent of the unobserved variable (in this case, the true exposure
value). He explained that, as a result, "the estimated risks [from the
simulation analyses] are most likely to be underestimates, or
conservatively estimating risk. This is an important aspect of
measurement error with significant implications for risk assessment and
should not be overlooked." (Document ID 3574, pp. 116-117). Addressing
Dr. Cox's broader point, Dr. Seixas in his peer review stated that the
"simulation of exposure measurement error in assessing the degree of
bias that may have been present is a reasonable approach to assessing
this source of uncertainty" (Document ID 3574, pp. 116). Dr. Crump
similarly characterized the uncertainty analysis used in the Steenland
and Bartell study as "a strong effort" that "appropriately applied"
this method (Document ID 3574, pp. 161-162). In this regard, OSHA
generally notes that the advantages and limitations of various methods
to address exposure measurement error in exposure-response models is an
area of ongoing investigation in risk assessment. As shown by the
comments of OSHA's peer reviewers above, there is no scientific
consensus to support Dr. Cox's opinion that the Monte Carlo analysis is
an inappropriate approach to analyze the effects of exposure
measurement error.
In conclusion, through use of high quality studies and modeling,
performance of an uncertainty analysis, and submission of the results
of that analysis to peer review, OSHA maintains that it has relied upon
the best available evidence. In addition, OSHA has carefully considered
the public comments criticizing ToxaChemica's uncertainty analysis and
has concluded that exposure estimation error did not substantially
affect the results in the majority of studies examined (Document ID
1711, pp. 299-314). As a result, it was not necessary to conduct
additional analyses modifying the approach adopted by Drs. Steenland
and Bartell. Accordingly, OSHA reaffirms its determination that the
conclusions of the Agency's risk assessment are correct and largely
unaffected by potential error in exposure measurement.
L. Comments and Responses Concerning Causation
As discussed in Section V.C, Summary of the Review of Health
Effects Literature and Preliminary QRA, OSHA finds, based upon the best
available evidence in the published, peer-reviewed scientific
literature, that exposure to respirable crystalline silica increases
the risk of silicosis, lung cancer, other non-malignant respiratory
disease (NMRD), and renal and autoimmune effects. Exposure to
respirable crystalline silica causes silicosis and is the only known
cause of silicosis. For other health endpoints like lung cancer that
have both occupational and non-occupational sources of exposure, OSHA
used a comprehensive weight-of-evidence approach to evaluate the
published, peer-reviewed scientific studies in the literature to
determine their overall quality and whether there is substantial
evidence that exposure to respirable crystalline silica increases the
risk of a particular health effect. For example, with respect to lung
cancer, OSHA reviewed 60 epidemiological studies covering more than 30
occupational groups in over a dozen industrial sectors and concluded
that exposure to respirable crystalline silica increases the risk of
lung cancer (Document ID 1711, pp. 77-170). This conclusion is
consistent with that of the World Health Organization's International
Agency for Research on Cancer (IARC), HHS' National Toxicology Program
(NTP), the National Institute for Occupational Safety and Health
(NIOSH), and many other organizations and individuals, as evidenced in
the rulemaking record and discussed throughout this section.
In spite of this, and in addition to asserting that OSHA's
Preliminary QRA was affected by many biases, Dr. Cox, on behalf of the
ACC, argued that OSHA failed to conduct statistical analyses of
causation, which led to inaccurate conclusions about causation. He
specifically challenged OSHA's reliance upon the IARC determination of
carcinogenicity, as discussed in Section V.F, Comments and Responses
Concerning Lung Cancer Mortality, and its use of the criteria for
evaluating causality developed by the noted epidemiologist Bradford
Hill (Document ID 2307, Attachment 4, pp. 13-14; 4027, p. 28). The Hill
criteria are nine aspects of an association that should be considered
when examining causation: (1) The strength of the association; (2) the
consistency of the association; (3) the specificity of the association;
(4) the temporal relationship of the association; (5) the biological
gradient (i.e., dose-response curve); (6) the biological plausibility
of the association; (7) coherency; (8) experimentation; and (9) analogy
(Document ID 3948, pp. 295-299).
Instead, Dr. Cox suggested that OSHA use the methods listed in
Table 1 of his 2013 paper, "Improving causal inferences in risk
analysis," which he described as "the most useful study designs and
methods for valid causal analysis and modeling of causal exposure-
response (CER) relations" (Document ID 2307, Attachment 4, p. 11).
Because OSHA did not use these methods, Dr. Cox maintained that the
Agency's Preliminary QRA "asserts causal conclusions based on non-
causal studies, data, and analyses" (Document ID 2307, Attachment 4,
p. 3). He also contended that OSHA "ha[d] conflated association and
causation, ignoring the fact that modeling choices can create findings
of statistical associations that do not predict correctly the changes
in health effects (if any) that would be caused by changes in
exposures" (Document ID 2307, Attachment 4, p. 3). He claimed that
"[t]his lapse all by itself invalidates the Preliminary QRA's
predictions and conclusions" (Document ID 2307, Attachment 4, p. 3).
As discussed below, since OSHA's methodology and conclusions regarding
causation are based on the best available evidence, they are sound.
Consequently, Dr. Cox's contrary position is unpersuasive.
1. IARC Determination
Dr. Cox asserted that OSHA erred in its reliance on the IARC
determination of carcinogenicity for crystalline silica inhaled in the
forms of quartz or cristobalite. He believed OSHA only relied on the
IARC findings because they aligned with the Agency's opinion, noting
that the "IARC analysis involved some of the same researchers, same
methodological flaws, and same gaps in explicit, well-documented
derivations of benefits and conclusions as OSHA's own preliminary QRA"
(Document ID 2307, Attachment 4, pp. 13-14). OSHA, however, relied on
IARC's determination to include lung cancer in its quantitative risk
assessment because it constitutes the best available evidence. For this
reason, Dr. Cox's position is without merit and OSHA's findings are supported
by substantial evidence in the record and reasonable.
As discussed in Section V.F, Comments and Responses Concerning Lung
Cancer Mortality, the IARC classifications and accompanying monographs
are well recognized in the scientific community, and have been
described by scientists as "the most comprehensive and respected
collection of systematically evaluated agents in the field of cancer
epidemiology" (Demetriou et al., 2012, Document ID 4131, p. 1273).
IARC's conclusions resulted from a thorough expert committee review of
the peer-reviewed scientific literature, in which crystalline silica
dust, in the form of quartz or cristobalite, was classified as Group 1,
"carcinogenic to humans," in 1997 (Document ID 2258, Attachment 8, p.
210). Since the publication of these conclusions, the scientific
community has reaffirmed their soundness. In March of 2009, 27
scientists from eight countries participated in an additional IARC
review of the scientific literature and reaffirmed that crystalline
silica dust is a Group 1 carcinogen, i.e., "carcinogenic to humans"
(Document ID 1473, p. 396). Additionally, the HHS' U.S. National
Toxicology Program also concluded that respirable crystalline silica is
a known human carcinogen (Document ID 1164, p. 1).
Further supporting OSHA's reliance on IARC's determination of
carcinogenicity for its quantitative risk assessment is testimony
offered by scientists during the informal public hearings. This
testimony highlighted IARC's carcinogenicity determinations as very
thorough examinations of the scientific literature that demonstrate
that exposure to respirable crystalline silica causes lung cancer. For
example, when asked about Dr. Cox's causation claims during the
informal public hearings, David Goldsmith, Ph.D., noted that causation
was very carefully examined by IARC. He believed that IARC, in its 1997
evaluation of evidence for cancer and silica, "...chose...the
best six studies that were the least confounded for inability to
control for smoking or other kinds of hazardous exposures like
radiation and asbestos and arsenic..." (Document ID 3577, Tr. 894-
896). He also believed it "...crucial...that we pay attention
to those kinds of studies, that we pay attention to the kinds of
studies that were looked at by the IARC cohort that Steenland did from
2001. That's where they had the best evidence" (Document ID 3577, Tr.
894-896).
Regarding IARC's evaluation of possible biases and confounders in
epidemiological studies, as well as its overall determination, Frank
Mirer, Ph.D., of CUNY School of Public Health, representing the AFL-
CIO, testified:
IARC has active practicing scientists review--I've been on two
IARC monographs, but not these monographs, monograph working groups.
It's been dealt with. It's been dealt with over a week of intense
discussion between the scientists who are on these committees, as to
whether there's chance bias in confounding which might have led to
these results, and by 1987 for foundries and 1997 for silica, and
it's been decided and reaffirmed.
So people who don't believe it are deniers, pure and simple.
This is the scientific consensus. I was on the NTP Board of
Scientific Counselors when we reviewed the same data. Known to be a
human carcinogen. Once you know it's a human carcinogen from studies
in humans, you can calculate risk rates (Document ID 3578, Tr. 937).
That OSHA relied on the best available evidence to draw its
conclusions was also affirmed by Dr. Cox's inability to provide
additional studies that would have cast doubt on the Agency's causal
analysis. Indeed, during the informal public hearings, Kenneth Crump,
Ph.D., an OSHA peer reviewer from the Louisiana Tech University
Foundation, asked Dr. Cox if he could identify "any causal studies of
silica that they [OSHA] should have used but did not use?" Dr. Cox
responded: "I think OSHA could look at a paper from around 2007 of
Brown's, on some of the issues and causal analysis, but I think the
crystalline silica area has been behind other particulate matter areas
...in not using causal analysis methods. So no, I can't point to a
good study that they should have included but didn't" (Document ID
3576, Tr. 401-402). In light of the above, OSHA maintains that in
relying on IARC's determination of carcinogenicity, its conclusions on
causation are rooted in the best available evidence.
2. Bradford Hill Criteria and Causality
Dr. Cox also challenged OSHA's use of Hill's criteria for
causation. He claimed that the Bradford Hill considerations were
neither necessary nor sufficient for establishing causation, which was
his reason for failing to include them in the statistical methods
listed in Table 1 of his written comments for objectively establishing
evidence about causation (Document ID 4027, p. 28). As explained below,
based on its review of the record, OSHA finds this position meritless,
as it is unsupported by the best available evidence.
As a preliminary matter, Hill's criteria for causation (Document ID
3948) are generally accepted as a gold standard for causation in the
scientific community. Indeed, OSHA heard testimony during the informal
public hearings and received post-hearing comments indicating that Dr.
Cox's assertion that statistical methods should be used to establish
causality is not consistent with common scientific practice. For
example, Andrew Salmon, Ph.D., an OSHA peer reviewer, wrote:
The identification of causality as opposed to statistical
association is, as described by Bradford Hill in his well-known
criteria, based mainly on non-statistical considerations such as
consistence, temporality and mechanistic plausibility: the role of
statistics is mostly limited to establishing that there is in fact a
quantitatively credible association to which causality may (or may
not) be ascribed. OSHA correctly cites the substantial body of
evidence supporting the association and causality for silicosis and
lung cancer following silica exposure, and also quotes previous
expert reviews (such as IARC). The causal nature of these
associations has already been established beyond any reasonable
doubt, and OSHA's analysis sufficiently reflects this (Document ID
3574, p. 38).
Similarly, Kyle Steenland, Ph.D., Professor, Department of
Environmental Health, Rollins School of Public Health, Emory
University, in response to a question about Dr. Cox's testimony on
causation from Darius Sivin, Ph.D., of the UAW Health and Safety
Department, stated that the Bradford Hill criteria are met for lung
cancer and silicosis:
[M]ost of the Bradford Hill criteria apply here. You know you
can never prove causality. But when the evidence builds up to such
an extent and you have 100 studies and they tend to be fairly
consistent, that's when we draw a causal conclusion. And that was
the case for cigarette smoke in lung cancer. That was the case for
asbestos in lung cancer. And when the evidence builds up to a
certain point, you say, yeah, it's a reasonable assumption that this
thing causes, X causes Y (Document ID 3580, pp. 1243-1244).
As a follow-up, OSHA asked if Dr. Steenland felt that the Bradford
Hill criteria were met for silica health endpoints. Dr. Steenland
replied, "For silicosis or for lung cancer. I had said they're met for
both" (Document ID 3580, p. 1262).
Gary Ginsberg, Ph.D., an OSHA peer reviewer, agreed with Dr.
Steenland, remarking to Dr. Cox during questioning, "I'm a little
dumbfounded about the concern over causality, given all the animal
evidence" (Document ID 3576, Tr. 406). Mr. Park from NIOSH's Risk
Evaluation Branch, in his question to Dr. Cox, echoed the sentiments of
Dr. Ginsberg, stating:
It's ludicrous to hear someone question causality. There's 100
years of research in occupational medicine, in exposure assessment.
People here even in industry would agree that silica they say causes
silicosis, which causes lung cancer. There's some debate about
whether the middle step is required. There's no question that
there's excess lung cancer in silica-exposed populations. We look at
literature, and we identify what we call good studies. Good studies
are ones that look at confounding, asbestos, whatever. We make
judgments. If there's data that allows one to control for
confounding, that's part of the analysis. If there is confounding
that we can't control for, we evaluate it. We ask how bad could it
be? There's a lot of empirical judgment from people who know these
populations, know these exposures, know these industries, who can
make very good judgments about that. We aren't stupid. So I don't
know where you're coming from (Document ID 3576, Tr. 410-411).
Indeed, Kenneth Mundt, Ph.D., testifying on behalf of the
International Diatomite Producers Association (part of the ACC
Crystalline Silica Panel, which included Dr. Cox), and whose research
study was the basis for the Morfeld et al. (2013, Document ID 3843)
paper that reportedly identified a high exposure threshold for
silicosis, also appeared to disagree with Dr. Cox's view of causation.
Dr. Mundt testified that while he thought he could appreciate Dr. Cox's
testimony, at some point there is sufficiently accumulated evidence of
a causal association; he concluded, "I think here, over time, we've
had the advantage with the reduction of exposure to see reduction in
disease, which I think just makes it a home run that the diseases are
caused by, therefore can be prevented by appropriate intervention"
(Document ID 3577, Tr. 639-640).
OSHA notes that Dr. Cox, upon further questioning by Mr. Park,
appeared to concede that exposure to respirable crystalline silica
causes silicosis; Dr. Cox stated, "I do not question that at
sufficiently high exposures, there are real effects" (Document ID
3576, Tr. 412). Later, when questioned by Anne Ryder, an attorney in
the Solicitor of Labor's office, he made a similar statement: "I do
take it as given that silica at sufficiently high and prolonged
exposures causes silicosis" (Document ID 3576, Tr. 426). Based upon
this testimony of Dr. Cox acknowledging that silica exposure causes
silicosis, OSHA interprets his concern with respect to silicosis to be
not one of causation, but rather a concern with whether there is a
silicosis threshold (i.e., that exposure to crystalline silica must
generally be above some level in order for silicosis to occur). Indeed,
OSHA peer reviewer Brian Miller, Ph.D., noted in his post-hearing
comments that Dr. Cox, when challenged, accepted that silica was causal
for silicosis, "but questioned whether there was evidence for
increased risks at low concentrations; i.e. whether there was a
threshold" (Document ID 3574, p. 31). Thresholds for silicosis are
addressed in great detail in Section V.I, Comments and Responses
Concerning Thresholds for Silica-Related Diseases.
Based on the testimony and written comments of numerous scientists
representing both public health and industry--all of whom agree that
causation is established by applying the Bradford Hill criteria and
examining the totality of the evidence--OSHA strongly disagrees with
Dr. Cox's claims that the Bradford Hill criteria are inadequate to
evaluate causation in epidemiology and that additional statistical
techniques are needed to establish causation. OSHA defends its reliance
on the IARC determination of 1997 and re-determination of 2012 that
crystalline silica is a causal agent for lung cancer. OSHA's own Review
of Health Effects Literature further demonstrates the totality of the
evidence supporting the causality determination (Document ID 1711).
Indeed, other than Dr. Cox representing the ACC, no other individual or
entity questioned causation with respect to silicosis. Even Dr. Cox's
questioning of causation for silicosis appears to be more of a question
about thresholds, which is discussed in Section V.I, Comments and
Responses Concerning Thresholds for Silica-Related Diseases.
3. Dr. Cox's Proposed Statistical Methods
OSHA reviewed the statistical methods provided by Dr. Cox in Table
1 of his 2013 paper, "Improving causal inferences in risk analysis,"
(Document ID 2307, Attachment 4, p. 11), and explains below why the
Agency did not adopt them. For example, Intervention Time Series
Analysis (ITSA), as proposed by Dr. Cox in his Table 1, is a method for
assessing the impact of an intervention or shock on the trend of
outcomes of interest (Gilmour et al., 2006, cited in Document ID 2307,
Attachment 4, p. 11). Implementing ITSA requires time series data
before and after the intervention for both the dependent variable
(e.g., disease outcome) and independent variables (e.g., silica
exposure and other predictors), as well as the point of occurrence of
the intervention. Although time-series data are frequently available in
epidemiological studies, for silica we do not have a specific
"intervention point" comparable to the implementation of a new OSHA
standard that can be identified and analyzed. Rather, changes in
exposure controls tend to be iterative and piecemeal, gradually
bringing workers' exposures down over the course of a facility's
history and affecting job-specific exposures differently at different
points in time. Furthermore, individual workers' exposures change
continually with new job assignments and employment. In addition, in a
situation where the intervention really reduces the adverse outcome to
a low level, such as 1/1000 lifetime excess risk, ITSA would require an
enormous observational database in order to be able to estimate the
actual post-intervention level of risk. OSHA believes the standard risk
analysis approach of estimating an exposure-response relationship based
on workers' exposures over time and using this model to predict the
effects of a new standard on risk appropriately reflects the typical
pattern of multiple and gradual changes in the workers' exposures over
time found in most industrial facilities.
Another method listed in Dr. Cox's Table 1, marginal structural
models (MSM), was introduced in the late 1990s (Robins, 1998, cited in
Document ID 2307, Attachment 4, p. 11) to address issues that can arise
in standard modeling approaches when time-varying exposure and/or time-
dependent confounders are present.\10\ These methods are actively being
explored in the epidemiological literature, but have not yet become a
standard method in occupational epidemiology. As such, OSHA faces some
of the same issues with MSM as were previously noted with BMA:
Published, peer-reviewed studies using this approach are not available
for the silica literature, and best practices are not yet well
established. Thus, the incorporation of MSM in the silica risk
assessment is not possible using the currently available literature and
would be premature for OSHA's risk assessment generally.
---------------------------------------------------------------------------
\10\ A time-dependent confounder is a covariate whose post-
baseline value is a risk factor for both the subsequent exposure and
the outcome.
---------------------------------------------------------------------------
In addition, in his post-hearing brief, Dr. Cox contended that
"[a] well-done QRA should explicitly address the causal fraction (and
explain the value used), rather than tacitly assuming that it is 1"
(Document ID 4027, p. 4). However, this claim is without grounds. OSHA
understands Dr. Cox's reference to the "causal fraction" to mean
that, when estimating risk from an exposure-response model, only a fraction
of the total estimated risk should be attributed to disease caused by
the occupational exposure of interest. The Agency notes that the
"causal fraction" of risk is typically addressed through the use of
life table analyses, which incorporate background rates for the disease
in question. Such analyses, which OSHA used in its Preliminary QRA,
calculate the excess risk, over and above background risk, that is
solely attributable to the exposure in question. Thus, there is no need
to estimate a causal fraction due to exposure. These approaches are
further discussed in Section V.M, Comments and Responses Concerning
Working Life, Life Tables, and Dose Metric. Furthermore, nowhere in the
silica epidemiological literature has the use of an alternative
"causal fraction" approach to ascribing the causal relationship
between silica exposure and silicosis and lung cancer been deemed
necessary to reliably estimate risk.
4. The Assertion That the Silica Scientific Literature May Be False
Dr. Cox also asserted that the same biases and issues with
causation in OSHA's Quantitative Risk Assessment (QRA) were likewise
present in the silica literature. He wrote, "In general, the
statistical methods and causal inferences described in this literature
are no more credible or sound than those in OSHA's Preliminary QRA, and
for the same reasons" (Document ID 2307, Attachment 4, p. 30).
The rulemaking record contains evidence that contradicts Dr. Cox's
claims with respect to the scientific foundation of the QRA. Such
evidence includes scientific testimony and the findings of many expert
bodies, including IARC, the HHS National Toxicology Program, and NIOSH,
concluding that exposure to respirable crystalline silica causes lung
cancer. At the public hearing, Dr. Steenland, Professor at Emory
University, testified that the body of evidence pertaining to silica
was of equal quality to that of other occupational health hazards
(Document ID 3580, pp. 1245-1246). Dr. Goldsmith similarly testified:
Silica dust...is like asbestos and cigarette smoking in that
exposure clearly increases the risk of many diseases. There have
been literally thousands of research studies on exposure to
crystalline silica in the past 30 years. Almost every study tells
the occupational research community that workers need better
protection to prevent severe chronic respiratory diseases, including
lung cancer and other diseases in the future. What OSHA is proposing
to do in revising the workplace standard for silica seems to be a
rational response to the accumulation of published evidence
(Document ID 3577, Tr. 865-866).
OSHA agrees with these experts, whose positive view of the science
supporting the need for better protection from silica exposures stands
in contrast to Dr. Cox's claim regarding what he believes to be the
problematic nature of the silica literature. Dr. Cox asserted in his
written statement:
Scientists with subject matter expertise in areas such as
crystalline silica health effects epidemiology are not necessarily
or usually also experts in causal analysis and valid causal
interpretation of data, and their causal conclusions are often
mistaken, with a pronounced bias toward declaring and publishing
findings of `significant' effects where none actually exists (false
positives). This has led some commentators to worry that `science is
failing us,' due largely to widely publicized but false beliefs
about causation (Lehrer, 2012); and that, in recent times, `Most
published research findings are wrong' (Ioannadis, 2005), with the
most sensational and publicized claims being most likely to be
wrong. (Document ID 2307, Attachment 4, pp. 15-16).
Moreover, during the public hearing, Dr. Cox stated that, with
respect to lung cancer in the context of crystalline silica, the
literature base may be false:
MR. PERRY [OSHA Director of the Directorate of Standards and
Guidance]: So as I understand it, you basically think there's a good
possibility that the entire literature base, with respect to lung
cancer now, I'm talking about, is wrong?
DR. COX: You mean with respect to lung cancer in the context of
crystalline silica?
MR. PERRY: Yes, sir.
DR. COX: I think that consistent with the findings of Lauer
[Lehrer] and Ioannidis and others, I think that it's very possible
and plausible that there is a consistent pattern of false positives
in the literature base, yes. And that implies, yes, they are wrong.
False positives are false (Document ID 3576, Tr. 423).
The Ioannidis paper (Document ID 3851) used mathematical constructs
to purportedly demonstrate that most claimed research findings are
false, and then provided suggestions for improvement (Document ID 3851,
p. 0696). Two of his suggestions appear particularly relevant to the
silica literature: "Better powered evidence, e.g., large studies or
low-bias meta-analyses, may help, as it comes closer to the unknown
`gold' standard. However, large studies may still have biases and these
should be acknowledged and avoided"; and "second, most research
questions are addressed by many teams, and it is misleading to
emphasize the statistically significant findings of any single team.
What matters is the totality of the evidence" (Document ID 3851, pp.
0700-0701). OSHA finds no merit in the claim that most claimed research
findings are false. Instead, it finds that the silica literature for
lung cancer is overall trustworthy, particularly because the "totality
of the evidence" characterized by large studies demonstrates a causal
relationship between crystalline silica exposure and lung cancer, as
IARC determined in 1997 and 2012 (Document ID 2258, Attachment 8, p.
210; 1473, p. 396).
OSHA likewise notes that there was disagreement on Ioannidis'
methods and conclusions. Jonathan D. Wren of the University of
Oklahoma, in a correspondence to the journal that published the paper,
noted that Ioannidis, "after all, relies heavily on other studies to
support his premise, so if most (i.e., greater than 50%) of his cited
studies are themselves false (including the eight of 37 that pertain to
his own work), then his argument is automatically on shaky ground"
(Document ID 4087, p. 1193). In addition, Steven Goodman of Johns
Hopkins School of Medicine and Sander Greenland of the University of
California, Los Angeles, performed a substantive mathematical review
(Document ID 4081) of the Ioannidis models and concluded in their
correspondence to the same journal that "the claims that the model
employed in this paper constitutes `proof' that most published medical
research claims are false, and that research in `hot' areas is most
likely to be false, are unfounded" (Document ID 4095, p. 0773).
Christiana A. Demetriou, Imperial College London, et al. (2012),
analyzed this issue of potential false positive associations in the
field of cancer epidemiology (Document ID 4131). They examined the
scientific literature for 509 agents classified by IARC as Group 3,
"not classifiable as to its carcinogenicity to humans" (Document ID
4131). Of the 509 agents, 37 had potential false positive associations
in the studies reviewed by IARC; this represented an overall frequency
of potential false positive associations between 0.03 and 0.10
(Document ID 4131). Regarding this overall false positive frequency of
about 10 percent, the authors concluded, "In terms of public health
care decisions, given that the production of evidence is historical,
public health care professionals are not expected to react immediately
to a single positive association. Instead, they are likely to wait for
further support or enough evidence to reach a consensus, and if a
hypothesis is repeatedly tested, then any initial false-positive
results will be quickly undermined" (Document ID 4131, p. 1277). The
authors also cautioned that "Reasons for criticisms that are most
common in studies with false-positive findings can also underestimate
an association and in terms of public health care, false-negative
results may be a more important problem than false-positives"
(Document ID 4131, pp. 1278-1279). Thus, this study suggested that the
false positive frequency in published literature is actually rather
low, and stressed the importance of considering the totality of the
literature, rather than a single study.
Given these responses to Ioannidis, OSHA fundamentally rejects the
claim that most published research findings are false. The Agency
concludes that, most likely, where, as here, there are multiple,
statistically significant positive findings of an association between
silica and lung cancer made by different researchers in independent
studies looking at distinct cohorts, the chances that there is a
consistent pattern of false positives are small; OSHA's mandate is met
when the weight of the evidence in the body of science constituting the
best available evidence supports such a conclusion.
M. Comments and Responses Concerning Working Life, Life Tables, and
Dose Metric
As discussed in Section V.C, Summary of the Review of Health
Effects Literature and Preliminary QRA, OSHA presented risk estimates
associated with exposure over a working lifetime to 25, 50, 100, 250,
and 500 [mu]g/m\3\ respirable crystalline silica (corresponding to
cumulative exposures over 45 years to 1.125, 2.25, 4.5, 11.25, and 22.5
mg/m\3\-yrs). For mortality from silica-related disease (i.e., lung
cancer, silicosis and non-malignant respiratory disease (NMRD), and
renal disease), OSHA estimated lifetime risks using a life table
analysis that accounted for background and competing causes of death.
The mortality risk estimates were presented as excess risk per 1,000
workers for exposures over an 8-hour working day, 250 days per year,
and a 45-year working lifetime. This is a legal standard that OSHA
typically uses in health standards to satisfy the statutory mandate to
"set the standard which most adequately assures, to the extent
feasible, 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. 655(b)(5). For silicosis morbidity, OSHA based its
risk estimates on cumulative risk models used by various investigators
to develop quantitative exposure-response relationships. These models
characterized the risk of developing silicosis (as detected by chest
radiography) up to the time that cohort members (including both active
and retired workers) were last examined. Thus, risk estimates derived
from these studies represent less-than-lifetime risks of developing
radiographic silicosis. OSHA did not attempt to estimate lifetime risk
(i.e., up to age 85) for silicosis morbidity because the relationships
between age, time, and disease onset post-exposure have not been well
characterized.
OSHA received critical comments from representatives of the ACC and
the Chamber. These commenters expressed concern that (1) the working
lifetime exposure of 45 years was not realistic for workers, (2) the
use of life tables was improper and alternative methods should be used,
and (3) the cumulative exposure metric does not consider the exposure
intensity and possible resulting dose-rate effects. OSHA examines these
comments in detail in this section, and shows why they do not alter its
conclusion that the best available evidence in the rulemaking record
fully supports the Agency's use of a 45-year working life in a life
table analysis with cumulative exposure as the exposure metric of
concern.
1. Working Life
The Chamber commented that 45-year career silica exposures do not
exist in today's working world, particularly in "short term work-site
industries" such as construction and energy production (Document ID
4194, p. 11; 2288, p. 11). The Chamber stated that careers in these
jobs are closer to 6 years, pointing out that OSHA's contractor, ERG,
estimated a 64 percent annual turnover rate in the construction
industry. Referring to Section 6(b)(5) of the Occupational Safety and
Health (OSH) Act of 1970, the Chamber concluded, "OSHA improperly
inflates risk estimates with its false 45-year policy, contradicting
the Act, which requires standards based on actual, `working life'
exposures--not dated hypotheticals" (Document ID 4194, pp. 11-12;
2288, pp. 11-12).
As stated previously, OSHA believes that the 45-year exposure
estimate satisfies its statutory obligation to evaluate risks from
exposure over a working life, and notes that the Agency has
historically based its significance-of-risk determinations on a 45-year
working life from age 20 to age 65 in each of its substance-specific
rulemakings conducted since 1980. The Agency's use of a 45-year working
life in risk assessment has also been upheld by the DC Circuit (Bldg &
Constr. Trades Dep't v. Brock, 838 F.2d 1258, 1264-65 (D.C. Cir. 1988))
(also see Section II, Pertinent Legal Authority). Even if most workers
are not exposed for such a long period, some will be, and OSHA is
legally obligated to set a standard that protects those workers to the
extent such standard is feasible. For reasons explained throughout this
preamble, OSHA has set the PEL for this standard at 50 [micro]g/m\3\
TWA. In setting the PEL, the Agency reasoned that while this level does
not eliminate all risk from 45 years of exposures for each employee, it
is the lowest level feasible for most operations.
In addition, OSHA heard testimony and received several comments
with accompanying data that support a 45-year working life in affected
industries. For example, six worker representatives of the
International Union of Bricklayers and Allied Craftworkers (BAC), which
represents a portion of the unionized masonry construction industry
(Document ID 4053, p. 2), raised their hands in the affirmative when
asked if they had colleagues who worked for longer than 40 years in
their trade (Document ID 3585, Tr. 3053). Following the hearings, BAC
reviewed its International Pension Fund and counted 116 members who had
worked in the industry for 40 years or longer. It noted that this
figure was likely an understatement, as many workers had previous
experience in the industry prior to being represented by BAC, and many
BAC affiliates did not begin participation in the Fund until
approximately a decade after its establishment in 1972 (Document ID
4053, p. 2).
OSHA heard similar testimony from representatives of other labor
groups and unions. Appearing with the Laborers' Health and Safety Fund
of North America (LHSFNA), Eddie Mallon, a long-time member of the New
York City tunnel workers' local union, testified that he had worked in
the tunnel business for 50 years, mainly on underground construction
projects (Document ID 3589, Tr. 4209). Appearing with the United
Steelworkers, Allen Harville, of the Newport News Shipbuilding Facility
and Drydock, testified that there are workers at his shipyard with more
than 50 years of experience. He also believed that 15 to 20 percent of
workers had 20 to 40 years of experience (Document ID 3584, Tr. 2571).
In addition, several union representatives appearing with the
Building and Construction Trades Department (BCTD) of the American
Federation of Labor and Congress of Industrial Organizations (AFL-CIO)
also commented on the working life exposure estimate. Deven Johnson, of the
Operative Plasterers' and Cement Masons' International Association,
testified that he thought 45 years was relevant, as many members of his
union had received gold cards for 50 and 60 years of membership; he
also noted that there was a 75-year member in his own local union
(Document ID 3581, Tr. 1625-1626). Similarly, Sarah Coyne, representing
the International Union of Painters and Allied Trades, testified that
45 years was adequate, as "we have many, many members who continue to
work out in the field with the 45 years" (Document ID 3581, Tr. 1626).
Charles Austin, of the International Association of Sheet Metal, Air,
Rail and Transportation Workers, added that thousands of workers in the
union's dust screening program have been in the field for 20 to 30
years (Document ID 3581, Tr. 1628-1629).
In its post-hearing comment, the BCTD submitted evidence on behalf
of the United Association of Plumbers, Fitters, Welders and HVAC
Service Techs, which represents a portion of the workers in the
construction industry. A review of membership records for this
association revealed 35,649 active members with 45 years or more of
service as a member of the union. Laurie Shadrick, Safety and Health
National Coordinator for the United Association, indicated that this
membership figure is considered an underestimate, as many members had
previous work experience in the construction industry prior to joining
the union, or were not tracked by the union after transitioning to
other construction trades (Document ID 4073, Attachment 1b). The post-
hearing comment of the BCTD also indicated a trend of an aging
workforce in the construction industry, with workers 65 years of age
and older predicted to increase from 5 percent in 2012 to 8.3 percent
in 2022 (Document ID 4073, Attachment 1a, p. 1). This age increase is
likely due to the fact that few construction workers have a defined
benefit pension plan, and the age for collecting Social Security
retirement benefits has been increasing; as a result, many construction
workers are staying employed for longer in the industry (Document ID
4073, Attachment 1a, p. 1). Thus, the BCTD expressed its support for
using a 45-year working life in the construction industry for risk
assessment purposes (Document ID 4073, Attachment 1a, p. 1).
In addition to BAC and BCTD, OSHA received post-hearing comments on
the 45-year working life from the International Union of Operating
Engineers (IUOE) and the American Federation of State, County and
Municipal Employees (AFSCME). The IUOE reviewed records of the Central
Pension Fund, in which IUOE construction and stationary local unions
participate, and determined that the average years of service amongst
all retirees (75,877 participants) was 21.34 years, with a maximum of
49.93 years of active service. Of these retirees, 15,836 participants
recorded over 30 years of service, and 1,957 participants recorded over
40 years of service (Document ID 4025, pp. 6-7). The IUOE also pointed
to the testimony of Anthony Bodway, Special Projects Manager at Payne &
Dolan, Inc. and appearing with the National Asphalt Pavement
Association (NAPA), who indicated that some workers in his company's
milling division had been with the company anywhere from 35 to 40 years
(Document ID 3583, Tr. 2227, 2228). Similarly, the AFSCME reported
that, according to its 2011 poll, 49 percent of its membership had over
10 years of experience, and 21 percent had over 20 years (Document ID
3760, p. 2).
The rulemaking record on this topic of the working life thus
factually refutes the Chamber's assertion that "no such 45-year career
silica exposures exist in today's working world, particularly in
construction, energy production, and other short term work-site
industries" (Document ID 4194, p. 11; 2288, p. 11). Instead, OSHA
concludes that the rulemaking record demonstrates that the Agency's use
of a 45-year working life as a basis for estimating risk is legally
justified and factually appropriate.
2. Life Tables
Dr. Cox, on behalf of the ACC, commented that OSHA should use
"modern methods," such as Bayesian competing-risks analyses,
expectation-maximization (EM) methods, and copula-based approaches that
account for subdistributions and interdependencies among competing
risks (Document ID 2307, Attachment 4, p. 61). Such methods, according
to Dr. Cox, are needed "[t]o obtain risk estimates...that have
some resemblance to reality, and that overcome known biases in the
na[iuml]ve life table method used by OSHA" (Document ID 2307,
Attachment 4, p. 61). Dr. Cox then asserted that the life table method
used in the following studies to estimate mortality risks is also
incorrect: Steenland et al. (2001a, Document ID 0452), Rice et al.
(2001, Document ID 1118), and Attfield and Costello (2004, Document ID
0285) (Document ID 2307, Attachment 4, pp. 61-63).
OSHA does not agree that the life table method it used to estimate
mortality risks is incorrect or inappropriate. Indeed, the Agency's
life table approach is a standard method commonly used to estimate the
quantitative risks of mortality. As pointed out by Rice et al. (2001),
the life table method was developed by the National Research Council's
BEIR IV Committee on the Biological Effects of Ionizing Radiations
(BEIR), Board of Radiation Effects Research, in its 1988 publication on
radon (Document ID 1118, p. 40). OSHA notes that the National Research
Council is the operating arm of the National Academy of Sciences and
the National Academy of Engineering, and is highly respected in the
scientific community. As further described by Rice et al., an
"advantage of this [actuarial] method is that it accounts for
competing causes of death which act to remove a fraction of the
population each year from the risk of death from lung cancer so that it
is not necessary to assume that all workers would survive these
competing causes to a given age" (Document ID 1118, p. 40). Because
this life table method is generally accepted in the scientific
community and has been used in a variety of peer-reviewed, published
journal articles, including some of the key studies relied upon by the
Agency in its Preliminary QRA (e.g., Rice et al., 2001, Document ID
1118, p. 40; Park et al., 2002, 0405, p. 38), OSHA believes it is
appropriate here.
Regarding the alternative methods proposed by Dr. Cox, OSHA
believes that these methods are not widely used in the occupational
epidemiology community. In addition, OSHA notes that Dr. Cox did not
provide any alternate risk estimates to support the use of his proposed
alternative methods, despite the fact that the Agency made its life
table data available in the Review of Health Effects Literature and
Preliminary QRA (Document ID 1711, pp. 360-378). Thus, for these
reasons, OSHA disagrees with Dr. Cox's claim that the life table method
used by the Agency to estimate quantitative risks was inappropriate.
3. Exposure Metric
In its risk assessment, OSHA uses cumulative exposure, i.e.,
average exposure concentration multiplied by duration of exposure, as
the exposure metric to quantify exposure-response relationships. It
uses this metric because each of the key epidemiological studies on
which the Agency relied to estimate risks used cumulative exposure as
the exposure metric to quantify exposure-response relationships,
although some also reported significant relationships based on exposure
intensity (Document ID 1711, p. 342). As noted in the Review of Health
Effects Literature, the majority of studies for lung cancer and silicosis
morbidity and mortality have consistently found significant positive
relationships between risk and cumulative exposure (Document ID 1711,
p. 343). For example, nine of the ten epidemiological studies included
in the pooled analysis by Steenland et al. (2001a, Document ID 0452)
showed positive exposure coefficients when exposure was expressed as
cumulative exposure (Document ID 1711, p. 343).
Commenting on this exposure metric, the ACC argued that cumulative
exposure undervalues the role of exposure intensity, as some studies of
silicosis have indicated a dose-rate effect, i.e., short-term exposure
to high concentrations results in greater risk than longer-term
exposure to lower concentrations at an equivalent cumulative exposure
level (Document ID 4209, p. 58; 2307, Attachment A, pp. 93-94). The ACC
added that, given that silica-related lung cancer and silicosis may
both involve an inflammation-mediated mechanism, a dose-rate effect
would also be expected for lung cancer (Document ID 4209, p. 58). It
concluded that "assessments of risk based solely on cumulative
exposure do not account adequately for the role played by intensity of
exposure and, accordingly, do not yield reliable estimates of risk"
(Document ID 4209, p. 68). Patrick Hessel, Ph.D., representing the
Chamber, pointed to the initial comments of OSHA peer reviewer Kenneth
Crump, Ph.D., who stated that "[n]ot accounting for a dose-rate
effect, if one exists, could overestimate risk at lower
concentrations" (Document ID 4016, p. 2, citing 1716, pp. 165-167).
OSHA acknowledges these concerns regarding the exposure metric and
finds them to have some merit. However, it notes that the best
available studies use cumulative exposure as the exposure metric, as in
common in occupational epidemiological studies. As discussed below,
there is also substantial good evidence in the record supporting the
use of cumulative exposure as the exposure metric for crystalline
silica risk assessment.
Paul Schulte, Ph.D., of NIOSH testified that "cumulative exposure
is a standard and appropriate metric for irreversible effects that
occur soon after actual exposure is experienced. For lung cancer and
nonmalignant respiratory disease, NMRD mortality, cumulative exposure
lagged for cancer is fully justified...For silicosis risk
assessment purposes, cumulative exposure is a reasonable and practical
choice" (Document ID 3579, Tr. 127). NIOSH also conducted a simulated
dose rate analysis for silicosis incidence with data from a Chinese tin
miners cohort and, in comparing exposure metrics, concluded that the
best fit to the data was cumulative exposure with no dose-rate effect
(Document ID 4233, pp. 36-39). This finding is consistent with the
testimony of Dr. Steenland, who stated, "Cumulative exposure, I might
say, is often the best predictor of chronic disease in general, in
epidemiology" (Document ID 3580, Tr. 1227). OSHA also notes that using
a cumulative exposure metric (e.g., mg/m\3\-yrs) factors in both
exposure intensity and duration, while using only an exposure intensity
metric (e.g., [mu]g/m\3\) ignores the influence of exposure duration.
Dr. Crump's comment that "[e]stimating risk based on an `incomplete'
exposure metric like average exposure is not recommended....
[E]xposure to a particular air concentration for one week is unlikely
to carry the same risk as exposure to that concentration for 20 years,
although the average exposures are the same" also supports the use of
a cumulative exposure metric (Document ID 1716, p. 166).
With regard to a possible dose-rate effect, OSHA agrees with Dr.
Crump that if one exists and is unaccounted for, the result could be an
overestimation of risks at lower concentrations (Document ID 1716, pp.
165-167). OSHA is aware of two studies discussed in its Review of
Health Effects Literature and Preliminary QRA that examined dose-rate
effects on silicosis exposure-response (Document ID 1711, pp. 342-344).
Neither study found a dose-rate effect relative to cumulative exposure
at silica concentrations near the previous OSHA PEL (Document ID 1711,
pp. 342-344). However, they did observe a dose-rate effect in instances
where workers were exposed to crystalline silica concentrations far
above the previous PEL (i.e., several-fold to orders of magnitude above
100 [mu]g/m\3\) (Buchanan et al., 2003, Document ID 0306; Hughes et
al., 1998, 1059). For example, the Hughes et al. (1998) study of
diatomaceous earth workers found that the relationship between
cumulative silica exposure and risk of silicosis was steeper for
workers hired prior to 1950 and exposed to average concentrations above
500 [micro]g/m\3\ compared to workers hired after 1950 and exposed to
lower average concentrations (Document ID 1059). Similarly, the
Buchanan et al. (2003) study of Scottish coal miners adjusted the
cumulative exposure metric in the risk model to account for the effects
of exposures to high concentrations where the investigators found that,
at concentrations above 2000 [micro]g/m\3\, the risk of silicosis was
about three times higher than the risk associated with exposure to
lower concentrations but at the same cumulative exposure (Document ID
0306, p. 162). OSHA concluded that there is little evidence that a
dose-rate effect exists at concentrations in the range of the previous
PEL (100 [micro]g/m\3\) (Document ID 1711, p. 344). However, at the
suggestion of Dr. Crump, OSHA used the model from the Buchanan et al.
study in its silicosis morbidity risk assessment to account for
possible dose-rate effects at high average concentrations (Document ID
1711, pp. 335-342). OSHA notes that the risk estimates in the exposure
range of interest (25-500 [mu]g/m\3\) derived from the Buchanan et al.
(2003) study were not appreciably different from those derived from the
other studies of silicosis morbidity (see Section VI, Final
Quantitative Risk Assessment and Significance of Risk, Table VI-1.).
In its post-hearing brief, NIOSH also added that a "detailed
examination of dose rate would require extensive and real time exposure
history which does not exist for silica (or almost any other agent)"
(Document ID 4233, p. 36). Similarly, Dr. Crump wrote, "Having noted
that there is evidence for a dose-rate effect for silicosis, it may be
difficult to account for it quantitatively. The data are likely to be
limited by uncertainty in exposures at earlier times, which were likely
to be higher" (Document ID 1716, p. 167). OSHA agrees with Dr. Crump,
and believes that it has used the best available evidence to estimate
risks of silicosis morbidity and sufficiently accounted for any dose-
rate effect at high silica average concentrations by using the Buchanan
et al. (2003) study.
For silicosis/NMRD mortality, the ACC noted that Vacek et al.
(2009, Document ID 2307, Attachment 6) reported that, in their
categorical analysis of the years worked at various levels of exposure
intensity, only years worked at >200 [micro]g/m\3\ for silicosis and
>300 [micro]g/m\3\ for NMRD were associated with increased mortality
(Document ID 2307, Attachment A, p. 93, citing 2307, Attachment 6, pp.
21, 23). However, OSHA believes it to be inappropriate to consider
these results in isolation from the other study findings, and notes
that Vacek et al. (2009) also reported statistically significant
associations of silicosis mortality with cumulative exposure, exposure
duration, and average exposure intensity in their continuous analyses
with univariate models; for NMRD mortality, there were statistically
significant associations with cumulative exposure and average exposure
intensity (Document ID 2307, Attachment 6, pp. 21, 23).
In addition, OSHA notes that Vacek et al. (2009) did not include
both an exposure intensity term and a cumulative exposure term in the
multivariate model, after testing for correlation between cumulative
exposure and years at particular exposure intensity; such a model would
indicate how exposure intensity affects any relationship with
cumulative exposure. As Dr. Crump stated in his comments:
To demonstrate evidence for a dose-rate effect that is not
captured by cumulative exposure, it would be most convincing to show
some effect of dose rate that is in addition to the effect of
cumulative exposure. To demonstrate such an effect one would need to
model both cumulative exposure and some effect of dose rate, and
show that adding the effect of dose rate makes a statistically
significant improvement to the model over that predicted by
cumulative exposure alone (Document ID 1716, p. 166).
Indeed, both Buchanan et al. (2003, Document ID 0306) and Hughes et
al. (1998, Document ID 1059), when examining possible dose-rate effects
for silicosis morbidity, specifically included both cumulative exposure
and exposure intensity in their multivariate models. Additionally, as
described in the lung cancer section of this preamble, the Vacek et al.
study may be affected by both exposure misclassification and the
healthy worker survivor effect. Both of these biases may flatten an
exposure-response relationship, obscuring the relationship at lower
exposure levels, which could be the reason why a significant effect was
not found at the lower exposure levels in the Vacek et al. (2009,
Document ID 2307, Attachment 6) multivariate analysis.
Regarding lung cancer mortality, the ACC pointed out that Steenland
et al. (2001a, Document ID 0452) acknowledged that duration of exposure
did not fit the data well in their pooled lung cancer study. The ACC
indicated that exposure intensity should be considered (Document ID
2307, Attachment A, p. 93; 4209, p. 58, citing 0452, p. 779). OSHA
interpreted the results of the Steenland et al. (2001, Document ID
0452) study to simply mean that duration of exposure alone was not a
good predictor for lung cancer mortality, where a lag period may be
important between the exposure and the development of disease. Indeed,
Steenland et al. found the model with logged cumulative exposure, with
a 15-year lag, to be a strong predictor of lung cancer (Document ID
0452, p. 779). Additionally, no new evidence of a dose-rate effect in
lung cancer studies was submitted to the record.
For these reasons, OSHA does not believe there to be any persuasive
data in the record that supports a dose-rate effect at exposure
concentrations near the revised or previous PELs. OSHA concludes that
cumulative exposure is a reasonable exposure metric on which to base
estimates of risk to workers exposed to crystalline silica in the
exposure range of interest (25 to 500 [mu]g/m\3\).
N. Comments and Responses Concerning Physico-Chemical and Toxicological
Properties of Respirable Crystalline Silica
As discussed in the Review of Health Effects Literature and
Preliminary Quantitative Risk Assessment (Document ID 1711, pp. 344-
350), the toxicological potency of crystalline silica is influenced by
a number of physical and chemical factors that affect the biological
activity of the silica particles inhaled in the lung. The toxicological
potency of crystalline silica is largely influenced by the presence of
oxygen free radicals on the surfaces of respirable particles; these
chemically-reactive oxygen species interact with cellular components in
the lung to promote and sustain the inflammatory reaction responsible
for the lung damage associated with exposure to crystalline silica. The
reactivity of particle surfaces is greatest when crystalline silica has
been freshly fractured by high-energy work processes such as abrasive
blasting, rock drilling, or sawing concrete materials. As particles age
in the air, the surface reactivity decreases and exhibits lower
toxicologic potency (Porter et al., 2002, Document ID 1114; Shoemaker
et al., 1995, 0437; Vallyathan et al., 1995, 1128). In addition,
surface impurities have been shown to alter silica toxicity. For
example, aluminum and aluminosilicate clay on silica particles has been
shown to decrease toxicity (Castranova et al., 1997, Document ID 0978;
Donaldson and Borm, 1998, 1004; Fubini, 1998, 1016; Donaldson and Borm,
1998, Document ID 1004; Fubini, 1998, 1016).
In the preamble to the proposed standard, OSHA preliminarily
concluded that although there is evidence that several environmental
influences can modify surface activity to either enhance or diminish
the toxicity of silica, the available information was insufficient to
determine to what extent these influences may affect risk to workers in
any particular workplace setting (Document 1711, p. 350). NIOSH
affirmed OSHA's preliminary conclusion regarding the silica-related
risks of exposure to clay-occluded quartz particles, which was based on
what OSHA believed to be the best available evidence. NIOSH stated:
NIOSH concurs with this assessment by OSHA. Currently available
information is not adequate to inform differential quantitative risk
management approaches for crystalline silica that are based on
surface property measurements. Thus, NIOSH recommends a single PEL
for respirable crystalline silica without consideration of surface
properties (Document ID 4233, p. 44).
Two rulemaking participants, the Brick Industry Association (BIA),
which represents distributors and manufacturers of clay brick, and the
Sorptive Minerals Institute (SMI), which represents many industries
that process and mine sorptive clays for consumer products and
commercial and industrial applications, provided comment and supporting
evidence that the crystalline silica encountered in their workplace
environments presents a substantially lower risk of silica-related
disease than that reflected in the Agency's Preliminary QRA.
BIA argued that the quartz particles found in clays and shales used
in clay brick are occluded in aluminum-rich clay coatings. BIA
submitted to the record several studies indicating reduced toxicity and
fibrogenicity from exposure to quartz in aluminum-rich clays (Document
ID 2343, Attachment 2, p. 2). It purported that "OSHA lacks the
statutory authority to impose the proposed rule upon the brick and
structural clay manufacturing industry because employees in that
industry do not face a significant risk of material impairment of
health or functional capacity" (Document ID 2242, pp. 2-3). BIA
concluded that its industry should be exempted from the rule, stating:
"OSHA should exercise its discretion to exempt the brickmaking
industry from compliance with the proposed rule unless and until it
determines how best to take into account the industry's low incidence
of adverse health effects from silica toxicity" (Document ID 2242, p.
11).
SMI argued that silica in sorptive clays exists as either amorphous
silica or as geologically ancient, occluded quartz, "neither of which
pose the health risk identified and studied in OSHA's risk assessment"
(Document ID 4230, p. 2). SMI further contended that OSHA's discussion
of aged silica "does not accurately reflect the risk of geologically
ancient, (occluded) silica formed millions of years ago found in
sorptive clays" (Document ID 4230, p. 2). Additionally, SMI noted that
clay products produced by the sorptive minerals industry are not heated
to high temperatures or fractured, making them different from brick and
pottery clays (Document ID 2377, p. 7). In support of its position, SMI
submitted to the record several toxicity studies of silica in sorptive
clays. It stated that the evidence does not provide the basis for a
finding of a significant risk of material impairment of health from
exposure to silica in sorptive clays (Document ID 4230, p. 2).
Consequently, SMI concluded that the application of a reduced PEL and
comprehensive standard is not warranted.
Having considered the evidence SMI submitted to the record, OSHA
finds that although quartz originating from bentonite deposits exhibits
some biological activity, it is clear that it is considerably less
toxic than unoccluded quartz. Moreover, evidence does not exist that
would permit the Agency to evaluate the magnitude of the lifetime risk
resulting from exposure to quartz in bentonite-containing materials and
similar sorptive clays. This finding does not extend to the brick
industry, where workers are exposed to silica through occluded quartz
in aluminum rich clays. The Love et al. study (1999, Document ID 0369),
which BIA claimed would be of useful quality for OSHA's risk
assessment, shows sufficient cases of silicosis to demonstrate
significant risk within the meaning used by OSHA for regulatory
purposes. In addition, OSHA found a reduced, although still
significant, risk of silicosis morbidity in the study of pottery
workers (Chen et al., 2005, Document ID 0985) that BIA put forth as
being representative of mortality in the brick industry (Document ID
3577, Tr. 674). These findings are discussed in detail below.
1. The Clay Brick Industry
BIA did not support a reduction in the PEL because although brick
industry employees are exposed to crystalline silica-bearing materials,
BIA believes silicosis is virtually non-existent in that industry. It
contended that silica exposure in the brick industry does not cause
similar rates of disease as in other industries because brick industry
workers are exposed to quartz occluded in aluminum-rich layers,
reducing the silica's toxicity. BIA concluded that "no significant
workplace risk for brick workers from crystalline silica exposure
exists at the current exposure limit" (Document ID 3577, Tr. 654) and
that reducing the PEL would have no benefit to workers in the brick
industry (Document ID 2300, p. 2). These concerns were also echoed by
individual companies in the brick industry, such as Acme Brick
(Document ID 2085, Attachment 1), Belden Brick Company (Document ID
2378), and Riverside Brick & Supply Company, Inc. (Document ID 2346,
Attachment 1). In addition, OSHA received over 50 letters as part of a
letter campaign from brick industry representatives referring to BIA's
comments on the lack of silicosis in the brick industry (e.g., Document
ID 2004).
The Tile Council of North America, Inc., also noted that "[c]lay
raw materials used in tile manufacturing are similar to those used in
brick and sanitary ware manufacturing" and also suggested that
aluminosilicates decrease toxicity (Document ID 3528, p. 1). OSHA
agrees with the Tile Council of North America, Inc., that their
concerns mirror those of the BIA and, therefore, the Agency's
consideration and response to BIA also applies to the tile industry.
a. Evidence on the Toxicity of Silica in Clay Brick.
On behalf of BIA, Mr. Robert Glenn presented a series of published
and unpublished studies (Document ID 3418), also summarized by BIA
(Document ID 2300, Attachment 1) as evidence that "no significant
workplace risk for brick workers from crystalline silica exposure
exists at the current exposure limit" (Document ID 3577, Tr. 654).
Most of these studies, including an unpublished report on West Virginia
brick workers (West Virginia State Health Department, 1939), a study of
North Carolina brick workers (Trice, 1941), a study of brick workers in
England (Keatinge and Potter, 1949), a study of Canadian brick workers
(Ontario Health Department, 1972), two studies of North Carolina brick
workers (NIOSH, 1978 and NIOSH, 1980), a study of English and Scottish
brick workers (Love et al., 1999, Document ID 0369), and an unpublished
study commissioned by BIA of workers at 13 of its member companies
(BIA, 2006), reported little or no silicosis among the workers examined
(Document ID 3418; 3577, Tr. 655-669).
Based on its review of the record evidence, OSHA finds that there
are many silica-containing materials (e.g., other clays, sand, etc.) in
brick and concludes that BIA's position is not supported by the best
available evidence. The analysis contained in the studies Mr. Glenn
presents does not meet the rigorous standards used in the studies on
which OSHA's risk assessment relies. Indeed the studies cited by Mr.
Glenn and BIA do not adequately support their contention that silicosis
is "essentially non-existent." Several studies were poorly designed
and applied inappropriate procedures for evaluating chest X-rays
(Document ID 3577, Tr. 682-685). Dr. David Weissman of NIOSH
underscored the significance of such issues, stating: "It's very
important, for example, to use multiple [B] readers [to evaluate chest
X-rays] and medians of readings, and it is very important for people to
be blinded to how readings are done" (Document ID 3577, Tr. 682). Also
problematic was Mr. Glenn's failure to provide key information on the
length of exposure or time since the first exposure in any of the
studies he presented, which examined only currently employed workers.
Information on duration of exposure or time since first exposure is
essential to evaluating risk of silicosis because silicosis typically
develops slowly and becomes detectable between 10 years and several
decades following a worker's first exposure. In the hearing, Dr. Ken
Rosenman also noted inadequacies related to silicosis latency,
testifying that "we know that silicosis occurs 20, 30 years after . .
. first exposure...if people have high exposure but short duration,
short latency, you are not going to see positive x-rays [even if
silicosis is developing] and so it's not going to be useful" (Document
ID 3577, Tr. 688-689).
Mr. Glenn acknowledged shortcomings in the studies he submitted for
OSHA's consideration, agreeing with Dr. Weissman's points about quality
assurance for X-ray interpretation and study design (e.g., Document ID
3577, Tr. 683). In response to Dr. Rosenman's concerns about silicosis
latency, he reported that no information on worker tenure or time since
first exposure was presented in Trice (1941), Keatings and Potter
(1949), Rajhans and Buldovsky (1972), the NIOSH studies (1978, 1980),
or Love et al. (1999), and that more than half of the West Virginia
brick workers studied by NIOSH (1939) had a tenure of less than 10
years (Document ID 4021, pp. 5-6), a time period that OSHA believes is
too short to see development of most forms of silicosis. He suggested
that high exposures in two areas of the West Virginia facilities could
trigger accelerated or acute silicosis, which could be observed in less
than 10 years, if the toxicity of the silica in clay brick was
comparable to silica found in other industries (post-hearing comments,
p. 5). However, OSHA notes that a cross-sectional report on actively
employed workers would not necessarily capture cases of accelerated or
acute silicosis, which are associated with severe symptoms that compromise
individuals' ability to continue work, and therefore would result in a
survivor effect where only unaffected workers remain at the time of study.
Mr. Glenn further argued that the Agency should assess risk to
brick workers based on studies from that industry because the incidence
of silicosis among brick workers appears to be lower than among workers
in other industries (Document ID 3577, Tr. 670). For the reasons
discussed above, OSHA does not believe the studies submitted by Mr.
Glenn provide an adequate basis for risk assessment. In addition,
studies presented did not: (1) Include retired workers; (2) report the
duration of workers' exposure to silica; (3) employ, in most cases,
quality-assurance practices for interpreting workers' medical exams; or
(4) include estimates of workers' silica exposures. Furthermore, Mr.
Glenn acknowledged in the informal public hearing that the Love et al.
(1999, Document ID 0369) study of 1,925 workers employed at brick
plants in England and Scotland in 1990-1991 is the only available study
of brick workers that presented exposure-response information (Document
ID 3577, Tr. 692). He characterized the results of that study as
contradictory to OSHA's risk assessment for silicosis morbidity because
the authors concluded that frequency of pneumoconiosis is low in
comparison to other quartz-exposed workers (Document ID 4021, p. 2). He
also cited an analysis by Miller and Soutar (Document ID 1098) (Dr.
Soutar is a co-author of the Love et al. study) that compared silicosis
risk estimates derived from Love et al. and those from Buchanan et
al.'s study of Scottish coal workers exposed to silica, and concluded
that silicosis risk among the coal workers far exceeded that among
brick workers (Document ID 3577, Tr. 671). He furthermore concluded
that the Love et al. study is "the only sensible study to be used for
setting an exposure limit for quartz in brick manufacturing."
(Document ID 3577, Tr. 679).
Based on review of the Love et al. study (Document ID 0369), OSHA
agrees with Mr. Glenn's claim that the silicosis risk among workers in
clay brick industries appears to be somewhat lower than might be
expected in other industries. However, OSHA is unconvinced by Mr.
Glenn's argument that risk to workers exposed at the previous PEL is
not significant because the cases of silicosis reported in this study
are sufficient to show significant risk within the meaning used by OSHA
for regulatory purposes (1 in 1,000 workers exposed for a working
lifetime).
Love et al. reported that 3.7 percent of workers with radiographs
were classified as ILO Category 0/1 (any signs of small opacities) and
1.4 percent of workers were classified as ILO Category 1/0 (small
radiographic opacities) or greater. Furthermore, among workers aged 55
and older, the age category most likely to have had sufficient time
since first exposure to develop detectable lung abnormalities from
silicosis exposure, Love et al. reported prevalences of abnormal
radiographs ranging from 2.9 percent (cumulative exposure below 0.5 mg/
yr-m\3\) to 16.4 percent (exposure at least 4 mg/yr-m\3\) (Love et al.
1999, Document ID 0369, Table 4, p. 129). According to the study
authors, these abnormalities "are the most likely dust related
pathology--namely, silicosis" (Document ID 0369, p. 132). Given that
OSHA considers a lifetime risk of 0.1 percent (1 in 1,000) to clearly
represent a significant risk, OSHA considers the Love et al. study to
have demonstrated a significant risk to brick workers even if only a
tiny fraction of the abnormalities observed in the study population
represent developing silicosis (see Benzene, 448 U.S. 607, 655 n. 2).
According to the study authors, "the estimated exposure-response
relation for quartz suggests considerable risks of radiological
abnormality even at concentrations of 0.1 mg/m\3\ [100 [mu]g/m\3\] of
quartz" (Document ID 0369, p. 132).
OSHA concludes that, despite the possibly lower toxicity of silica
in the clay brick industry compared to other forms, and despite the
Love et al. study's likely underestimation of risk due to exclusion of
retired workers, the study demonstrates significant risk among brick
workers exposed at the previous general industry PEL. It also suggests
that the silicosis risk among brick workers would remain significant
even at the new PEL. Furthermore, OSHA is unconvinced by Mr. Glenn's
argument that the Agency should develop a quantitative risk assessment
based on the Love et al. study, because that study excluded retired
workers and had inadequate worker follow-up. As explained earlier in
this section, adequate follow-up time and inclusion of retired workers
is extremely important to allow for latency in the development of
silicosis. Therefore, OSHA relied on studies including retired workers
in its QRA for silicosis morbidity.
Mr. Glenn additionally argued that the risk of lung cancer from
silica exposure among brick workers is likely to be lower than among
workers exposed to silica in other work settings. Mr. Glenn
acknowledged that "there are no published mortality studies of brick
workers that look at cause of death or lung cancer death" (Document ID
3577, Tr. 674). However, he stated that "pottery clays are similar to
the structural clays used in brickmaking in that the quartz is occluded
in aluminum-rich layers of bentonite, kaolinite, and illite," and that
OSHA should consider studies of mortality among pottery workers as
representative of the brick industry (Tr. 674). Mr. Glenn cited the
Chen et al. (2005) study of Chinese pottery workers, which reported a
weak exposure-response relationship between silica exposure and lung
cancer mortality, and which appeared to be affected by PAH-related
confounding. He concluded that the Chen et al. study "provides strong
evidence for aluminum-rich clays suppressing any potential
carcinogenesis from quartz" (Document ID 3577, Tr. 675).
OSHA acknowledges that occlusion may weaken the carcinogenicity of
silica in the brick clay industry, but does not believe that the Chen
et al. study provides conclusive evidence of such an effect. This is
because of the relatively low carcinogenic potential of silica and the
difficulty involved in interpreting one cohort with known issues of
confounding (see Section V.F, Comments and Responses Concerning Lung
Cancer Mortality). OSHA also notes, however, that it estimated risks of
silicosis morbidity from the cited Chen et al. (2005, Document ID 0985)
study, and found the risk among pottery workers to be significant, with
60 deaths per 1,000 workers at the previous PEL of 100 [mu]g/
m3 and 20 deaths per 1,000 workers at the revised PEL of 50
[mu]g/m3 (as indicated in Section VI, Final Quantitative
Risk Assessment and Significance of Risk, Table VI-1). Thus, given Mr.
Glenn's assertion that pottery clays are similar to the clays used in
brickmaking, OSHA believes that while the risk of silicosis morbidity
may be lower than that seen in other industry sectors, it is likely to
still be significant in the brickmaking industry.
Thus, OSHA concludes that the BIA's position is not supported by
the best available evidence. The studies cited by Mr. Glenn to support
his contention that brick workers are not at significant risk of
silica-related disease do not have the same standards as those studies
used by OSHA in its quantitative risk assessment. Furthermore, in the
highest-quality study brought forward by Mr. Glenn (Love et al. 1999,
Document ID 0369), there are sufficient cases of silicosis to
demonstrate significant risk within the meaning used by OSHA for
regulatory purposes. Even if the commenters' arguments that silica in
clay brick is less toxic were, to some extent, legitimate, this would
not significantly affect OSHA's own estimates from the epidemiological
evidence of the risks of silicosis.
2. Sorptive Minerals (Bentonite Clay) Processing
SMI asserted that the physico-chemical form of respirable
crystalline silica in sorptive clays reduces the toxicologic potency of
crystalline silica relative to the forms of silica common to most
studies relied on in OSHA's Preliminary QRA. In other words, the risk
associated with exposure to silica in sorptive clays is assertedly
lower than the risk associated with exposure to silica in other
materials. SMI based this view on what it deemed the "best available
scientific literature," epidemiological, in vitro, and animal evidence
OSHA had not previously considered. It believed the evidence showed
reduced risk from exposure to occluded quartz found in the sorptive
clays and that occluded quartz does not create a risk similar to that
posed by freshly fractured quartz (Document ID 2377, p. 7). Based on
this, SMI contended that the results of OSHA's Preliminary QRA were not
applicable to the sorptive minerals industry, and a more stringent
standard for crystalline silica is "neither warranted nor legally
permissible" (Document ID 4230, p. 1). As discussed below, OSHA
reviewed the evidence submitted by SMI and finds that although the
studies provide evidence of some biological activity in quartz
originating from bentonite deposits, there is not quantitative evidence
that would permit the Agency to evaluate the magnitude of the lifetime
risk resulting from exposure to quartz in bentonite-containing
materials and similar sorptive clays.
a. Evidence on the Toxicity of Silica in Sorptive Minerals
SMI submitted a number of studies to the rulemaking record. First,
it summarized a retrospective study by Waxweiler et al. (Document ID
3998, Attachment 18e) of attapulgite clay workers in Georgia in which
the authors concluded that there was a significant deficit of non-
malignant respiratory disease mortality and no clear excess of lung
cancer mortality among these workers. It used the study as the basis
for its recommendation to OSHA that the study "be cited and that
exposures in the industry be recognized in the final rule as not posing
the same hazard as those in industries with reactive crystalline
silica" (Document ID 2377, p. 10).
Based on its review of the rulemaking record, OSHA concludes that
the Waxweiler et al. study is of limited value for assessing the hazard
potential of quartz in bentonite clay because of the low airborne
levels of silica to which the workers were exposed. The Agency's
conclusion is supported by NIOSH's summary of the time-weighted average
(TWA) exposures calculated for each job category in Waxweiler et al.
(1988, Document ID 3998, Attachment 18e), which were found to be
"within the acceptable limits as recommended by NIOSH (i.e., < 0.05 mg/
m3 [50 [mu]g/m3])...and most were
substantially lower" (Document ID 4233, p. 41). It cannot be known to
what extent the low toxicity of the dust or the low exposures
experienced by the workers each contributed to the lack of observed
disease.
SMI also presented a World Health Organization (WHO) document
(2005, Document ID 3929), which recognized that "studies of workers
exposed to sorptive clays have not identified significant silicosis
risk" (Document ID 2377, p. 10). However, although WHO did find that
there were no reported cases of fibrotic reaction in humans exposed to
montmorillonite minerals in the absence of crystalline silica (Document
ID 3929, p. 130), the WHO report does discuss the long-term effects
from exposure to crystalline silica, including silicosis and lung
cancer. In fact, with respect to evaluating the hazards associated with
exposure to bentonite clay, WHO regarded silica as a potential
confounder (Document ID 3929, p. 136). Thus, WHO did not specifically
make any findings with respect to the hazard potential of quartz in the
bentonite clay mineral matrix but instead recognized the hazard
presented by exposure to crystalline silica generally.
Additionally, the WHO (Document ID 3929, pp. 114, 118) cited two
case/case series reports of bentonite-exposed workers, one
demonstrating increasing prevalence of silicosis with increasing
exposure to bentonite dust (Rombola and Guardascione, 1955, Document ID
3998, Attachment 18) and another describing cases of silicosis among
workers exposed to bentonite dust (Phibbs et al. 1971, Document ID
3998, Attachment 18b). Rombola and Guardascione (1955) found silicosis
prevalences of 35.5 and 12.8 percent in two bentonite processing
factories, and 6 percent in a bentonite mine. In the factory where the
highest exposures occurred, 10 of the 26 cases found were severe and
all cases developed with seven or fewer years of exposure, indicating
that exposure levels were extremely high (Document ID 4233, p. 42,
citing 3998, Attachment 18). Phibbs et al. (1971) reviewed chest x-rays
of 32 workers in two bentonite plants, of which x-ray films for 14
indicated silicosis ranging from minimal to advanced. Although the
exposure of affected workers to respirable dust or quartz is not known,
industrial hygiene surveys conducted in four bentonite plants showed
some areas having particle counts in excess of 3 to 11 times the ACGIH
particle count limit (Document ID 3998, Attachment 18b, p. 4). This is
roughly equivalent to exposure levels between 8 and 28 times OSHA's
former general industry PEL of 100 [mu]g/m3 (given that the
particle count limit is about 2.5 or more times higher than the
gravimetric limit for respirable quartz (see Section V.C, Summary of
the Review of Health Effects Literature and Preliminary QRA). Exposures
of this magnitude are considerably higher than those experienced by
worker cohorts of the studies relied on by OSHA in its Final Risk
Assessment and discussed in Section V.C, Summary of the Review of
Health Effects Literature and Preliminary QRA. For example, the median
of average exposures reported in the ten cohort studies used by
Steenland et al. (2001, Document ID 0684, p. 775) ranged from about
one-half to six times the former general industry PEL.
The lack of specific exposure information on bentonite workers
found with silicosis, combined with the extraordinary exposures
experienced by workers in the bentonite plants studied by Phibbs et al.
(1971), make this study, while concerning, unsuitable for evaluating
risks in the range of the former and final rule PELs. OSHA notes that
the WHO report also concluded that available data were inadequate to
conclusively establish a dose-response relationship or even a cause-
and-effect relationship for bentonite dust, and that its role in
inducing pneumoconiosis remains uncertain.
SMI also presented evidence from animal and in vitro studies that
it believes shows that respirable crystalline quartz present in
sorptive clays exists in a distinct occluded form, which significantly
mitigates adverse health effects due to the physico-chemical
characteristics of the occluded quartz. As discussed below, based on
careful review of the studies SMI cited, OSHA believes these studies
indicate that silica in bentonite clay is of lower toxicologic potency
than that found in other industry sectors.
SMI submitted two studies: an animal study (Creutzenberg et al.
2008, Document ID 3891) and a study of the characteristics of quartz samples
isolated from bentonite (Miles et al. 2008, Document ID 4173). SMI
contended that these studies demonstrate the low toxicity potential of
geologically ancient occluded quartz found in sorptive clays (Document
ID 2377, pp. 8-9).
Creutzenberg et al. (2008) summarized the findings from a rat study
aimed at "characterizing the differences in biological activity
between crystalline ground reference quartz (DQ12) and a quartz with
occluded surfaces (quartz isolate) obtained from a clay deposit formed
110-112 million years ago" (Document ID 3891, p. 995). Based on
histopathological assessment of the lungs in each treatment group,
Creutzenberg et al. (2008, Document ID 3891) found that the DQ12
reference quartz group exhibited a significantly stronger inflammatory
reaction than the quartz isolate, which showed a slight but still
statistically significant inflammatory response compared to the control
group. The increased inflammatory response was observed at day 3 but
not at 28 or 90 days. Thus, reaction elicited by the quartz isolate,
thought to have similar properties to bentonite, was considered by the
investigators to represent a moderate effect that did not progress. In
light of this, the implications of this study for development of
silicosis are unclear.
SMI also cited Miles et al. (2008, Document ID 4173), who studied
the mineralogical and chemical characteristics of quartz samples
isolated from bentonite, including the quartz isolate used by
Creutzenberg et al. (2008) in their animal study. Their evaluation
identified several differences in the chemical and physical properties
of the quartz isolates and unoccluded quartz that could help explain
the observed differences in toxicity (Document ID 4173); these included
differences in crystal structure, electrical potential of particle
surfaces, and, possibly, differences in the reactivity of surface-free
radicals owing to the presence of iron ions in the residual clay
material associated with the quartz isolates.
With respect to the two studies just discussed, animal evidence
cited by SMI demonstrates that quartz in bentonite induces a modest
inflammatory reaction in the lung that does not persist (Creutzenberg
et al., 2008, Document ID 3891). Such a reaction is notably different
from the persistent and stronger response seen with standard
experimental quartz material without surface occlusion (Creutzenberg et
al., 2008, Document ID 3891). Physical and chemical characteristics of
quartz from bentonite deposits have been shown to differ from standard
experimental quartz in ways that can explain its reduced toxicity
(Miles et al., 2008, Document ID 4173). However, the animal studies
cited by SMI are not suitable for risk assessment since they were
short-term (90 days), single-dose experiments.
In sum, human evidence on the toxicity of quartz in bentonite clay
includes one study cited by SMI that did not find an excess risk of
respiratory disease (Waxweiller et al., Document ID 3998, Attachment
18e). However, because exposures experienced by the workers were low
with most less than that of the final rule PEL, the lack of an observed
effect cannot be solely attributed to the nature of the quartz
particles. Two studies of bentonite workers found a high prevalence of
silicosis based on x-ray findings (Rombola and Guardascione, 1955,
Document ID 3998, Attachment 18; Phibbs et al., 1971, Document ID 3998,
Attachment 18b). Limited exposure data provided in the studies as well
as the relatively short latencies seen among cases of severe silicosis
make it clear that the bentonite workers were exposed to extremely high
dust levels. Neither of these studies can be relied on to evaluate
disease risk in the exposure range of the former and revised respirable
crystalline silica PELs.
OSHA finds that the evidence for quartz originating from bentonite
deposits indicates some biological activity, but also indicates lower
toxicity than standard experimental quartz (which has similar
characteristics to quartz encountered in most workplaces where
exposures occur). For regulatory purposes, however, OSHA finds that the
evidence does not exist that would permit the Agency to evaluate the
magnitude of the lifetime risk resulting from exposure to quartz in
sorptive clays at the 100 [mu]g/m\3\ PEL. Instead, OSHA finds that the
record provides no sound basis for determining the significance of risk
for exposure to sorptive clays containing respirable quartz. Thus, OSHA
is excluding sorptive clays (as described specifically in the Scope
part of Section XV, Summary and Explanation) from the scope of the
rule, until such time that sufficient science has been developed to
permit evaluation of the significance of the risk. However, in
excluding sorptive clays from the rule, the general industry PEL, as
described in 29 CFR 1910.1000 Table Z-3, will continue to apply.
VI. Final Quantitative Risk Assessment and Significance of Risk
A. Introduction
To promulgate a standard that regulates workplace exposure to toxic
materials or harmful physical agents, OSHA must first determine that
the standard reduces a "significant risk" of "material impairment."
Section 6(b)(5) of the OSH Act, 29 U.S.C. 655(b). The first part of
this requirement, "significant risk," refers to the likelihood of
harm, whereas the second part, "material impairment," refers to the
severity of the consequences of exposure. Section II, Pertinent Legal
Authority, of this preamble addresses the statutory bases for these
requirements and how they have been construed by the Supreme Court and
federal courts of appeals.
It is the Agency's practice to estimate risk to workers by using
quantitative risk assessment and determining the significance of that
risk based on the best available evidence. Using that evidence, OSHA
identifies material health impairments associated with potentially
hazardous occupational exposures, and, when possible, provides a
quantitative assessment of exposed workers' risk of these impairments.
The Agency then evaluates whether these risks are severe enough to
warrant regulatory action and determines whether a new or revised rule
will substantially reduce these risks. For single-substance standards
governed by section 6(b)(5) of the OSH Act, 29 U.S.C. 655(b)(5), OSHA
sets a permissible exposure limit (PEL) based on that risk assessment
as well as feasibility considerations. These health and risk
determinations are made in the context of a rulemaking record in which
the body of evidence used to establish material impairment, assess
risks, and identify affected worker population, as well as the Agency's
preliminary risk assessment, are placed in a public rulemaking record
and subject to public comment. Final determinations regarding the
standard, including final determinations of material impairment and
risk, are thus based on consideration of the entire rulemaking record.
In this case, OSHA reviewed extensive toxicological,
epidemiological, and experimental research pertaining to the adverse
health effects of occupational exposure to respirable crystalline
silica, including silicosis, other non-malignant respiratory disease
(NMRD), lung cancer, and autoimmune and renal diseases. Using the
information collected during this review, the Agency
developed quantitative estimates of the excess risk of mortality and
morbidity attributable to the previously allowed and revised respirable
crystalline silica PELs; these estimates were published with the
proposed rule. The Agency subsequently reexamined these estimates in
light of the rulemaking record as a whole, including comments,
testimony, data, and other information, and has determined that long-
term exposure at and above the previous PELs would pose a significant
risk to workers' health, and that adoption of the new PEL and other
provisions of the final rule will substantially reduce this risk. Based
on these findings, the Agency is adopting a new PEL of 50 [mu]g/m\3\.
Even though OSHA's risk assessment indicates that a significant
risk also exists at the revised action level of 25 [mu]g/m\3\, the
Agency is not adopting a PEL below the revised 50 [mu]g/m\3\ limit
because OSHA must also consider the technological and economic
feasibility of the standard in determining exposure limits. As
explained in the Summary and Explanation for paragraph (c), Permissible
Exposure Limit (PEL), of the general industry/maritime standard
(paragraph (d) for construction), OSHA has determined that, with the
adoption of additional engineering and work practice controls, the
revised PEL of 50 [mu]g/m\3\ is technologically and economically
feasible in most operations in the affected general industrial and
maritime sectors and in the construction industry, but that a lower PEL
of 25 [mu]g/m\3\ is not technologically feasible for most of these
operations (see Section VII, Summary of the Final Economic Analysis and
Final Regulatory Flexibility Analysis (FEA) and Chapter IV,
Technological Feasibility, of the FEA). Therefore, OSHA concludes that
by establishing the 50 [mu]g/m\3\ PEL, the Agency has reduced
significant risk to the extent feasible.
B. OSHA's Findings of Material Impairments of Health
As discussed below and in OSHA's Review of Health Effects
Literature and Preliminary QRA (Document ID 1711, pp. 7-229), there is
convincing evidence that inhalation exposure to respirable crystalline
silica increases the risk of a variety of adverse health effects,
including silicosis, NMRD (such as chronic bronchitis and emphysema),
lung cancer, kidney disease, immunological effects, and infectious
tuberculosis (TB). OSHA considers each of these conditions to be a
material impairment of health. These diseases make it difficult or
impossible to work and result in significant and permanent functional
limitations, reduced quality of life, and sometimes death. When these
diseases coexist, as is common, the effects are particularly
debilitating (Rice and Stayner, 1995, Document ID 0418; Rosenman et
al., 1999, 0421). Based on these findings and on the scientific
evidence that respirable crystalline silica substantially increases the
risk of each of these conditions, OSHA has determined that exposure to
respirable crystalline silica increases the risk of "material
impairment of health or functional capacity" within the meaning of the
Occupational Safety and Health Act.
1. Silicosis
OSHA considers silicosis, an irreversible and potentially fatal
disease, to be a clear material impairment of health. The term
"silicosis" refers to a spectrum of lung diseases attributable to the
inhalation of respirable crystalline silica. As described more fully in
the Review of Health Effects Literature (Document ID 1711, pp. 16-71),
the three types of silicosis are acute, accelerated, and chronic. Acute
silicosis can occur within a few weeks to months after inhalation
exposure to extremely high levels of respirable crystalline silica.
Death from acute silicosis can occur within months to a few years of
disease onset, with the affected person drowning in his or her own lung
fluid (NIOSH, 1996, Document ID 0840). Accelerated silicosis results
from exposure to high levels of airborne respirable crystalline silica,
and disease usually occurs within 5 to 10 years of initial exposure
(NIOSH, 1996, Document ID 0840). Both acute and accelerated silicosis
are associated with exposures that are substantially above the previous
general industry PEL, although no precise information on the
relationships between exposure and occurrence of disease exists.
Chronic silicosis is the most common form of silicosis seen today,
and is a progressive and irreversible condition characterized as a
diffuse nodular pulmonary fibrosis (NIOSH, 1996, Document ID 0840).
Chronic silicosis generally occurs after 10 years or more of inhalation
exposure to respirable crystalline silica at levels below those
associated with acute and accelerated silicosis. Affected workers may
have a dry chronic cough, sputum production, shortness of breath, and
reduced pulmonary function. These symptoms result from airway
restriction caused by the development of fibrotic scarring in the lower
regions of the lungs. The scarring can be detected in chest x-ray films
when the lesions become large enough to appear as visible opacities.
The result is a restriction of lung volumes and decreased pulmonary
compliance with concomitant reduced gas transfer. Chronic silicosis is
characterized by small, rounded opacities that are symmetrically
distributed in the upper lung zones on chest radiograph (Balaan and
Banks, 1992, Document ID 0289, pp. 347, 350-351).
The diagnosis of silicosis is based on a history of exposure to
respirable crystalline silica, chest radiograph findings, and the
exclusion of other conditions that appear similar. Because workers
affected by early stages of chronic silicosis are often asymptomatic,
the finding of opacities in the lung is key to detecting silicosis and
characterizing its severity. The International Labour Organization
(ILO) International Classification of Radiographs of Pneumoconioses
(ILO, 1980, Document ID 1063; 2002, 1064) is the currently accepted
standard against which chest radiographs are evaluated for use in
epidemiological studies, medical surveillance, and clinical evaluation.
The ILO system standardizes the description of chest x-rays, and is
based on a 12-step scale of severity and extent of silicosis as
evidenced by the size, shape, and density of opacities seen on the x-
ray film. Profusion (frequency) of small opacities is classified on a
4-point major category scale (0-3), with each major category divided
into three, giving a 12-point scale between 0/- and 3/+. Large
opacities are defined as any opacity greater than 1 cm that is present
in a film (ILO, 1980, Document ID 1063; 2002, 1064, p. 6).
The small rounded opacities seen in early stage chronic silicosis
(ILO major category 1 profusion) may progress (through ILO major
categories 2 and/or 3) and develop into large fibrotic masses that
destroy the lung architecture, resulting in progressive massive
fibrosis (PMF). This stage of advanced silicosis is usually
characterized by impaired pulmonary function, permanent disability, and
premature death. In cases involving PMF, death is commonly attributable
to progressive respiratory insufficiency (Balaan and Banks, 1992,
Document ID 0289).
Patients with ILO category 2 or 3 background profusion of small
opacities are at increased risk, compared to those with category 1
profusion, of developing the large opacities characteristic of PMF. In
one study of silicosis patients in Hong Kong, Ng and Chan (1991,
Document ID 1106, p. 231) found the risk of PMF increased by 42 and 64
percent among patients whose chest x-ray films were classified as
ILO major category 2 or 3, respectively. Research has shown that
people with silicosis advanced beyond ILO major category 1 have
reduced life expectancy compared to the general population
(Infante-Rivard et al., 1991, Document ID 1065; Ng et al., 1992a,
0383; Westerholm, 1980, 0484).
Silicosis is the oldest known occupational lung disease and is
still today the cause of significant premature mortality. As discussed
further in Section V.E, Comments and Responses Concerning Surveillance
Data on Silicosis Morbidity and Mortality, in 2013, there were 111
deaths in the U.S. where silicosis was recorded as an underlying or
contributing cause of death on a death certificate (NCHS data). Between
1996 and 2005, deaths attributed to silicosis resulted in an average of
11.6 years of life lost by affected workers (NIOSH, 2007, Document ID
1362). In addition, exposure to respirable crystalline silica remains
an important cause of morbidity and hospitalizations. National
inpatient hospitalization data show that in the year 2011, 2,082
silicosis-related hospitalizations occurred, indicating that silicosis
continues to be a significant health issue in the U.S. (Document ID
3577, Tr. 854-855). Although there is no national silicosis disease
surveillance system in the U.S., a published analysis of state-based
surveillance data from the time period 1987-1996 estimated that between
3,600-7,000 new cases of silicosis occurred in the U.S. each year
(Rosenman et al., 2003, Document ID 1166).
It has been widely reported that available statistics on silicosis-
related mortality and morbidity are likely to be understated due to
misclassification of causes of death (for example, as tuberculosis,
chronic bronchitis, emphysema, or cor pulmonale), lack of occupational
information on death certificates, or misdiagnosis of disease by health
care providers (Goodwin et al., 2003, Document ID 1030; Windau et al.,
1991, 0487; Rosenman et al., 2003, 1166). Furthermore, reliance on
chest x-ray findings may miss cases of silicosis because fibrotic
changes in the lung may not be visible on chest radiograph; thus,
silicosis may be present absent x-ray signs or may be more severe than
indicated by x-ray (Hnizdo et al., 1993, Document ID 1050; Craighhead
and Vallyahan, 1980, 0995; Rosenman et al., 1997, 4181).
Although most workers with early-stage silicosis (ILO categories 0/
1 or 1/0) typically do not experience respiratory symptoms, the primary
risk to the affected worker is progression of disease with progressive
decline of lung function. Several studies of workers exposed to
crystalline silica have shown that, once silicosis is detected by x-
ray, a substantial proportion of affected workers can progress beyond
ILO category 1 silicosis, even after exposure has ceased (e.g., Hughes,
1982, Document ID 0362; Hessel et al., 1988, 1042; Miller et al., 1998,
0374; Ng et al., 1987a, 1108; Yang et al., 2006, 1134). In a population
of coal miners whose last chest x-ray while employed was classified as
major category 0, and who were examined again 10 years after the mine
had closed, 20 percent had developed opacities consistent with a
classification of at least 1/0, and 4 percent progressed further to at
least 2/1 (Miller et al., 1998, Document ID 0374). Although there were
periods of extremely high exposure to respirable quartz in the mine
(greater than 2,000 [mu]g/m\3\ in some jobs between 1972 and 1976, and
more than 10 percent of exposures between 1969 and 1977 were greater
than 1,000 [mu]g/m\3\), the mean cumulative exposure for the cohort
over the period 1964-1978 was 1.8 mg/m\3\-yrs, corresponding to an
average silica concentration of 120 [mu]g/m\3\. In a population of
granite quarry workers exposed to an average respirable silica
concentration of 480 [mu]g/m\3\ (mean length of employment was 23.4
years), 45 percent of those diagnosed with simple silicosis (i.e.,
presence of small opacities only on chest x-ray films) showed
radiological progression of disease after 2 to 10 years of follow up
(Ng et al., 1987a, Document ID 1108). Among a population of gold
miners, 92 percent progressed in 14 years; exposures of high-, medium-,
and low-exposure groups were 970, 450, and 240 [mu]g/m\3\, respectively
(Hessel et al., 1988, Document ID 1042). Chinese mine and factory
workers categorized under the Chinese system of x-ray classification as
"suspected" silicosis cases (analogous to ILO 0/1) had a progression
rate to stage I (analogous to ILO major category 1) of 48.7 percent,
and the average interval was about 5.1 years (Yang et al., 2006,
Document ID 1134).
The risk of silicosis carries with it an increased risk of reduced
lung function as the disease irreversibly progresses. There is strong
evidence in the literature for the finding that lung function
deteriorates more rapidly in workers exposed to silica, especially
those with silicosis, than what is expected from a normal aging process
(Cowie, 1988, Document ID 0993; Hughes et al., 1982, 0362; Malmberg et
al., 1993, 0370; Ng and Chan, 1992, 1107). The rates of decline in lung
function are greater in those whose disease showed evidence of
radiologic progression (Begin et al., 1987, Document ID 0295; Cowie,
1988, 0993; Ng and Chan, 1992, 1107; Ng et al., 1987a, 1108).
Additionally, the average deterioration of lung function exceeds that
in smokers (Hughes et al., 1982, Document ID 0362).
Several studies have reported no decrease in pulmonary function
with an ILO category 1 level of profusion of small opacities but found
declines in pulmonary function with categories 2 and 3 (Ng et al.,
1987a, Document ID 1108; Begin et al., 1988, 0296; Moore et al., 1988,
1099). However, one study found a statistically significantly greater
annual loss in forced vital capacity (FVC) and forced expiratory volume
in one second (FEV1) among those with category 1 profusion
compared to category 0 (Cowie, 1988, Document ID 0993). In another
study, the degree of profusion of opacities was associated with
reductions in several pulmonary function metrics (Cowie and Mabena,
1991, Document ID 0342). Some studies have reported no associations
between radiographic silicosis and decreases in pulmonary function (Ng
et al., 1987a, Document ID 1108; Wiles et al., 1972, 0485; Hnizdo,
1992, 1046), while other studies (Ng et al., 1987a, Document ID 1108;
Wang et al., 1997, 0478) have found that measurable changes in
pulmonary function are evident well before the changes seen on chest x-
ray. Findings of pulmonary function decrements absent radiologic signs
of silicosis may reflect the general insensitivity of chest radiography
in detecting lung fibrosis, or may also reflect that exposure to
respirable silica has been shown to increase the risk of non-malignant
respiratory disease (NMRD) and its attendant pulmonary function losses
(see Section V.C, Summary of the Review of Health Effects Literature
and Preliminary QRA).
Moreover, exposure to respirable crystalline silica in and of
itself, with or without silicosis, increases the risk that latent
tuberculosis infection can convert to active disease. Early
descriptions of dust diseases of the lung did not distinguish between
TB and silicosis, and most fatal cases described in the first half of
this century were a combination of silicosis and TB (Castranova et al.,
1996, Document ID 0314). More recent findings demonstrate that exposure
to silica, even without silicosis, increases the risk of infectious
(i.e., active) pulmonary TB (Sherson and Lander, 1990, Document ID
0434; Cowie, 1994, 0992; Hnizdo and Murray, 1998, 0360; teWaterNaude et
al., 2006, 0465). Both conditions together can hasten the development
of respiratory impairment and increase mortality risk even beyond that
experienced by persons with active TB who have not been exposed to
respirable crystalline silica (Banks, 2005, Document ID 0291).
Based on the information presented above and in its review of the
health literature, OSHA concludes that silicosis remains a significant
cause of early death and of serious illness, despite the existence of
an enforceable exposure limit over the past 40 years. Silicosis in its
later stages of progression (i.e., with chest x-ray findings of ILO
category 2 or 3 profusion of small opacities, or the presence of large
opacities) is characterized by the likely appearance of respiratory
symptoms and decreased pulmonary function, as well as increased risk of
progression to PMF, disability, and early mortality. Early-stage
silicosis, although without symptoms among many who are affected,
nevertheless reflects the formation of fibrotic lesions in the lung and
increases the risk of progression to later stages, even after exposure
to respirable crystalline silica ceases. In addition, the presence of
silicosis increases the risk of pulmonary infections, including
conversion of latent TB infection to active TB. Silicosis is not a
reversible condition, and there is no specific treatment for the
disease, other than administration of drugs to alleviate inflammation
and maintain open airways, or administration of oxygen therapy in
severe cases. Based on these considerations, OSHA finds that silicosis
of any form, and at any stage of progression, is a material impairment
of health and that fibrotic scarring of the lungs represents loss of
functional respiratory capacity.
2. Lung Cancer
OSHA considers lung cancer, an irreversible and frequently fatal
disease, to be a clear material impairment of health (see Homer et al.,
2009, Document ID 1343). According to the National Cancer Institute
(SEER Cancer Statistics Review, 2006, Document ID 1343), the five-year
survival rate for all forms of lung cancer is only 15.6 percent, a rate
that has not improved in nearly two decades. After reviewing the record
as a whole, OSHA finds that respirable crystalline silica exposure
substantially increases the risk of lung cancer. This finding is based
on the best available toxicological and epidemiological data, reflects
substantial supportive evidence from animal and mechanistic research,
and is consistent with the conclusions of other government and public
health organizations, including the International Agency for Research
on Cancer (1997, Document ID 1062; 2012, Document ID 1473), the HHS
National Toxicology Program (2000, Document ID 1417), the CDC's
National Institute for Occupational Safety and Health (2002, Document
ID 1110), the American Thoracic Society (1997, Document ID 0283), and
the American Conference of Governmental Industrial Hygienists (2010,
Document ID 0515).
The Agency's primary evidence comes from evaluation of more than 50
studies of occupational cohorts from many different industry sectors in
which exposure to respirable crystalline silica occurs, including:
Granite and stone quarrying; the refractory brick industry; gold, tin,
and tungsten mining; the diatomaceous earth industry; the industrial
sand industry; and construction. In addition, the association between
exposure to respirable crystalline silica and lung cancer risk was
reported in a national mortality surveillance study (Calvert et al.,
2003, Document ID 0309) and in two community-based studies (Pukkala et
al., 2005, Document ID 0412; Cassidy et al., 2007, 0313), as well as in
a pooled analysis of 10 occupational cohort studies (Steenland et al.,
2001a, Document ID 0452). Toxicity studies provide supportive evidence
of the carcinogenicity of crystalline silica, in that they demonstrate
biologically plausible mechanisms by which crystalline silica in the
deep lung can give rise to biochemical and cellular events leading to
tumor development (see Section V.H, Mechanisms of Silica-Induced
Adverse Health Effects).
3. Non-Malignant Respiratory Disease (NMRD) (Other Than Silicosis)
Although many of the stakeholders in this rule have focused their
attention on the evidence related to silicosis and lung cancer, the
available evidence shows that exposure to respirable crystalline silica
also increases the risk of developing NMRD, in particular chronic
bronchitis and emphysema. OSHA has determined that NMRD, which results
in loss of pulmonary function that restricts normal activity in
individuals afflicted with these conditions (see American Thoracic
Society, 2003, Document ID 1332), constitutes a material impairment of
health. Both chronic bronchitis and emphysema can occur in conjunction
with the development of silicosis. Several studies have documented
increased prevalence of chronic bronchitis and emphysema among silica-
exposed workers even absent evidence of silicosis (see Document ID
1711, pp. 182-192; NIOSH, 2002, 1110; American Thoracic Society, 2003,
1332). There is also evidence that smoking may have an additive or
synergistic effect on silica-related NMRD morbidity or mortality
(Hnizdo, 1990, Document ID 1045; Hnizdo et al., 1990, 1047; Wyndham et
al., 1986, 0490; NIOSH, 2002, 1110). In a study of diatomaceous earth
workers, Park et al. (2002, Document ID 0405) found a positive
exposure-response relationship between exposure to respirable
cristobalite (a form of silica) and increased mortality from NMRD.
Decrements in pulmonary function have often been found among
workers exposed to respirable crystalline silica absent radiologic
evidence of silicosis. Several cross-sectional studies have reported
such findings among granite workers (Theriault et al., 1974a, Document
ID 0466; Wallsh, 1997, 0477; Ng et al., 1992b, 0387; Montes II et al.,
2004b, 0377), gold miners (Irwig and Rocks, 1978, Document ID 1067;
Hnizdo et al., 1990, 1047; Cowie and Mabena, 1991, 0342), gemstone
cutters (Ng et al., 1987b, Document ID 1113), concrete workers (Meijer
et al., 2001, Document ID 1243), refractory brick workers (Wang et al.,
1997, Document ID 0478), hard rock miners (Manfreda et al., 1982,
Document ID 1094; Kreiss et al., 1989, 1079), pottery workers (Neukirk
et al., 1994, Document ID 0381), slate workers (Surh, 2003, Document ID
0462), and potato sorters exposed to silica in diatomaceous earth
(Jorna et al, 1994, Document ID 1071).
OSHA also evaluated several longitudinal studies where exposed
workers were examined over a period of time to track changes in
pulmonary function. Among both active and retired granite workers
exposed to an average of 60 [mu]g/m \3\, Graham et al. did not find
exposure-related decrements in pulmonary function (1981, Document ID
1280; 1984, 0354). However, Eisen et al. (1995, Document ID 1010) did
find significant pulmonary decrements among a subset of granite workers
(termed "dropouts") who left work and consequently did not
voluntarily participate in the last of a series of annual pulmonary
function tests. This group of workers experienced steeper declines in
FEV1 compared to the subset of workers who remained at work and
participated in all tests (termed "survivors"), and these declines
were significantly related to dust exposure. Thus, in this study,
workers who had left work had exposure-related declines in pulmonary
function to a greater extent than did workers who remained on the job,
clearly demonstrating a survivor effect among the active workers.
Exposure-related changes in lung function were also reported in a
12-year study of granite workers (Malmberg, 1993, Document ID 0370),
in two 5-year studies of South African miners (Hnizdo, 1992,
Document ID 1046; Cowie, 1988, 0993), and in a study of foundry workers
whose lung function was assessed between 1978 and 1992 (Hertzberg et
al., 2002, Document ID 0358).
Each of these studies reported their findings in terms of rates of
decline in any of several pulmonary function measures, such as FVC,
FEV1, and FEV1/FVC. To put these declines in
perspective, Eisen et al. (1995, Document ID 1010) reported that the
rate of decline in FEV1 seen among the dropout subgroup of
Vermont granite workers was 4 ml per mg/m\3\-yrs of exposure to
respirable granite dust; by comparison, FEV1 declines at a
rate of 10 ml/year from smoking one pack of cigarettes daily. From
their study of foundry workers, Hertzberg et al., reported finding a
1.1 ml/year decline in FEV1 and a 1.6 ml/year decline in FVC
for each mg/m\3\-yrs of respirable silica exposure after controlling
for ethnicity and smoking (2002, Document ID 0358, p. 725). From these
rates of decline, they estimated that exposure to the previous OSHA
general industry quartz standard of 100 [micro]g/m\3\ for 40 years
would result in a total loss of FEV1 and FVC that is less
than but still comparable to smoking a pack of cigarettes daily for 40
years. Hertzberg et al. also estimated that exposure to the current
standard for 40 years would increase the risk of developing abnormal
FEV1 or FVC by factors of 1.68 and 1.42, respectively (2002, Document
ID 0358, pp. 725-726). OSHA believes that this magnitude of reduced
pulmonary function, as well as the increased morbidity and mortality
from non-malignant respiratory disease (NMRD) that has been documented
in the studies summarized above, constitute material impairments of
health and loss of functional respiratory capacity.
4. Renal and Autoimmune Effects
Finally, OSHA's review of the literature reflects substantial
evidence that exposure to crystalline silica increases the risk of
renal and autoimmune diseases, both of which OSHA considers to be
material impairments of health (see Section V.C, Summary of the Review
of Health Effects Literature and Preliminary QRA). Epidemiological
studies have found statistically significant associations between
occupational exposure to silica dust and chronic renal disease (e.g.,
Calvert et al., 1997, Document ID 0976), subclinical renal changes
including proteinurea and elevated serum creatinine (e.g., Ng et al.,
1992c, Document ID 0386; Rosenman et al., 2000, 1120; Hotz, et al.,
1995, 0361), end-stage renal disease morbidity (e.g., Steenland et al.,
1990, Document ID 1125), chronic renal disease mortality (Steenland et
al., 2001b, Document ID 0456; 2002a, 0448), and granulomatosis with
polyangitis (Nuyts et al., 1995, Document ID 0397). Granulomatosis with
polyangitis is characterized by inflammation of blood vessels, leading
to damaging granulomatous formation in the lung and damage to the
glomeruli of the kidneys, a network of capillaries responsible for the
first stage of blood filtration. If untreated, this condition often
leads to renal failure (Nuyts et al., 1995, Document ID 0397, p. 1162).
Possible mechanisms for silica-induced renal disease include a direct
toxic effect on the kidney and an autoimmune mechanism (see Section
V.H, Mechanisms of Silica-Induced Adverse Health Effects; Calvert et
al., 1997, Document ID 0976; Gregorini et al., 1993, 1032). Steenland
et al. (2002a, Document ID 0448) demonstrated a positive exposure-
response relationship between exposure to respirable crystalline silica
and end-stage renal disease mortality.
In addition, there are a number of studies that show exposure to be
related to increased risks of autoimmune disease, including scleroderma
(e.g., Sluis-Cremer et al., 1985, Document ID 0439), rheumatoid
arthritis (e.g., Klockars et al., 1987, Document ID 1075; Rosenman and
Zhu, 1995, 0424), and systemic lupus erythematosus (e.g., Brown et al.,
1997, Document ID 0974). Scleroderma is a degenerative disorder that
leads to over-production of collagen in connective tissue that can
cause a wide variety of symptoms including skin discoloration and
ulceration, joint pain, swelling and discomfort in the extremities,
breathing problems, and digestive problems. Rheumatoid arthritis is
characterized by joint pain and tenderness, fatigue, fever, and weight
loss. Systemic lupus erythematosus is a chronic disease of connective
tissue that can present a wide range of symptoms including skin rash,
fever, malaise, joint pain, and, in many cases, anemia and iron
deficiency. OSHA considers chronic renal disease, end-stage renal
disease mortality, granulomatosis with polyangitis, scleroderma,
rheumatoid arthritis, and systemic lupus erythematosus clearly to be
material impairments of health.
C. OSHA's Final Quantitative Risk Estimates
To evaluate the significance of the health risks that result from
exposure to hazardous chemical agents, OSHA relies on epidemiological
and experimental data, as well as statistical methods. The Agency uses
these data and methods to characterize the risk of disease resulting
from workers' exposure to a given hazard over a working lifetime at
levels of exposure reflecting both compliance with previous standards
and compliance with the new standard. In the case of respirable
crystalline silica, the previous general industry, construction, and
shipyard PELs were formulas that limit 8-hour TWA exposures to
respirable dust; the limit on exposure decreased with increasing
crystalline silica content of the dust. OSHA's previous general
industry PEL for respirable quartz was expressed both in terms of a
particle count and a gravimetric concentration, while the previous
construction and shipyard employment PELs for respirable quartz were
only expressed in terms of a particle count formula. For general
industry, the gravimetric formula PEL for quartz approaches 100
[micro]g/m\3\ of respirable crystalline silica when the quartz content
of the dust is about 10 percent or greater. The previous PEL's particle
count formula for the construction and shipyard industries is equal to
a range of about 250 [mu]g/m\3\ to 500 [mu]g/m\3\ expressed as
respirable quartz. In general industry, the previous PELs for
cristobalite and tridymite, which are forms (polymorphs) of silica,
were one-half the PEL for quartz.
In this final rule, OSHA has established a uniform PEL for
respirable crystalline silica by revising the PELs applicable to
general industry, construction, and maritime to 50 [mu]g/m\3\ TWA of
respirable crystalline silica. OSHA has also established an action
level of 25 [micro]g/m\3\ TWA. In this section of the preamble, OSHA
presents its final estimates of health risks associated with a working
lifetime (45 years) of exposure to 25, 50, and 100 [micro]g/m\3\
respirable crystalline silica. These levels represent the risks
associated with exposure over a working lifetime to the new action
level, new PEL, and previous general industry PEL, respectively. OSHA
also presents estimates associated with exposure to 250 and 500
[micro]g/m\3\ to represent a range of risks likely to be associated
with exposure to the former construction and shipyard PELs. Risk
estimates are presented for mortality due to lung cancer, silicosis and
other non-malignant respiratory disease (NMRD), and end-stage renal
disease, as well as silicosis morbidity. These estimates are the
product of OSHA's risk assessment, following the Agency's
consideration of new data introduced into the rulemaking record and
of the numerous comments in the record that raised questions about
OSHA's preliminary findings and analysis.
After reviewing the evidence and testimony in the record, OSHA has
determined that it is appropriate to base its final risk estimates on
the same studies and models as were used in the NPRM (see Section V.C,
Summary of the Review of Health Effects Literature and Preliminary
QRA). For mortality risk estimates, OSHA used the models developed by
various investigators and employed a life table analysis to implement
the models using the same background all-cause mortality data and
consistent assumption for length of lifetime (85 years). The life table
is a technique that allows estimation of excess risk of disease
mortality factoring in the probability of surviving to a particular age
assuming no exposure to the agent in question and given the background
probability of dying from any cause at or before that age (see Section
V.M, Comments and Responses Concerning Working Life, Life Tables, and
Dose Metric). Since the time of OSHA's preliminary analysis, the
National Center for Health Statistics (NCHS) released updated all-cause
mortality background rates from 2011; these rates are available in an
internet web-based query by year and 2010 International Classification
of Diseases (ICD) code through the Centers of Disease Control and
Prevention (CDC) Wonder database (http://wonder.cdc.gov/udc-icd10.html).
Using these updated statistics, OSHA revised its life table analyses
to estimate lifetime risks of mortality that result from 45 years
of exposure to respirable crystalline silica. OSHA's final quantitative
mortality risk estimates are presented in Table VI-1 below.
For silicosis morbidity risk estimates, OSHA relied on the
cumulative risk models developed by investigators of five studies who
conducted studies relating cumulative disease risk to cumulative
exposure to respirable crystalline silica (see footnotes to Table VI-
1). Of these, only one, the study by Steenland and Brown (1995) of U.S.
gold miners, employed a life-table analysis. Table VI-1 also presents
OSHA's final quantitative estimates of silicosis morbidity risks.
BILLING CODE 4510-26-P
BILLING CODE 4510-26-C
OSHA notes that the updated risk estimates are not substantially
different from those presented in the Preliminary QRA; for example, for
exposure at the previous general industry PEL approaching 100 [mu]g/
m\3\, the excess lung cancer mortality risk ranged from 13 to 60 deaths
per 1,000 workers using the original 2006 background data, and from 11
to 54 deaths per 1,000 workers using the updated 2011 background data.
For exposure at the revised PEL of 50 [mu]g/m\3\, the risk estimates
ranged from 6 to 26 deaths per 1,000 workers using the 2006 background
data, and 5 to 23 deaths per 1,000 workers using the 2011 background
data. Similarly, the updated risk estimates for NMRD are not
substantially different; for example, for exposure for 45 working years
at the previous general industry PEL approaching 100 [mu]g/m\3\, the
excess NMRD mortality risk, using the Park et al. (2002, Document 0405)
model was 83 deaths per 1,000 workers using the original 2006
background data, and 85 deaths per 1,000 workers using the updated 2011
background data. For exposure at the revised PEL of 50 [mu]g/m\3\, the
risk estimate was 43 deaths per 1,000 workers using the 2006 background
data, and 44 deaths per 1,000 workers using the 2011 background data.
OSHA also presents in the table the excess lung cancer mortality
risk associated with 45 years of exposure to the previous construction/
shipyard PEL (in the range of 250 to 500 [micro]g/m\3\). It should be
noted, however, that exposure to 250 or 500 [micro]g/m\3\ over 45 years
represents cumulative exposures of 11.25 and 22.5 mg/m\3\-yrs,
respectively, which are well above the median cumulative exposure for
most of the cohorts used in the risk assessment. Estimating excess
risks over this higher range of cumulative exposures required some
degree of extrapolation, which adds uncertainty. In addition, at
cumulative exposures as high as permitted by the previous construction
and maritime PELs, silica-related causes of mortality will compete with
each other and it is difficult to determine the risk of any single
cause of mortality in the face of such competing risks.
OSHA's final risk estimates for renal disease reflect the 1998
background all-cause mortality and renal mortality rates for U.S.
males, rather than the 2011 rates used for lung cancer and NMRD, as
updated in the previous sections. Background rates were not adjusted
for the renal disease risk estimates because the CDC significantly
changed the classification of renal diseases after 1998; they are now
inconsistent with those used by Steenland et al. (2002a, Document ID
0448), the study relied on by OSHA, to ascertain the cause of death of
workers in their study. OSHA notes that the change in classification
system, from ICD-9 to ICD-10, did not materially affect background
rates for diseases grouped as lung cancer or NMRD. The findings from
OSHA's final risk assessment are summarized below.
OSHA notes that the key studies in its final risk assessment were
composed of cohorts with cumulative exposures relevant to those permitted
by the preceding General Industry PEL (45 years of exposure at 100 [mu]g/m\3\
equals 4.5 mg/m\3\-yrs). Table VI-2 provides the reported cumulative
exposure information for each of the cohorts of the key studies. Most
of these cohorts had mean or median cumulative exposures below 4.5 mg/
m\3\-yrs. Based on this data, OSHA concludes that the cumulative
exposures experienced by the cohorts are relevant and reasonable for
use in the Agency's final risk assessment.
1. Summary of Excess Risk Estimates for Lung Cancer Mortality
For estimates of lung cancer risk from crystalline silica exposure,
OSHA has relied upon studies of exposure-response relationships
presented in a pooled analysis of 10 cohort studies (Steenland et al.,
2001a, Document ID 0452; ToxaChemica, Inc., 2004, 0469) as well as on
individual studies of granite (Attfield and Costello, 2004, Document ID
0543), diatomaceous earth (Rice et al., 2001, Document ID 1118), and
industrial sand (Hughes et al., 2001, Document ID 1060) worker cohorts,
and a study of coal miners exposed to respirable crystalline silica
(Miller et al., 2007, Document ID 1305; Miller and MacCalman, 2009,
1306). OSHA found these studies to have been suitable for use to
quantitatively characterize health risks to exposed workers because:
(1) Study populations were of sufficient size to provide adequate
statistical power to detect low levels of risk; (2) sufficient
quantitative exposure data were available over a sufficient span of
time to characterize cumulative exposures of cohort members to
respirable crystalline silica; (3) the studies either adjusted for or
otherwise adequately addressed confounding factors such as smoking and
exposure to other carcinogens; and (4) investigators developed
quantitative assessments of exposure-response relationships using
appropriate statistical models or otherwise provided sufficient
information that permits OSHA to do so. OSHA implemented all risk
models in its own life table analysis so that the use of background
lung cancer rates and assumptions regarding length of exposure and
lifetime were consistent across each of the models, and so OSHA could
estimate lung cancer risks associated with exposure to specific levels
of silica of interest to the Agency.
The Steenland et al. (2001a, Document ID 0452) study consisted of a
pooled exposure-response analysis and risk assessment based on raw data
obtained for ten cohorts of silica-exposed workers (65,980 workers,
1,072 lung cancer deaths). The cohorts in this pooled analysis include
U.S. gold miners (Steenland and Brown, 1995a, Document ID 0450), U.S.
diatomaceous earth workers (Checkoway et al., 1997, Document ID 0326),
Australian gold miners (de Klerk and Musk, 1998, Document ID 0345),
Finnish granite workers (Koskela et al., 1994, Document ID 1078), South
African gold miners (Hnizdo et al., 1997, Document ID 1049), U.S.
industrial sand workers (Steenland et al., 2001b, Document ID 0456),
Vermont granite workers (Costello and Graham, 1988, Document ID 0991),
and Chinese pottery workers, tin miners, and tungsten miners (Chen et
al., 1992, Document ID 0329). To determine the exposure-response
relationship between silica exposures and lung cancer, the
investigators used a nested case-control design with cases and controls
matched for race, sex, age (within five years), and study; 100 controls
were matched for each case. An extensive exposure assessment for this
pooled analysis was developed and published by Mannetje et al. (2002a,
Document ID 1090).
Using ToxaChemica's study (2004, Document ID 0469) of this pooled
data, the estimated excess lifetime lung cancer risk associated with 45
years of exposure to 100 [mu]g/m\3\ (about equal to the previous
general industry PEL) is between 20 and 26 deaths per 1,000 workers.
The estimated excess lifetime risk associated with 45 years of exposure
to silica concentrations in the range of 250 and 500 [mu]g/m\3\ (about
equal to the previous construction and shipyard PELs) is between 24 and
33 deaths per 1,000. At the final PEL of 50 [mu]g/m\3\, the estimated
excess lifetime risk ranges from 16 to 23 deaths per 1,000, and, at the
action level of 25 [mu]g/m\3\, from 10 to 21 deaths per 1,000.
In addition to the pooled cohort study, OSHA's Final Quantitative
Risk Assessment presents risk estimates in Table VI-1 derived from four
individual studies where investigators presented either lung cancer
risk estimates or exposure-response coefficients. Two of these studies,
one on diatomaceous earth workers (Rice et al., 2001, Document ID 1118)
and one on Vermont granite workers (Attfield and Costello, 2004,
Document ID 0543), were included in the 10-cohort pooled study
(Steenland et al., 2001a, Document ID 0452; ToxaChemica Inc., 2004,
0469). The other two were of British coal miners (Miller et al., 2007,
Document ID 1305; Miller and MacCalman, 2009,1306) and North American
industrial sand workers (Hughes et al., 2001, Document ID 1060).
Rice et al. (2001, Document ID 1118) presented an exposure-response
analysis of the diatomaceous worker cohort studied by Checkoway et al.
(1993, Document ID 0324; 1996, 0325; 1997, 0326), who found a
significant relationship between exposure to respirable cristobalite
and increased lung cancer mortality. From this cohort the estimates of
the excess risk of lung cancer mortality are 30, 15, and 8 deaths per
1,000 workers for 45 years of exposure to 100, 50, and 25 [mu]g/m\3\,
respectively. For exposures in the range of the current construction
and shipyard PELs over 45 years, estimated risks lie in a range between
72 and 137 excess deaths per 1,000 workers.
Somewhat higher risk estimates are derived from the analysis
presented by Attfield and Costello (2004, Document ID 0543) of Vermont
granite workers. OSHA's use of this analysis yielded a risk estimate of
54 excess deaths per 1,000 workers for 45 years of exposure to the
previous general industry PEL of 100 [mu]g/m\3\, 22 excess deaths per
1,000 for 45 years of exposure to the final PEL of 50 [mu]g/m\3\, and
10 excess deaths per 1,000 for 45 years of exposure at the action level
of 25 [mu]g/m\3\. Estimated excess risks associated with 45 years of
exposure at the current construction PEL range from 231 to 657 deaths
per 1,000.
Hughes et al. (2001, Document ID 1060) conducted a study of
industrial sand workers in the U.S. and Canada. Using this study, OSHA
estimated cancer risks of 33, 14, and 7 deaths per 1,000 for 45 years
exposure to the previous general industry PEL of 100 [mu]g/m\3\, the
final PEL of 50 [mu]g/m\3\, and the final action level of 25 [mu]g/m\3\
respirable crystalline silica, respectively. For 45 years of exposure
to the previous construction PEL, estimated risks range from 120 to 407
deaths per 1,000 workers.
Miller and MacCalman (2010, Document ID 1306; also reported in
Miller et al., 2007, Document ID 1305) presented a study of miners from
10 coal mines in the U.K. Based on this study, OSHA estimated the
lifetime lung cancer mortality risk to be 11 per 1,000 workers for 45
years of exposure to 100 [mu]g/m\3\ respirable crystalline silica. For
the final PEL of 50 [mu]g/m\3\ and action level of 25 [mu]g/m\3\, the
lifetime risks are estimated to be 5 and 3 deaths per 1,000,
respectively. The range of risks estimated to result from 45 years of
exposure to the previous construction and shipyard PELs is from 33 to
86 deaths per 1,000 workers.
2. Summary of Risk Estimates for Silicosis and Other Chronic Lung
Disease Mortality
OSHA based its quantitative assessment of silicosis mortality risks
on a pooled analysis conducted by Mannetje et al. (2002b, Document ID
1089) of data from six of the ten epidemiological studies in the
Steenland et al. (2001a, Document ID 0452) pooled analysis of lung
cancer mortality that also included extensive data on silicosis.
Cohorts included in the silicosis study were: U.S. diatomaceous earth
workers (Checkoway et al., 1997, Document ID 0326); Finnish granite
workers (Koskela et al., 1994, Document ID 1078); U.S. granite workers
(Costello and Graham, 1988, Document ID 0991); U.S. industrial sand workers
(Silicosis and Silicate Disease Committee, 1988, Document ID 0455);
U.S. gold miners (Steenland and Brown, 1995b, Document ID 0451); and
Australian gold miners (de Klerk and Musk, 1998, Document ID 0345).
These six cohorts contained 18,634 workers and 170 silicosis deaths,
where silicosis mortality was defined as death from silicosis (ICD-9
502, n = 150) or from unspecified pneumoconiosis (ICD-9 505, n = 20).
Although Mannetje et al, (2002b, Document ID 1089) estimated silicosis
risks from a Poisson regression, a subsequent analysis was conducted by
Steenland and Bartell (ToxaChemica, 2004, Document ID 0469) based on a
case control design. Based on the Steenland and Bartell analysis, OSHA
estimated that the lifetime risk of silicosis mortality associated with
45 years of exposure to the previous general industry PEL of 100 [mu]g/
m\3\ is 11 deaths per 1,000 workers. Exposure for 45 years to the final
PEL of 50 [mu]g/m\3\ results in an estimated 7 silicosis deaths per
1,000, and exposure for 45 years to the final action level of 25 [mu]g/
m\3\ results in an estimated 4 silicosis deaths per 1,000. Lifetime
risks associated with exposure at the previous construction and
shipyard PELs range from 17 to 22 deaths per 1,000 workers.
To study non-malignant respiratory diseases (NMRD), of which
silicosis is one, Park et al. (2002, Document ID 0405) analyzed the
California diatomaceous earth cohort data originally studied by
Checkoway et al. (1997, Document ID 0326). The authors quantified the
relationship between exposure to cristobalite and mortality from NMRD.
Diseases in this category included pneumoconiosis (which includes
silicosis), chronic bronchitis, and emphysema, but excluded pneumonia
and other infectious diseases. Because of the broader range of silica-
related diseases examined by Park et al., OSHA's estimates of the
lifetime chronic lung disease mortality risk based on this study are
substantially higher than those that OSHA derived from the Mannetje et
al. (2002b, Document ID 1089) silicosis analysis. For the previous
general industry PEL of 100 [mu]g/m\3\, exposure for 45 years is
estimated to result in 85 excess deaths per 1,000 workers. At the final
PEL of 50 [mu]g/m\3\ and action level of 25 [mu]g/m\3\, OSHA estimates
the lifetime risk from 45 years of exposure to be 44 and 22 excess
deaths per 1,000, respectively. The range of risks associated with
exposure at the former construction and shipyard PELs over a working
lifetime is from 192 to 329 excess deaths per 1,000 workers.
3. Summary of Risk Estimates for Renal Disease Mortality
OSHA's analysis of the health effects literature included several
studies that have demonstrated that exposure to respirable crystalline
silica increases the risk of renal and autoimmune disease (see Document
ID 1711, Review of Health Effects Literature and Preliminary QRA, pp.
208-229). For autoimmune disease, there was insufficient data on which
to base a quantitative risk assessment. OSHA's assessment of the renal
disease risks that result from exposure to respirable crystalline
silica is based on an analysis of pooled data from three cohort studies
(Steenland et al., 2002a, Document ID 0448). The combined cohort for
the pooled analysis (Steenland et al., 2002a, Document ID 0448)
consisted of 13,382 workers and included industrial sand workers
(Steenland et al., 2001b, Document ID 0456), U.S. gold miners
(Steenland and Brown, 1995a, Document ID 0450), and Vermont granite
workers (Costello and Graham, 1988, Document ID 0991). Exposure data
were available for 12,783 workers and analyses conducted by the
original investigators demonstrated monotonically increasing exposure-
response trends for silicosis, indicating that exposure estimates were
not likely subject to significant random misclassification. The mean
duration of exposure, cumulative exposure, and concentration of
respirable silica for the combined cohort were 13.6 years, 1.2 mg/m\3\-
years, and 70 [mu]g/m\3\, respectively. There were highly statistically
significant trends for increasing renal disease mortality with
increasing cumulative exposure for both multiple cause analysis of
mortality (p < 0.000001) and underlying cause analysis (p = 0.0007).
OSHA's estimates of renal disease mortality risk based on this study
are 39 deaths per 1,000 for 45 years of exposure at the previous
general industry PEL of 100 [mu]g/m\3\, 32 deaths per 1,000 for
exposure at the final PEL of 50 [mu]g/m\3\, and 25 deaths per 1,000 at
the action level of 25 [mu]g/m\3\. OSHA also estimates that 45 years of
exposure at the previous construction and shipyard PELs would result in
a renal disease excess mortality risk ranging from 52 to 63 deaths per
1,000 workers. OSHA acknowledges that the risk estimates for end-stage
renal disease mortality are less robust than those for silicosis, lung
cancer, and NMRD, and are thus more uncertain.
4. Summary of Risk Estimates for Silicosis Morbidity
OSHA's Final Quantitative Risk Assessment is based on several
cross-sectional studies designed to characterize relationships between
exposure to respirable crystalline silica and development of silicosis
as determined by chest radiography. Due to the long latency periods
associated with silicosis, OSHA relied on those studies that were able
to contact and evaluate many of the workers who had retired. OSHA
believes that relying on studies that included retired workers comes
closest to characterizing lifetime risk of silicosis morbidity. OSHA
identified studies of six cohorts for which the inclusion of retirees
was deemed sufficient to adequately characterize silicosis morbidity
risks well past employment (Hnizdo and Sluis-Cremer, 1991, Document ID
1051; Steenland and Brown, 1995b, 0451; Miller et al., 1998, 0374;
Buchanan et al., 2003, 0306; Chen et al., 2001, 0332; Chen et al.,
2005, 0985). Study populations included five mining cohorts and a
Chinese pottery worker cohort. With the exception of a coal miner study
(Buchanan et al., 2003, Document ID 0306), risk estimates reflected the
risk that a worker will acquire an abnormal chest x-ray classified as
ILO major category 1 or greater; the coal miner study evaluated the
risk of acquiring an abnormal chest x-ray classified as major category
2 or higher.
For miners exposed to freshly cut respirable crystalline silica,
OSHA estimates the risk of developing lesions consistent with an ILO
classification of category 1 or greater to range from 120 to 773 cases
per 1,000 workers exposed at the previous general industry PEL of 100
[mu]g/m\3\ for 45 years; from 20 to 170 cases per 1,000 workers exposed
at the final PEL of 50 [mu]g/m\3\; and from 5 to 40 cases per 1,000
workers exposed at the new action level of 25 [mu]g/m\3\. From the coal
miner study of Buchanan et al., (2003, Document ID 0306), OSHA
estimates the risks of acquiring an abnormal chest x-ray classified as
ILO category 2 or higher to be 301, 55, and 21 cases per 1,000 workers
exposed for 45 years to 100, 50, and 25 [mu]g/m\3\, respectively. These
estimates are within the range of risks obtained by OSHA from the other
mining studies. At exposures at or above 250 [mu]g/m\3\ (equivalent to
the previous construction and shipyard PELs) for 45 years, the risk of
acquiring an abnormal chest x-ray approaches 100 percent. OSHA's risk
estimates based on the pottery cohort are 60, 20, and 5 cases per 1,000
workers exposed for 45 years to 100, 50, and 25 [mu]g/m\3\,
respectively, which is generally below the range of risks estimated
from the other studies and may reflect a lower toxicity of quartz
particles in that work environment due to the presence of
aluminosilicates on the particle surfaces (see Section V.N, Comments
and Responses Concerning Physico-chemical and Toxicological Properties
of Respirable Crystalline Silica); they are still well over OSHA's 1 in
a 1,000 workers benchmark for setting standards, however. According to
Chen et al. (2005, Document ID 0985), adjustment of the exposure metric
to reflect the unoccluded surface area of silica particles resulted in
an exposure-response of pottery workers that was similar to the mining
cohorts, indicating that the occluded surface reduced the toxic potency
of the quartz particles. The finding of a reduced silicosis risk among
pottery workers is consistent with other studies of clay and brick
industries that have reported finding a lower prevalence of silicosis
compared to that experienced in other industry sectors (Love et al.,
1999, Document ID 0369; Hessel, 2006, 1299; Miller and Soutar, 2007,
1098) as well as a lower silicosis risk per unit of cumulative exposure
(Love et al., 1999, Document ID 0369; Miller and Soutar, 2007, 1098).
D. Significance of Risk and Risk Reduction
In this section, OSHA presents its final findings with respect to
the significance of the risks summarized above and the potential of the
proposed standard to reduce those risks. Findings related to mortality
risk will be presented first, followed by silicosis morbidity risks.
1. Mortality Risks
OSHA's Final Quantitative Risk Assessment described above presents
risk estimates for four causes of excess mortality: Lung cancer,
silicosis, non-malignant respiratory disease (including silicosis), and
renal disease. Table VI-1 above presents OSHA's estimated excess
lifetime risks (i.e., to age 85, following 45 years of occupational
exposure) of these fatal diseases associated with various levels of
respirable crystalline silica exposure allowed under the former PELs
and the final PEL and action level promulgated herein. OSHA's mortality
risk estimates represent "excess" risks in the sense that they
reflect the risk of dying from disease over and above that of persons
who are not occupationally exposed to respirable crystalline silica.
Assuming a 45-year working life, as OSHA has done in significant
risk determinations for previous standards, the Agency finds that the
excess risk of disease mortality related to exposure to respirable
crystalline silica at levels permitted by the previous OSHA standards
is clearly significant. The Agency's estimate of such risk falls well
above the level of risk the Supreme Court indicated a reasonable person
would consider unacceptable (Benzene, 448 U.S. 607, 655). For lung
cancer, OSHA estimates the range of risk at the previous general
industry PEL to be between 11 and 54 deaths per 1,000 workers. The
estimated risk for silicosis mortality is 11 deaths per 1,000 workers;
however, the estimated lifetime risk for non-malignant respiratory
disease (NMRD) mortality, including silicosis, is about 8-fold higher
than that for silicosis alone, at 85 deaths per 1,000. This higher
estimate for NMRD is better than the estimate for silicosis mortality
at capturing the total respiratory disease burden associated with
exposure to crystalline silica dust. The former captures deaths related
to other non-malignant diseases, including chronic bronchitis and
emphysema, for which there is strong evidence of a causal relationship
with exposure to silica, and is also more likely to capture those
deaths where silicosis was a contributing factor but where the cause of
death was misclassified. Finally, there is an estimated lifetime risk
of renal disease mortality of 39 deaths per 1,000. Exposure for 45
years at levels of respirable crystalline silica in the range of the
previous limits for construction and shipyards results in even higher
risk estimates, as presented in Table VI-1. It should be noted that
these risk estimates are not additive because some individuals may
suffer from multiple diseases caused by exposure to silica.
To further demonstrate significant risk, OSHA compares the risks at
the former PELs and the revised PEL for respirable crystalline silica
to risks found across a broad variety of occupations. OSHA also
compares the lung cancer risk associated with the former PELs and
revised PEL to the risks for other carcinogens OSHA regulates. The
Agency has used similar occupational risk comparisons in the
significant risk determinations for other substance-specific standards.
Fatal injury rates for most U.S. industries and occupations may be
obtained from data collected by the Department of Labor's Bureau of
Labor Statistics (BLS). Table VI-3 shows annual fatality rates per
1,000 employees for several industries for 2013, as well as projected
fatalities per 1,000 employees assuming exposure to workplace hazards
for 45 years based on these annual rates. While it is difficult to
meaningfully compare aggregate industry fatality rates to the risks
estimated in the quantitative risk assessment for respirable
crystalline silica, which address one specific hazard (inhalation
exposure to respirable crystalline silica) and several health outcomes
(lung cancer, silicosis, NMRD, renal disease mortality), these rates
provide a useful frame of reference for considering risk from
inhalation exposure to crystalline silica. For example, OSHA's
estimated range of 5-54 excess lung cancer deaths per 1,000 workers
from regular occupational exposure to respirable crystalline silica in
the range of 50-100 [mu]g/m\3\ is roughly comparable to, or higher
than, the expected risk of fatal injuries over a working life in high-
risk occupations such as mining and construction (see Table VI-3).
Regular exposures at higher levels, including the previous construction
and shipyard PELs for respirable crystalline silica, are expected to
cause substantially more deaths per 1,000 workers from lung cancer
alone (ranging from 24 to 657 per 1,000) than result from occupational
injuries in most private industry. At the final PEL of 50 [mu]g/
m3 respirable crystalline silica, the Agency's estimate of
excess lung cancer mortality, from 5 to 23 deaths per 1,000 workers, is
still 3- to 15-fold higher than private industry's average fatal injury
rate, given the same employment time, and substantially exceeds those
rates found in lower-risk industries such as finance and educational
and health services. Adding in the mortality from silicosis, NMRD, and
renal disease would make these comparisons even more stark.
Because there is little available information on the incidence of
occupational cancer across all industries, risk from crystalline silica
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, as with the current assessment for respirable crystalline
silica, were based on animal or human data of reasonable or high
quality and used the best information then available. Table VI-4 shows
the Agency's best estimates of cancer risk from 45 years of
occupational exposure to several carcinogens, as published in the
preambles to final rules promulgated since the Benzene decision in
1980.
The estimated excess lung cancer mortality risks associated with
respirable crystalline silica at the previous general industry PEL, 11-
54 deaths per 1,000 workers, are comparable to, and in some cases
higher than, the estimated excess cancer risks for many other workplace
carcinogens for which OSHA made a determination of significant risk
(see Table VI-4, "Selected OSHA Risk Estimates for Prior and Current
PELs"). The estimated excess lung cancer risks associated with
exposure to the previous construction and shipyard PELs are even
higher. The estimated risk from lifetime occupational exposure to
respirable crystalline silica at the final PEL of 50 [mu]g/m\3\ is 5-23
excess lung cancer deaths per 1,000 workers, a range still higher than
the risks from exposure to many other carcinogens regulated by OSHA.
OSHA's risk assessment also shows that reduction of the PELs for
respirable crystalline silica to the final level of 50 [mu]g/m\3\ will
result in substantial reduction in risk, although quantitative
estimates of that reduction vary depending on the statistical models
used. Risk models that reflect attenuation of the risk with increasing
exposure, such as those relating risk to a log transformation of
cumulative exposure, will result in lower estimates of risk reduction
compared to linear risk models. Thus, for lung cancer risks, the
assessment based on the 10-cohort pooled analysis by Steenland et al.
(2001, Document ID 0455; also 0469; 1312) suggests risk will be reduced
by about 14 percent from the previous general industry PEL and by 28-41
percent from the previous construction/shipyard PEL (based on the
midpoint of the ranges of estimated risk derived from the three models
used for the pooled cohort data). These risk reduction estimates,
however, are much lower than those derived from the single cohort
studies (Rice et al., 2001, Document ID 1118; Attfield and Costello,
2004, 0543; Hughes et al., 2001, 1060; Miller and MacCalman 2009,
1306). These single cohort studies suggest that reducing the previous
PELs to the final PEL will reduce lung cancer risk by more than 50
percent in general industry and by more than 80 percent in construction
and shipyards.
For silicosis mortality, OSHA's assessment indicates that risk will
be reduced by 36 percent and by 58-68 percent as a result of reducing
the previous general industry and construction/shipyard PELs,
respectively. NMRD mortality risks will be reduced by 48 percent and by
77-87 percent as a result of reducing the general industry and
construction/shipyard PELs, respectively, to the new PEL. There is also
a substantial reduction in renal disease mortality risks; an 18-percent
reduction associated with reducing the previous general industry PEL
and a 38-49 percent reduction associated with reducing the previous
construction/shipyard PEL.
Thus, OSHA believes that the final PEL of 50 [mu]g/m\3\ respirable
crystalline silica will substantially reduce the risk of material
health impairments associated with exposure to silica. However, even at
this final PEL, as well as the action level of 25 [mu]g/m\3\, the risk
posed to workers with 45 years of regular exposure to respirable
crystalline silica is greater than 1 per 1,000 workers and is still
clearly significant.
2. Silicosis Morbidity Risks
OSHA's Final Quantitative Risk Assessment also characterizes the
risk of developing silicosis, defined as developing lung fibrosis
detected by chest x-ray. For 45 years of exposure at the previous
general industry PEL of 100 [mu]g/m\3\, OSHA estimates that the risk of
developing lung fibrosis consistent with an ILO category 1+ degree of
small opacity profusion ranges from 60 to 773 cases per 1,000. For
exposure at the previous construction and shipyard PELs, the risk
approaches 100 percent. The wide range of risk estimates derived from
the underlying studies relied on for the risk assessment may reflect
differences in the relative toxicity of quartz particles in different
workplaces; nevertheless, OSHA finds that each of these risk estimates
clearly represents a significant risk of developing fibrotic lesions in
the lung. Exposure to the final PEL of 50 [mu]g/m\3\ respirable
crystalline silica for 45 years yields an estimated risk of between 20
and 170 cases per 1,000 for developing fibrotic lesions consistent with
an ILO category of 1+. These risk estimates indicate that the final PEL
will result in a reduction in risk by about two-thirds or more, which
the Agency finds is a substantial reduction of the risk of developing
abnormal chest x-ray findings consistent with silicosis.
One study of coal miners also permitted the agency to evaluate the
risk of developing lung fibrosis consistent with an ILO category 2+
degree of profusion of small opacities (Buchanan et al., 2003, Document
ID 0306). This level of profusion has been shown to be associated with
a higher prevalence of lung function decrement and an increased rate of
early mortality (Ng et al., 1987a, Document ID 1108; Begin et al.,
1988, 0296; Moore et al., 1988, 1099; Ng et al., 1992a, 0383; Infante-
Rivard, 1991, 1065). From this study, OSHA estimates that the risk
associated with 45 years of exposure to the previous general industry
100 [mu]g/m\3\ PEL is 301 cases per 1,000 workers, again a clearly
significant risk. Exposure to the final PEL of 50 [mu]g/m\3\ respirable
crystalline silica for 45 years yields an estimated risk of 55 cases
per 1,000 for developing lesions consistent with an ILO category 2+
degree of small opacity profusion. This represents a reduction in risk
of over 80 percent, again a clearly substantial reduction of the risk
of developing radiologic silicosis consistent with ILO category 2+.
3. Sources of Uncertainty and Variability in OSHA's Risk Assessment
Throughout the development of OSHA's risk assessment for silica-
related health effects, sources of uncertainty and variability have
been identified by the Agency, peer reviewers, interagency reviewers,
stakeholders, scientific experts, and the general public. This
subsection reviews and summarizes several general areas of uncertainty
and variability in OSHA's risk assessment. As used in this section,
"uncertainty" refers to lack of knowledge about factors affecting
exposure or risk, and "variability" refers to heterogeneity, for
example, across people, places, or time. For more detailed discussion
and evaluation of sources of uncertainty in the risk assessment and a
comprehensive review of comments received by OSHA on the risk
assessment, (see discussions provided throughout the previous section,
Section V, Health Effects).
As shown in Table VI-1, OSHA's risk estimates for lung cancer are a
range derived from a pooled analysis of 10 cohort studies (Steenland et
al., 2001a, Document ID 0452; ToxaChemica, Inc., 2004, 0469), a study
of granite workers (Attfield and Costello, 2004, Document ID 0543), a
study of diatomaceous earth workers (Rice et al., 2001, Document ID
1118), a multi-cohort study of industrial sand workers (Hughes et al.,
2001, Document ID 1060), and a study of coal miners exposed to
respirable crystalline silica (Miller et al., 2007, Document ID 1305;
Miller and MacCalman, 2009, 1306). Similarly, a variety of studies in
several different working populations was used to derive risk estimates
of silicosis mortality, silicosis morbidity, and renal disease
mortality. The ranges of risks presented in Table VI-1 for silica
mortality and the other health endpoints thus reflect silica exposure-
response across a variety of industries and worker populations, which
may differ for reasons such as the processes in which silica exposure
occurs and the various kinds of minerals that co-exist with crystalline
silica in the dust particles (see discussion on variability in
toxicological potency of crystalline silica later in this section). The
ranges presented in Table VI-1 do not reflect statistical uncertainty
(e.g., 95% confidence intervals) or model uncertainty (e.g., the slope
of the exposure-response curve at exposures higher or lower than the
exposures of the study population) but do reflect variability in the
sources of data for the different studies.
The risks presented in Table VI-1, however, do not reflect
variability in the consistency, duration or frequency of workers'
exposures. As discussed previously in this section, OSHA's final
estimates of health risks represent risk associated with exposure to an
8-hour time weighted average of 25, 50, 100, 250 and 500 [mu]g/m\3\
respirable crystalline silica. These levels represent the risks
associated with continuous occupational exposure over a working
lifetime of 45 years to the new action level, new PEL, previous general
industry PEL, and the range in exposure (250-500 [mu]g/m\3\) that
approximates the previous construction and shipyard PELs, respectively.
OSHA estimates risks assuming exposure over a working life so that it
can evaluate the significance of the risk associated with exposure at
the previous PELs in a manner consistent with Section 6(b)(5) of the
Act, which requires OSHA to set standards that substantially reduce
these risks to the extent feasible even if workers are exposed over a
full working lifetime. However, while the risk assessment is based on
the assumed working life of 45 years, OSHA recognizes that risks
associated with shorter-term or intermittent exposures at a given
airborne concentration of silica will be less than the risk associated
with continuous occupational exposure at the same concentration over a
working lifetime. OSHA thus also uses alternatives to the 45-year full-
time exposure metric in its projections of the benefits of the final
rule (Section VII of this preamble and the FEA) that reflect the
reduction in silica-related disease that the Agency expects will result
from implementation of the revised standard, using the various
estimates of workers' typical exposure levels and patterns.
The remainder of this discussion reviews several general areas of
uncertainty and variability in OSHA's risk assessment that are not
quantitatively reflected in the risk estimates shown in Table VI-1, but
that provide important context for understanding these estimates,
including differences in the degree of uncertainty among the estimates.
These areas include exposure estimation error, dose-rate effects, model
form uncertainty, variability in toxicological potency of crystalline
silica, and additional sources of uncertainty specific to particular
endpoints, (e.g., the small number of cases in the renal disease
analysis), differing conclusions in the literature on silica as a
causative factor in renal disease and lung cancer, and reporting error
in silicosis mortality and morbidity. These different sources of
uncertainty have varying effects that can lead either to under- or
over-estimation of risks. OSHA has taken these sources of uncertainty into
account in concluding that the body of scientific literature supports
the finding that there is significant risk at existing levels of
exposure. The Agency is not required to support the finding that a
"significant risk exists with anything approaching scientific
certainty" (Benzene, 448 U.S. at 656).
a. Exposure Estimation Error
As discussed in Section V, OSHA identified exposure estimation
error as a key source of uncertainty in most of the studies and thus
the Agency's risk assessment. OSHA's contractor, ToxaChemica, Inc.,
commissioned Drs. Kyle Steenland and Scott Bartell to perform an
uncertainty analysis to examine the effect of uncertainty due to
exposure estimation error in the pooled studies (Steenland et al.,
2001a, Document ID 0452; Mannetje 2002b, 1089) on the lung cancer and
silicosis mortality risk estimates (ToxaChemica, Inc., 2004, Document
ID 0469). Drs. Steenland and Bartell addressed two main sources of
error in the silica exposure estimates. The first arises from the
assignment of individual workers' exposures based either on exposure
measurements for a sample of workers in the same job or estimated
exposure levels for specific jobs in the past when no measurements were
available, via a job-exposure matrix (JEM) (Mannetje et al., 2002a,
Document ID 1090). The second arises from the conversion of
historically-available dust measurements, typically particle count
concentrations, to gravimetric respirable silica concentrations.
ToxaChemica, Inc. conducted an uncertainty analysis using the raw data
from the IARC multi-centric study to address these sources of error
(2004, Document ID 0469).
To explore the potential effects of both kinds of uncertainty
described above, ToxaChemica, Inc. (2004, Document ID 0469) used the
distributions representing the error in job-specific exposure
assignment and the error in converting exposure metrics to generate 50
exposure simulations for each cohort. A study-specific coefficient and
a pooled coefficient were fit for each new simulation. The results
indicated that the only lung cancer cohort for which the mean of the
exposure coefficients derived from the simulations differed
substantially from the previously calculated exposure coefficient was
the South African gold cohort (simulation mean of 0.181 vs. original
coefficient of 0.582). This suggests that the results of exposure-
response analyses conducted using the South African cohort are
sensitive to error in exposure estimates; therefore, there is greater
uncertainty due to potential exposure estimation error in an exposure-
response model based on this cohort than is the case for the other nine
cohorts in Steenland et al's analysis (or, put another way, the
exposure estimation for the other nine cohorts was less sensitive to
the effects of exposure measurement uncertainty).
For the pooled analysis, the mean coefficient estimate from the
simulations was 0.057, just slightly lower than the previous estimate
of 0.060. Based on these results, OSHA concluded that random error in
the underlying exposure estimates in the Steenland et al. (2001a,
Document ID 0452) pooled cohort study of lung cancer is not likely to
have substantially influenced the original findings.
Following the same procedures described above for the lung cancer
analysis, ToxaChemica, Inc. (2004, Document ID 0469) combined both
sources of random measurement error in a Monte Carlo analysis of the
silicosis mortality data from Mannetje et al. (2002b, Document ID
1089). The silicosis mortality dataset appeared to be more sensitive to
possible error in exposure measurement than the lung cancer dataset,
for which the mean of the simulation coefficients was virtually
identical to the original. To reflect this exposure measurement
uncertainty, OSHA's final risk estimates derived from the pooled
analysis (Mannetje et al., 2002b, Document ID 1089), incorporated
ToxaChemica, Inc.'s simulated measurement error (2004, Document ID
0469).
b. Uncertainty Related to Dose-Rate Effects
OSHA received comments citing uncertainty in its risk assessment
related to possible dose-rate effects in the silica exposure-response
relationships, particularly for silicosis. For example, the ACC
commented that extrapolating risks from the high mean exposure levels
in the Park et al. 2002 cohort (Document ID 0405) to the much lower
mean exposure levels relevant to OSHA's risk assessment contributes
uncertainty to the analysis (Document ID 4209, pp. 84-85), because of
the possibility that risk accrues differently at different exposure
concentrations. The ACC thus argued that the risk associated with any
particular level of cumulative exposure may be higher for exposure to a
high concentration of respirable crystalline silica over a short period
of time than for an equivalent cumulative exposure resulting from
exposure to a low concentration of respirable crystalline silica over a
long period of time (Document ID 4209, p. 58; 2307, Attachment A, pp.
93-94). These and similar comments on dose-rate effects questioned
OSHA's use of workers' cumulative exposure levels to estimate risk, as
the cumulative exposure metric does not capture dose-rate effects.
Thus, according to the ACC, if there are significant dose-rate effects
in the exposure-response relationship for a disease or other health
endpoint, use of the cumulative exposure metric could lead to error in
risk estimates.
The rationale for OSHA's reliance on a cumulative exposure metric
to assess the risks of respirable crystalline silica is discussed in
Section V. With respect to this issue of uncertainty related to dose-
response effects, OSHA finds limited evidence in the record to either
support or refute the effects hypothesized by the ACC. As such, OSHA
acknowledges some uncertainty. Furthermore, use of an alternative
metric such as concentration would not provide assurance that
uncertainties would be mitigated or reduced.
Two studies discussed in OSHA's Review of Health Effects Literature
and Preliminary QRA examined dose-rate effects on silicosis exposure-
response (Document ID 1711, pp. 342-344). Neither study found a dose-
rate effect relative to cumulative exposure at silica concentrations
near the previous OSHA PEL (Document ID 1711, pp. 342-344). However,
they did observe a dose-rate effect in instances where workers were
exposed to crystalline silica concentrations far above the previous PEL
(i.e., several-fold to orders of magnitude above 100 [mu]g/m\3\)
(Buchanan et al., 2003, Document ID 0306; Hughes et al., 1998, 1059).
The Hughes et al. (1998) study of diatomaceous earth workers found that
the relationship between cumulative silica exposure and risk of
silicosis was steeper for workers hired prior to 1950 and exposed to
average concentrations above 500 [micro]g/m\3\ compared to workers
hired after 1950 and exposed to lower average concentrations (Document
ID 1059). Hughes et al. reported that subdivisions for workers with
exposure to concentrations below 500 [mu]g/m\3\ were examined, but that
no differences were observed across these groups (Document ID 1059, p.
809). It is unclear whether sparse data at the low end of the
concentration range contributed to this finding, as the authors did not
provide detailed information on the distribution of exposures in the
study population.
The Buchanan et al. (2003) study of Scottish coal miners adjusted
the cumulative exposure metric in the risk model to account for the
effects of exposures to high concentrations where the investigators
found that, at concentrations above 2000 [mu]g/m\3\, the risk of
silicosis was about three times higher than the risk associated with
exposure to lower concentrations but at the same cumulative exposure
(Document ID 0306, p. 162). Buchanan et al. noted that only 16 percent
of exposure hours among the workers in the study occurred at levels
below 10 [mu]g/m\3\ (Document ID 0306, p. 161), and cautioned that
insufficient data are available to predict effects at very low
concentrations where data are sparse (Document ID 0306, p. 163).
However, 56 percent of hours occurred at levels between 10 and
100 [mu]g/m\3\. Detailed information on the hours worked at
concentrations within this range was not provided.
Based on its review of these studies, OSHA concluded that there is
little evidence that a dose-rate effect exists at concentrations in the
range of the previous PEL (100 [mu]g/m\3\) (Document ID 1711, p. 344).
However, there remains some uncertainty related to dose-rate effects in
the Agency's silicosis risk assessment. Even if a dose-rate effect
exists only at concentrations far higher than the previous PEL, it is
possible for the dose-rate effect to impact model form if not properly
accounted for in study populations with high-concentration exposures.
This is one reason that OSHA presents a range of risk estimates based
on a variety of study populations exposed under different working
conditions. For example, as OSHA noted in its Review of Health Effects
Literature and Preliminary QRA (Document ID 1711, pp. 355-356), the
Park et al. study is complemented by the Mannetje et al. multi-cohort
silicosis mortality pooled study. Mannetje et al.'s study included
several cohorts that had exposure concentrations in the range of
interest for this rulemaking and also showed clear evidence of
significant risk of silicosis mortality at the previous general
industry and construction PELs (2002b, Document ID 1089). In addition,
OSHA used the model from the Buchanan et al. study in its silicosis
morbidity risk assessment to account for possible dose-rate effects at
high average concentrations (Document ID 1711, pp. 335-342). OSHA notes
that the risk estimates in the exposure range of interest (25-500
[mu]g/m\3\) derived from the Buchanan et al. (2003) study were not
appreciably different from those derived from the other studies of
silicosis morbidity (see Table VI-1).
c. Model Form Uncertainty
Another source of uncertainty in OSHA's risk analysis is
uncertainty with respect to the form of the statistical models used to
characterize the relationship between exposure level and risk of
adverse health outcomes. As discussed in Section V, some commenters
expressed concern that studies relied on by OSHA may not have
considered all potential exposure-response relationships and might be
unable to discern differences between monotonic and non-monotonic
characteristics (e.g., Document ID 2307, Attachment A, p. 113-114).
OSHA acknowledges that the possibility of error in selection of
exposure-response model forms is a source of uncertainty in the silica
risk assessment. To address this uncertainty, the Agency included
studies in the risk assessment that explored a variety of model forms.
For example, as discussed in Section V, the ToxaChemica reanalyses of
the Mannetje et al. silicosis mortality dataset and the Steenland et
al. lung cancer mortality data set examined several model forms
including a five-knot restricted spline analysis, which is a highly
flexible model form able to capture a variety of exposure-response
shapes (Document ID 0469, p. 50). The ToxaChemica reanalysis addresses
the issue of model form uncertainty by finding similar exposure-
response relationships regardless of the type of model used.
d. Uncertainty Related to Silica Exposure as a Risk Factor for Lung
Cancer
As discussed in Section V, OSHA has reviewed the best available
evidence on the relationship between silica exposure and lung cancer
mortality, and has concluded that the weight of evidence supports the
finding that exposure to silica at the preceding and new PELs increases
the risk of lung cancer. However, OSHA acknowledges that not every
study in the literature on silica-related lung cancer reached the same
conclusions. This variability is to be expected in epidemiology, as
there are different cohorts, measurements, study designs, and
analytical methods, among other factors. OSHA further acknowledges that
there is uncertainty with respect to the magnitude of the risk of lung
cancer from silica exposure. In the case of silica, the exposure-
response relationship with lung cancer may be easily obscured, as
crystalline silica is a comparably weaker carcinogen (i.e., the
increase in risk per unit exposure is smaller) than other well-studied,
more potent carcinogens such as hexavalent chromium (Steenland et al.,
2001, Document ID 0452, p. 781) and tobacco smoke, a common co-exposure
in silica-exposed populations.
A study by Vacek et al. (2011) illustrates the uncertainties
involved in evaluating risk of lung cancer from silica exposure. This
study found no significant association between respirable silica
exposure and lung cancer mortality in a cohort of Vermont granite
workers (Document ID 1486, pp. 75-81). Some commenters criticized
OSHA's preliminary risk assessment for rejecting the Vacek et al.
(2011) study and instead relying upon the Attfield and Costello (2004,
Document ID 0284) study of Vermont granite workers (Document ID 2307,
Attachment A, pp. 36-47; 4209, pp. 34-36). As discussed in detail in
Section V, OSHA reviewed the Vacek et al. study and all comments
received by the Agency on this issue, and has decided not to reject the
Attfield and Costello (2004) study in favor of the Vacek et al. (2011)
study as a basis for risk assessment. OSHA acknowledges that
comprehensive studies, such as those of Attfield and Costello (2004)
and Vacek et al. (2011), in the Vermont granite industry have shown
conflicting results with respect to lung cancer mortality (Document ID
0284; 1486). Although OSHA believes that the Attfield and Costello
(2004) study is the most appropriate Vermont granite study to use in
its QRA, it also relied upon other studies, and that the risk estimates
for lung cancer mortality based on those studies (i.e., Document ID
0543, 1060, 1118, 1306) still provide substantial evidence that
respirable crystalline silica poses a significant risk of lung cancer
to exposed workers.
e. Uncertainty Related to Renal Disease
As discussed in Section V, OSHA acknowledges that there are
considerably less data for renal disease mortality than those for
silicosis, lung cancer, and non-malignant respiratory disease (NMRD)
mortality. Although the Agency believes the renal disease risk findings
are based on credible data, the risk findings based on them are less
robust than the findings for silicosis, lung cancer, and NMRD.
Based upon its overall analysis of the literature, including the
negative studies, OSHA has concluded that there is substantial evidence
suggesting an association between exposure to crystalline silica and
increased risks of renal disease. This conclusion is supported by a
number of case reports and epidemiological studies that found
statistically significant associations between occupational exposure to
silica dust and chronic renal disease (Calvert et al., 1997, Document
ID 0976), subclinical renal changes (Ng et al., 1992c, Document ID
0386), end-stage renal disease morbidity (Steenland et al., 1990,
Document ID 1125), end-stage renal disease incidence (Steenland et al.,
2001b, Document ID 0456), chronic renal disease mortality
(Steenland et al., 2002a, 0448), and granulomatosis with
polyangitis (Nuyts et al., 1995, Document ID 0397). However, as
discussed in the Review of Health Effects Literature and Preliminary
QRA, the studies reviewed by OSHA included a number of studies that did
not show an association between crystalline silica and renal disease
(Document ID 1711, pp. 211-229). Additional negative studies by Birk et
al. (2009, Document ID 1468), and Mundt et al. (2011, Document ID 1478)
were reviewed in the Supplemental Literature Review of the Review of
Health Effects Literature and Preliminary QRA, which noted the short
follow-up period as a limitation, which reduces the likelihood that an
increased incidence of renal mortality would have been detected
(Document ID 1711, Supplement, pp. 6-12). Comments submitted to OSHA by
the ACC additionally cited several studies that did not show a
statistically significant association between exposure to crystalline
silica and renal disease mortality, including McDonald et al. (2005,
Document ID 1092), Vacek et al. (2011, Document ID 2340), Davis et al.
(1983, Document ID 0999), Koskela et al. (1987, Document ID 0363),
Cherry et al. (2012, article included in Document ID 2340), Steenland
et al. (2002b, Document ID 0454), Rosenman et al. (2000, Document ID
1120), and Calvert et al. (2003, Document ID 0309) (Document ID 2307,
Attachment A, pp. 140-145).
As discussed in detail in Section V, OSHA concludes that the
evidence supporting causality regarding renal risk outweighs the
evidence casting doubt on that conclusion, but acknowledges this
divergence in the renal disease literature as a source of uncertainty.
OSHA estimated quantitative risks for renal disease mortality
(Document ID 1711, pp. 314-316) using data from a pooled analysis of
renal disease, conducted by Steenland et al. (2002a, Document ID 0448).
The data set included 51 deaths from renal disease as an underlying
cause, which the authors of the pooled study, Drs. Kyle Steenland and
Scott Bartell, acknowledged to be insufficient to provide robust
estimates of risk (Document ID 2307, Attachment A, p. 139, citing 0469,
p. 27). OSHA agrees with Dr. Steenland and acknowledges, as it did in
its Review of Health Effects Literature and Preliminary QRA (Document
ID 1711, p. 357), that its quantitative risk estimates for renal
disease mortality are less robust than those for the other health
effects examined (i.e., lung cancer mortality, silicosis and NMRD
mortality, and silicosis morbidity).
f. Uncertainty in Reporting and Diagnosis of Silicosis Mortality and
Silicosis Morbidity
OSHA's final quantitative risk assessment includes risk estimates
for silicosis mortality and morbidity. Silicosis mortality is
ascertained by analysis of death certificates for cause of death, and
morbidity is ascertained by the presence of chest radiographic
abnormalities consistent with silicosis among silica-exposed workers.
Each of these kinds of studies are associated with uncertainties in
case ascertainment and use of chest roentgenograms to detect lung
scarring due to silicosis.
For silicosis mortality, OSHA's analysis includes a pooled analysis
of six epidemiological studies first published by Mannetje et al.
(2002b, Document ID 1089) and re-analyzed by OSHA's contractor
ToxaChemica (2004, Document ID 0469). OSHA finds that the estimates
from Mannetje et al. and ToxaChemica's analyses are likely to
understate the actual risk because silicosis is under-reported as a
cause of death, as discussed in Sections VC.2.iv and V.E in the context
of silicosis disease surveillance systems. To help address this
uncertainty, OSHA's risk analysis also included an exposure-response
analysis of diatomaceous earth (DE) workers (Park et al., 2002,
Document ID 0405), which better captures the totality of silica-related
respiratory disease than do the datasets analyzed by Mannetje et al.
and ToxaChemica. Park et al.. quantified the relationship between
cristobalite exposure and mortality caused by NMRD, which includes
silicosis, pneumoconiosis, emphysema, and chronic bronchitis. Because
NMRD captures much of the silicosis misclassification that results in
underestimation of the disease and includes risks from other lung
diseases associated with crystalline silica exposures, OSHA finds the
risk estimates derived from the Park et al. study are important to
include as part of OSHA's range of estimates of the risk of death from
silica-related respiratory diseases, including silicosis. (Document ID
1711, pp. 297-298). OSHA concludes that the range of silicosis and NMRD
risks presented in the final risk assessment, based on both the
ToxaChemica reanalysis of Mannetje et al.'s silicosis mortality data
and Park et al.'s study of NMRD mortality, provide a credible range of
estimates of mortality risk from silicosis and NMRD across a range of
industrial workplaces. The upper end of this range, based on the Park
et al. study, is less likely to underestimate risk as a result of
under-reporting of silicosis mortality, but cannot be directly compared
to risk estimates from studies that focused on cohorts of workers from
different industries.
OSHA's estimates of silicosis morbidity risks are based on studies
of active and retired workers for which exposure histories could be
constructed and chest x-ray films could be evaluated for signs of
silicosis. There is evidence in the record that chest x-ray films are
relatively insensitive to detecting lung fibrosis. Hnizdo et al. (1993,
Document ID 1050) found chest x-ray films to have low sensitivity for
detecting lung fibrosis related to silicosis, compared to pathological
examination at autopsy. To address the low sensitivity of chest x-rays
for detecting silicosis, Hnizdo et al. (1993, Document ID 1050)
recommended that radiographs consistent with an ILO category of 0/1 or
greater be considered indicative of silicosis among workers exposed to
a high concentration of silica-containing dust. In like manner, to
maintain high specificity, chest x-rays classified as category 1/0 or
1/1 should be considered as a positive diagnosis of silicosis. Studies
relied on in OSHA's risk assessment typically used an ILO category of
1/0 or greater to identify cases of silicosis. According to Hnizdo et
al., they are unlikely to include many false positives (diagnoses of
silicosis where there is none), but may include false negatives
(failure to identify cases of silicosis). Thus, the use of chest
roentgenograms to ascertain silicosis cases in the morbidity studies
relied on by OSHA in its risk assessment could lead to an
underestimation of risk given the low sensitivity of chest
roentgenograms for detecting silicosis.
g. Variability in Toxicological Potency of Crystalline Silica
As discussed in Section V, the toxicological potency of crystalline
silica is influenced by a number of physical and chemical factors that
affect the biological activity of inhaled silica particles. The
toxicological potency of crystalline silica is largely influenced by
the presence of oxygen free radicals on the surfaces of respirable
particles. These chemically-reactive oxygen species interact with
cellular components in the lung to promote and sustain the inflammatory
reaction responsible for the lung damage associated with exposure to
crystalline silica. The reactivity of particle surfaces is greatest
when crystalline silica has been freshly fractured by high-energy
work processes such as abrasive blasting, rock drilling, or sawing
concrete materials. As particles age in the air, the surface reactivity
decreases and exhibits lower toxicologic potency (Porter et al., 2002,
Document ID 1114; Shoemaker et al., 1995, 0437; Vallyathan et al.,
1995, 1128). In addition, surface impurities have been shown to alter
silica toxicity. For example, aluminum and aluminosilicate clay on
silica particles has been shown to decrease toxicity (Castranova et
al., 1997, Document ID 0978; Donaldson and Borm, 1998, 1004; Fubini,
1998, 1016; Donaldson and Borm, 1998, Document ID 1004; Fubini, 1998,
1016).
In the preamble to the proposed standard, OSHA preliminarily
concluded that although there is evidence that several environmental
influences can modify surface activity to either enhance or diminish
the toxicity of silica, the available information was insufficient to
determine to what extent these influences may affect risk to workers in
any particular workplace setting (Document 1711, p. 350). OSHA
acknowledges that health risks are probably in the low end of the range
for workers in the brick manufacturing industry, although the evidence
still indicates that there is a significant risk at the previous
general industry PEL for those workers. OSHA also acknowledges that
there was a lack of evidence for a significant risk in the sorbent
minerals industry due to the nature of crystalline silica present in
those operations; as a result, it decided to exclude sorptive clay
processing from this rule. Furthermore, Dudley and Morriss (2015) raise
concerns about the whether the exposures reflected in the historical
cohorts used in the risk assessment are sufficiently reflective of
rapidly changing working conditions over the last 45 years.\11\
However, the risk estimates presented in Table VI-1 are based on
studies from a variety of industries, such that the risk ranges
presented are likely to include estimates appropriate to most working
populations. Thus, in OSHA's view, its significant risk finding is well
supported by the weight of best available evidence, notwithstanding
uncertainties that may be present to varying degrees in the numerous
studies relied upon and the even greater number of studies that the
Agency considered.
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\11\ Dudley, S. E. and Morriss, A. P. (2015), Will the
Occupational Safety and Health Administration's Proposed Standards
for Occupational Exposure to Respirable Crystalline Silica Reduce
Workplace Risk?. Rish Analysis, 35: 1191-1196. doi:10.1111/
risa.12341
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4. OSHA's Response to Comments on Significant Risk of Material
Impairment
OSHA received several comments pertaining to the Agency's
determination of a significant risk of material impairment of health
posed to workers exposed for a working life to the previous PELs.
Although many of these comments were supportive of OSHA's conclusions
regarding the significance of risk, others were critical or suggested
that OSHA has an obligation to further reduce the risk below that
estimated to remain at the revised PEL.
Referring to the previous PELs for respirable crystalline silica,
the AFL-CIO commented that "[w]orkers face a significant risk of harm
from silica exposure at the current permissible exposure limits," and
that "[t]here is overwhelming evidence in the record that exposure to
respirable crystalline silica poses a significant health risk to
workers" (Document ID 4204, pp. 10-11). The AFL-CIO noted that OSHA's
mortality risk estimates well exceeded the benchmark of 1/1,000 excess
risk over a working lifetime of exposure to the previous PELs, and also
highlighted the risks of silicosis morbidity (Document ID 4204, p. 13).
The AFL-CIO further pointed out that there is no cure for silicosis,
and quoted oral testimony from workers at the informal public hearings
demonstrating that "[s]ilica-related diseases are still destroying
workers' lives and livelihoods" (Document ID 4204, p. 19).
Both the UAW and the Building and Construction Trades Department
(BCTD) concurred with the AFL-CIO that the previous PEL needs to be
lowered to adequately protect workers. Referring to the previous PEL,
the BCTD stated that "[t]he record supports OSHA's determination that
exposures at the current PEL present a significant risk" (Document ID
4223, p. 6). Although supportive of OSHA's proposed standard, the UAW
also suggested the adoption of a PEL of 25 [micro]g/m\3\ or lower where
feasible (Document ID 2282, Attachment 3, p.1), noting that a PEL set
at this level "will significantly reduce workers' exposure to deadly
silica dust and prevent thousands of illnesses and deaths every year"
(Document ID 2282, Attachment 3, p. 25). Similarly, Charles Gordon, a
retired occupational safety and health attorney, commented that the
revised PEL "leaves a remaining risk of 97 deaths per 1,000 workers
from silicosis, lung cancer, and renal disease combined" (Document ID
4236, p. 2). Again, it should be noted that these risk estimates are
not additive because some individuals may suffer from multiple diseases
caused by exposure to silica. Instead, OSHA presents risk estimates for
each health endpoint.
As discussed above, OSHA acknowledges that there remains a
significant risk of material impairment of health at the revised PEL; a
further reduction in the PEL, however, is not currently technologically
feasible (see Section VII, Summary of the Final Economic Analysis and
Final Regulatory Flexibility Analysis, in which OSHA summarizes its
assessment of the technological feasibility of the revised PEL).
Despite this, the final PEL will provide a very substantial reduction
in the risk of material impairment of health to silica-exposed workers,
as described in the Benzene decision (Benzene, 448 U.S. at 642).
In contrast to the foregoing comments from labor groups contending
that OSHA would be setting the PEL too high if it made a final
determination to lower the preceding PELs to 50 [micro]g/m\3\, critical
comments came from industry groups including the American Chemistry
Council (ACC), which disagreed with OSHA's determination of a
significant risk of material impairment of health at the previous PELs.
The ACC stated, "OSHA's assessment of these risks is flawed, and its
conclusions that the risks are significant at a PEL of 100 [micro]g/
m\3\ and would be substantially reduced by lowering the PEL to 50
[micro]g/m\3\ are unsupported" (Document ID 4209, p. 12). The ACC then
asserted several "fundamental shortcomings" in OSHA's QRA on which
OSHA based its significant risk determination (Document ID 4209, pp.
16-17), including a variety of purported biases in the key studies on
which OSHA relied. OSHA addresses the ACC's concerns in detail in
Section V of this preamble dealing with the key studies relied upon by
the Agency for each health endpoint, as well as separate sections
addressing the issues of biases, causation, thresholds, the uncertainty
analysis, and the life table and exposure assumptions used in the QRA.
As more fully discussed in those sections, OSHA finds these concerns to
be unpersuasive. As discussed in Section V, the scientific community
and regulators in other advanced industrial societies agree on the need
for a PEL of at most 50 [micro]g/m\3\ based on demonstrated health
risks, and OSHA has used the best available evidence in the scientific
literature to estimate quantitative risks of silica-related illnesses
and thereby reach the same conclusion. OSHA's preliminary review of the
health effects literature and OSHA's preliminary QRA were, further,
examined by an independent, external peer review panel of
accomplished scientists, which lent credibility to the Agency's methods
and findings and led to some adjustments in the analysis that
strengthened OSHA's final risk assessment. There is, additionally,
widespread support for the Agency's methods and conclusions in the
rulemaking record. As such, OSHA is confident in its conclusion that
there is a significant risk of material impairment of health to workers
exposed to respirable crystalline silica at the levels of exposure
permitted under the previous PELs and under this final standard, and
finds no merit in broad assertions purporting to debunk this
conclusion.
In summary, as discussed throughout Section V and this final rule,
OSHA concludes, based on the best available evidence in the scientific
literature, that workers' exposure to respirable crystalline silica at
the previous PELs results in a clearly significant risk of material
impairment of health. The serious, and potentially fatal, health
effects suffered by exposed workers include silicosis, lung cancer,
NMRD, renal disease, and autoimmune effects. OSHA finds that the risk
is substantially decreased, though still significant, at the new PEL of
50 [micro]g/m\3\ and below, including at the new action level of 25
[micro]g/m\3\. The Agency is constrained, however, from lowering the
PEL further by its finding that a lower PEL would be infeasible in many
operations across several industries. Given the significant risks faced
by workers exposed to respirable crystalline silica under the
previously-existing exposure limits, OSHA believes that it is
imperative that it issue this final standard pursuant to its statutory
mandate under the OSH Act.
VII. Summary of the Final Economic Analysis and Final Regulatory
Flexibility Analysis
A. Introduction
OSHA's Final Economic Analysis and Final Regulatory Flexibility
Analysis (FEA) addresses issues related to the costs, benefits,
technological and economic feasibility, and the economic impacts
(including impacts on small entities) of this final respirable
crystalline silica rule and evaluates regulatory alternatives to the
final rule. Executive Orders 13563 and 12866 direct agencies to assess
all costs and benefits of available regulatory alternatives and, if
regulation is necessary, to select regulatory approaches that maximize
net benefits (including potential economic, environmental, and public
health and safety effects; distributive impacts; and equity). Executive
Order 13563 emphasized the importance of quantifying both costs and
benefits, of reducing costs, of harmonizing rules, and of promoting
flexibility. The full FEA has been placed in OSHA rulemaking docket
OSHA-2010-0034. This rule is an economically significant regulatory
action under Sec. 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 the FEA is to:
Identify the establishments and industries potentially
affected by the final rule;
Estimate current exposures and the technologically
feasible methods of controlling these exposures;
Estimate the benefits resulting from employers coming into
compliance with the final rule in terms of reductions in cases of
silicosis, lung cancer, other forms of chronic obstructive pulmonary
disease, and renal failure;
Evaluate the costs and economic impacts that
establishments in the regulated community will incur to achieve
compliance with the final rule;
Assess the economic feasibility of the final rule for
affected industries; and
Assess the impact of the final rule on small entities
through a Final Regulatory Flexibility Analysis (FRFA), to include an
evaluation of significant regulatory alternatives to the final rule
that OSHA has considered.
Significant Changes to the FEA Between the Proposed Standards and the
Final Standards
OSHA changed the FEA for several reasons:
Changes to the rule, summarized in Section I of this
preamble and discussed in detail in the Summary and Explanation;
Comments on the Preliminary Economic Analysis (PEA);
Updates of economic data; and
Recognition of errors in the PEA.
OSHA revised its technological and economic analysis in response to
these changes and to comments received on the NPRM. The FEA contains
some costs that were not included in the PEA and updates data to use
more recent data sources and, in some cases, revised methodologies.
Detailed discussions of these changes are included in the relevant
sections throughout the FEA.
The FEA contains the following chapters:
Chapter I. Introduction
Chapter II. Market Failure and the Need for Regulation
Chapter III. Profile of Affected Industries
Chapter IV. Technological Feasibility
Chapter V. Costs of Compliance
Chapter VI. Economic Feasibility Analysis and Regulatory Flexibility
Determination
Chapter VII. Benefits and Net Benefits
Chapter VIII. Regulatory Alternatives
Chapter IX. Final Regulatory Flexibility Analysis
Chapter X. Environmental Impacts
Table VII-1 provides a summary of OSHA's best estimate of the costs
and estimated benefits of the final rule using a discount rate of 3
percent. As shown, the final rule is estimated to prevent 642
fatalities and 918 silica-related illnesses annually once it is fully
effective, and the estimated cost of the rule is $1,030 million
annually. Also as shown in Table VII-1, the discounted monetized
benefits of the final rule are estimated to be $8.7 billion annually,
and the final rule is estimated to generate net benefits of $7.7
billion annually. Table VII-1 also presents the estimated costs and
estimated benefits of the final rule using a discount rate of 7
percent.
The remainder of this section (Section VII) of the preamble is
organized as follows:
B. Market Failure and the Need for Regulation
C. Profile of Affected Industries
D. Technological Feasibility
E. Costs of Compliance
F. Economic Feasibility Analysis and Regulatory Flexibility
Determination
G. Benefits and Net Benefits
H. Regulatory Alternatives
I. Final Regulatory Flexibility Analysis.
B. Market Failure and the Need for Regulation
Employees in work environments addressed by the final silica rule
are exposed to a variety of significant hazards that can and do cause
serious injury and death. As described in Chapter II of the FEA in
support of the final rule, OSHA concludes there is a failure of private
markets to protect workers from exposure to unnecessarily high levels
of respirable crystalline silica and that private markets, as well as
information dissemination programs, workers' compensation systems, and
tort liability options, each may fail to protect workers from silica
exposure, resulting in the need for a more protective OSHA silica rule.
After carefully weighing the various potential advantages and
disadvantages of using a regulatory approach to improve upon the
current situation, OSHA concludes that, in the case of silica exposure,
the final mandatory standards represent the best choice for reducing
the risks to employees. In addition, rulemaking is necessary in this
case in order to replace older existing standards with updated, clear,
and consistent health standards.
C. Profile of Affected Industries
Introduction
Chapter III of the FEA presents profile data for industries
potentially affected by the final silica rule. The discussion below
summarizes the findings in that chapter. As a first step, OSHA
identifies the North American Industrial Classification System (NAICS)
industries, both in general industry and maritime and in the
construction sector, with potential worker exposure to silica. Next,
OSHA provides summary statistics for the affected industries, including
the number of affected entities and establishments, the number of
workers whose exposure to silica could result in disease or death
("at-risk workers"), and the average revenue for affected entities
and establishments.\12\ Finally, OSHA presents silica exposure profiles
for at-risk workers. These data are presented by sector and job
category. Summary data are also provided for the number of workers in
each affected industry who are currently exposed above the final silica
PEL of 50 [mu]g/m\3\, as well as above an alternative PEL of 100 [mu]g/
m\3\ for economic analysis purposes.
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\12\ The Census Bureau defines an establishment as a single
physical location at which business is conducted or services or
industrial operations are performed. The Census Bureau defines a
business firm or entity as a business organization consisting of one
or more domestic establishments in the same state and industry that
were specified under common ownership or control. The firm and the
establishment are the same for single-establishment firms. For each
multi-establishment firm, establishments in the same industry within
a state will be counted as one firm; the firm employment and annual
payroll are summed from the associated establishments. (US Census
Bureau, Statistics of US Businesses, Definitions. 2015,
http://www.census.gov/econ/susb/definitions.html?cssp=SERP).
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The methodological basis for the industry and at-risk worker data
presented in this chapter comes from the PEA, the Eastern Research
Group (ERG) analysis supporting the PEA (2007a, 2007b, 2008a, and
2008b),\13\ and ERG's analytic support in preparing the FEA. The data
used in this chapter come from the rulemaking record (Docket OSHA-2010-
0034), the technological feasibility analyses presented in Chapter IV
of the FEA, and from OSHA (2016), which updated its earlier
spreadsheets to reflect the most recent industry data available. To do
so, ERG first matched the BLS Occupational Employment Statistics (OES)
survey occupational titles with the at-risk job categories, by NAICS
industry. ERG then calculated the percentages of production employment
represented by each at-risk job title within industry (see OSHA, 2016
for details on the calculation of employment percentages and the
mapping of at-risk job categorizations into OES occupations).\14\ ERG's
expertise for identifying the appropriate OES occupations and
calculating the employment percentages enabled OSHA to estimate the
number of employees in the at-risk job categories by NAICS industry
(Id.).
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\13\ Document ID, 1709, 1608, 1431, and 1365, respectively.
\14\ Production employment includes workers in building and
grounds maintenance; forestry, fishing, and farming; installation
and maintenance; construction; production; and material handling
occupations.
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In the NPRM and PEA, OSHA invited the public to submit additional
information and data that might help improve the accuracy and
usefulness of the preliminary industry profile; the profile presented
here and in Chapter III of the FEA reflects public comment.
Selection of NAICS Industries for Analysis
The technological feasibility analyses presented in Chapter IV of
the FEA identify the general industry and maritime sectors and the
construction activities potentially affected by the final silica
standard.
General Industry and Maritime
Employees engaged in various activities in general industry and
maritime routinely encounter crystalline silica as a molding material,
as an inert mineral additive, as a component of fluids used to
stimulate well production of oil or natural gas, as a refractory
material, as a sandblasting abrasive, or as a natural component of the
base materials with which they work. Some industries use various forms
of silica for multiple purposes. As a result, employers are faced with
the challenge of limiting worker exposure to silica in dozens of job
categories throughout the general industry and maritime sectors.
Job categories in general industry and maritime were selected for
analysis based on data from the technical industrial hygiene
literature, evidence from OSHA Special Emphasis Program (SEP) results,
and, in several cases, information from ERG site visit reports and
public comment submitted into the record. These data sources provided
evidence of silica exposures in numerous sectors. While the available
data are not entirely comprehensive, OSHA believes that silica
exposures in other sectors are quite limited.
The industry subsectors in the overall general industry and
maritime application groups that OSHA identified as being potentially
affected by the final silica standard are as follows:
Asphalt Paving Products
Asphalt Roofing Materials
Hydraulic Fracturing
Industries with Captive Foundries
Concrete Products
Cut Stone
Dental Equipment and Supplies
Dental Laboratories
Flat Glass
Iron Foundries
Jewelry
Mineral Processing
Mineral Wool
Nonferrous Sand Casting Foundries
Non-Sand Casting Foundries
Other Ferrous Sand Casting Foundries
Other Glass Products
Paint and Coatings
Porcelain Enameling
Pottery
Railroads
Ready-Mix Concrete
Refractories
Refractory Repair
Shipyards
Structural Clay
In some cases, affected industries presented in the technological
feasibility analysis have been disaggregated to facilitate the cost and
economic impact analysis. In particular, flat glass, mineral wool, and
other glass products are subsectors of the glass industry described in
Chapter IV, Section IV-9, of the FEA, and captive foundries,\15\ iron
foundries, nonferrous sand casting foundries, non-sand cast foundries,
and other ferrous sand casting foundries are subsectors of the
overall foundries industry presented in Chapter IV, Section IV-8, of
the FEA.
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\15\ Captive foundries include establishments in other
industries with foundry processes incidental to the primary products
manufactured. ERG (2008b, Document ID 1365) provides a discussion of
the methodological issues involved in estimating the number of
captive foundries and in identifying the industries in which they
are found. Since the 2008 ERG report, through comment in the public
record and the public hearings, OSHA has gained additional
information on the presence of captive foundries throughout general
industry.
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As described in ERG (2008b, Document ID 1365) and updated in OSHA
(2016), OSHA identified the six-digit NAICS codes for these subsectors
to develop a list of industries potentially affected by the final
silica standard. Table VII-2 presents the sectors listed above with
their corresponding six-digit NAICS industries. The NAICS codes and
associated industry definitions in the FEA are consistent with the 2012
NAICS edition.
BILLING CODE 4510-26-P
BILLING CODE 4510-26-C
Construction
The construction sector is an integral part of the nation's
economy, accounting for approximately 4.5 percent of total private
sector employment. Establishments in this industry are involved in a
wide variety of activities, including land development and subdivision,
homebuilding, construction of nonresidential buildings and other
structures, heavy construction work (including roadways and bridges),
and a myriad of special trades such as plumbing, roofing, electrical,
excavation, and demolition work.
Construction activities were selected for analysis based on
historical data of recorded samples of construction worker exposures
from the OSHA Integrated Management Information System (IMIS) and the
National Institute for Occupational Safety and Health (NIOSH). In
addition, OSHA reviewed the industrial hygiene literature across the
full range of construction activities and focused on dusty operations
where silica sand was most likely to be fractured or abraded by work
operations. These physical processes have been found to cause the
silica exposures that pose the greatest risk of silicosis for workers.
The construction activities, by equipment or task, that OSHA
identified as being potentially affected by the final silica standard
are as follows:
Earth drilling
Heavy Equipment Operators and Ground Crew Laborers--I
(Abrading or fracturing silica containing materials or demolishing
concrete or masonry structures)
Heavy Equipment Operators and Ground Crew Laborers--II
(Grading and Excavating)
Hole Drillers Using Handheld or Stand-Mounted Drills
Jackhammers and Other Powered Handheld Chipping Tools
Masonry and Concrete Cutters Using Portable Saws--I (Handheld
power saws)
Masonry and Concrete Cutters Using Portable Saws--II (Handheld
power saws for cutting fiber-cement board)
Masonry and Concrete Cutters Using Portable Saws--III (Walk-
behind saws)
Masonry and Concrete Cutters Using Portable Saws--IV (Drivable
or ride-on concrete saws)
Masonry and Concrete Cutters Using Portable Saws--V (Rig-
mounted core saws or drills)
Masonry Cutters Using Stationary Saws
Millers Using Portable or Mobile Machines--I (Walk-behind
milling machines and floor grinders)
Millers Using Portable or Mobile Machines--II (Small drivable
milling machine (less than half-lane))
Millers Using Portable or Mobile Machines--III (Milling
machines (half-lane and larger with cuts of any depth on asphalt only
and for cuts of four inches in depth or less on any other substrate))
Rock and Concrete Drillers--I (Vehicle-mounted drilling rigs
for rock and concrete)
Rock and Concrete Drillers--II (Dowel drilling rigs for
concrete)
Mobile Crushing Machine Operators and Tenders
Tuckpointers and Grinders--I (Handheld grinders for mortar
removal (e.g., tuckpointing))
Tuckpointers and Grinders--II (Handheld grinders for uses
other than mortar removal)
As shown in OSHA (2016) and in Chapter IV of the FEA, these
construction activities occur in the following industries and
governmental bodies, accompanied by their four-digit NAICS codes: \16\
\17\
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\16\ ERG and OSHA used the four-digit NAICS codes for the
construction sector both because the BLS's Occupational Employment
Statistics survey only provides data at this level of detail ad
because, unlike the case in general industry and maritime, job
categories in the construction sector are task-specific, not
industry-specific. Furthermore, as far as economic impacts are
concerned, IRS data on profitability are reported only at the four-
digit NAICS code level of detail.
\17\ Some public employees in state and local governments are
exposed to elevated levels of respirable crystalline silica. These
exposures are included in the construction sector because they are
the result of construction activities.
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2361 Residential Building Construction
2362 Nonresidential Building Construction
2371 Utility System Construction
2372 Land Subdivision
2373 Highway, Street, and Bridge Construction
2379 Other Heavy and Civil Engineering Construction
2381 Foundation, Structure, and Building Exterior Contractors
2382 Building Equipment Contractors
2383 Building Finishing Contractors
2389 Other Specialty Trade Contractors
2211 Electric Utilities
9992 State Government
9993 Local Government
Characteristics of Affected Industries
Table VII-3 provides an overview of the industries and estimated
number of workers affected by the final rule. Included in Table VII-3
are summary statistics for each of the affected industries, subtotals
for construction and for general industry and maritime, and grand
totals for all affected industries combined.
The first five columns in Table VII-3 identify the NAICS code for
each industry in which workers are routinely exposed to respirable
crystalline silica and the name or title of the industry, followed by
the total number of entities, establishments, and employees for that
industry. Note that, while the industries are characterized by such
exposure, not every entity, establishment, and employee in these
affected industries engage in activities involving silica exposure.
The next three columns in Table VII-3 show, for each affected
industry, the number of entities and establishments in which workers
are actually exposed to silica and the total number of workers exposed
to silica. The number of affected establishments was set equal to the
total number of establishments in an industry (based on Census data)
unless the number of affected establishments would exceed the number of
affected employees in the industry. In that case, the number of
affected establishments in the industry was set equal to the number of
affected employees, and the number of affected entities in the industry
was reduced so as to maintain the same ratio of entities to
establishments in the industry.\18\
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\18\ OSHA determined that removing this assumption would have a
negligible impact on total costs and would reduce the cost and
economic impact on the average affected establishment or entity.
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BILLING CODE 4510-26-P
BILLING CODE 4510-26-C
As shown in Table VII-3, OSHA estimates that a total of 652,600
entities (586,800 in construction; 65,900 in general industry and
maritime), 675,800 establishments (600,700 in construction; 75,100 in
general industry and maritime), and 2.3 million workers (2.0 million in
construction; 0.3 million in general industry and maritime) would be
affected by the final silica rule. Note that only 67 percent of the
entities and establishments, and about 21 percent of the workers in
affected industries, actually engage in activities involving silica
exposure.\19\
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\19\ It should be emphasized that these percentages vary
significantly depending on the industry sector and, within an
industry sector, depending on the NAICS industry. For example, about
35 percent of the workers in construction, but only 6 percent of
workers in general industry, actually engage in activities involving
silica exposure. As an example within construction, about 35 percent
of workers in highway, street, and bridge construction, but only 3
percent of workers in state and local governments, actually engage
in activities involving silica exposure.
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The ninth column in Table VII-3, with data only for construction,
shows for each affected NAICS construction industry the number of full-
time-equivalent (FTE) affected workers that corresponds to the total
number of affected construction workers in the previous column.\20\
This distinction is necessary because affected construction workers may
spend large amounts of time working on tasks with no risk of silica
exposure. As shown in Table VII-3, the 2.0 million affected workers in
construction converts to approximately 387,700 FTE affected workers. In
contrast, OSHA based its analysis of the affected workers in general
industry and maritime on the assumption that they were engaged full
time in activities with some silica exposure.
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\20\ FTE affected workers becomes a relevant variable in the
estimation of control costs in the construction industry. The reason
is that, consistent with the costing methodology, control costs
depend only on how many worker-days there are in which exposures are
above the PEL. These are the worker-days in which controls are
required. For the derivation of FTEs, see Tables IV-8 and IV-22 and
the associated text in ERG (2007a, Document ID 1709).
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The last three columns in Table VII-3 show combined total revenues
for all entities (not just affected entities) in each affected
industry, and the average revenue per entity and per establishment in
each affected industry. Because OSHA did not have data to distinguish
revenues for affected entities and establishments in any industry,
average revenue per entity and average revenue per affected entity (as
well as average revenue per establishment and average revenue per
affected establishment) are estimated to be equal in value.
Silica Exposure Profile of At-Risk Workers
The technological feasibility analyses presented in Chapter IV of
the FEA contain data and discussion of worker exposures to silica
throughout industry. Exposure profiles, by job category, were developed
from individual exposure measurements that were judged to be
substantive and to contain sufficient accompanying description to allow
interpretation of the circumstance of each measurement. The resulting
exposure profiles show the job categories with current overexposures to
silica and, thus, the workers for whom silica controls would be
implemented under the final rule.
Chapter IV of the FEA includes a section with a detailed
description of the methods used to develop the exposure profile and to
assess the technological feasibility of the final standard. The final
exposure profiles take the exposure data that were used for the same
purpose in OSHA's PEA and build upon them, using new data in the
rulemaking record. The sampling data that were used to identify the
affected industries and to develop the exposure profiles presented in
the PEA were obtained from a comprehensive review of the following
sources of information: OSHA compliance inspections conducted before
2011, OSHA contractor (ERG) site visits performed for this rulemaking,
NIOSH site visits, NIOSH Health Hazard Evaluation reports (HHEs),
published literature, submissions by individual companies or
associations and, in a few cases, data from analogous operations
(Document ID 1720, pp. IV-2-IV-3). The exposure profiles presented in
the PEA were updated for the FEA using exposure measurements from the
OSHA Information System (OIS) that were taken during compliance
inspections conducted between 2011 and 2014 (Document ID 3958). In
addition, exposure data submitted to the record by rulemaking
participants were used to update the exposure profiles. The criteria
used for determining whether to include exposure data in the exposure
profiles are described in Section IV-2--Methodology in Chapter IV of
the FEA. As explained there, some of the original data are no longer
used in the exposure profiles based on those selection or screening
criteria. OSHA considers the exposure data relied upon for its analysis
to be the best available evidence of baseline silica exposure
conditions.
Table VII-4 summarizes, from the exposure profiles, the total
number of workers at risk from silica exposure at any level, and the
distribution of 8-hour TWA respirable crystalline silica exposures by
job category for general industry and maritime sectors and for
construction activities. Exposures are grouped into the following
ranges: Less than 25 [mu]g/m\3\; >= 25 [mu]g/m\3\ and <= 50 [mu]g/m\3\;
> 50 [mu]g/m\3\ and <= 100 [mu]g/m\3\; > 100 [mu]g/m\3\ and <= 250
[mu]g/m\3\; and greater than 250 [mu]g/m\3\. These frequencies
represent the percentages of production employees in each job category
and sector currently exposed at levels within the indicated range.
Table VII-5 presents data by NAICS code--for each affected general,
maritime, and construction industry--on the estimated number of workers
currently at risk from silica exposure, as well as the estimated number
of workers at risk of silica exposure at or above 25 [mu]g/m\3\, above
50 [mu]g/m\3\, and above 100 [mu]g/m\3\. As shown, an estimated
1,249,250 workers (1,097,000 in construction; 152,300 in general
industry and maritime) currently have silica exposures at or above the
new action level of 25 [mu]g/m\3\; an estimated 948,100 workers
(847,700 in construction; 100,400 in general industry and maritime)
currently have silica exposures above the new PEL of 50 [mu]g/m\3\; and
an estimated 578,000 workers (519,200 in construction; 58,800 in
general industry and maritime) currently have silica exposures above
100 [mu]g/m\3\--an alternative PEL investigated by OSHA for economic
analysis purposes.
BILLING CODE 4510-26-P
BILLING CODE 4510-26-C
D. Technological Feasibility
In Chapter IV of OSHA's FEA, OSHA assesses the technological
feasibility of the standard in all affected industry sectors and
application groups. The analysis presented in this chapter is organized
by industry sectors in general industry and maritime and by application
groups in the construction industry. Employee exposures were analyzed
at the operation, job category or task/activity level to the extent
that the necessary data were available.
OSHA collected exposure data to characterize current (baseline)
exposures and to identify the tasks, operations, and job categories for
which employers will need to either improve their process controls or
implement additional controls to reduce respirable crystalline silica
exposures to 50 [micro]g/m\3\ or below. In the few instances where
there were insufficient exposure data, OSHA used analogous operations
to characterize these operations.
The technological feasibility analysis informed OSHA's selection of
the rule's permissible exposure limit (PEL) of 50 [micro]g/m\3\
respirable crystalline silica, consistent with the requirements of the
Occupational Safety and Health Act ("OSH Act"), 29 U.S.C. 651 et seq.
Section 6(b)(5) of the OSH Act requires that OSHA "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" (29 U.S.C. 655(b)(5)). In
fulfilling this statutory directive, OSHA is guided by the legal
standard expressed by the Court of Appeals for the D.C. Circuit for
demonstrating the technological feasibility of reducing occupational
exposure to a hazardous substance:
OSHA must prove a reasonable possibility that the typical firm
will be able to develop and install engineering and work practice
controls that can meet the PEL in most of its operations....The
effect of such proof is to establish a presumption that industry can
meet the PEL without relying on respirators....Insufficient
proof of technological feasibility for a few isolated operations
within an industry, or even OSHA's concession that respirators will
be necessary in a few such operations, will not undermine this
general presumption in favor of feasibility. Rather, in such
operations firms will remain responsible for installing engineering
and work practice controls to the extent feasible, and for using
them to reduce...exposure as far as these controls can do so
(United Steelworkers of Am, AFL-CIO-CLC v. Marshall, 647 F.2d 1189,
1272 (D.C. Cir. 1980)).
Additionally, the D.C. Circuit explained that "[f]easibility of
compliance turns on whether exposure levels at or below [the PEL] can
be met in most operations most of the time..." (Am. Iron & Steel
Inst. v. OSHA, 939 F.2d 975, 990 (D.C. Cir. 1991)); (see Section II,
Pertinent Legal Authority).
Consistent with the legal standard described above, Chapter IV of
the FEA, which can be found at www.regulations.gov (docket OSHA-2010-
0034), describes OSHA's examination of the technological feasibility of
this rule on occupational exposure to respirable crystalline silica.
The chapter provides a description of the methodology and data used by
OSHA to analyze the technological feasibility of the standard, as well
as a discussion of the accuracy and reliability of current methods used
for the sampling and analysis of respirable crystalline silica. Chapter
IV contains OSHA's analyses, for 21 general industry sectors, 1
maritime sector, and 12 construction industry application groups, of
the technological feasibility of meeting the rule's requirements for
reducing exposures to silica. For each sector and application group,
OSHA addresses the extent to which the evidence in the record indicates
that engineering and work practice controls can reduce respirable
crystalline silica exposures to the PEL or below and maintain them at
that level. These individual technological feasibility analyses form
the basis for OSHA's overall finding that employees' exposures can be
reduced to the rule's PEL or below in most of the affected sectors'
operations. Throughout Chapter IV, OSHA describes and responds to
issues raised in the comments and testimony it received from interested
parties during the comment periods and public hearing OSHA held on the
proposed rule. The material below summarizes the detailed discussion
and presentation of OSHA's findings contained in Chapter IV of the FEA.
1. Methodology
As noted above, OSHA's technological feasibility analysis for this
rule largely involved describing engineering and work practice controls
that OSHA concludes can be expected to control respirable crystalline
silica exposures to the PEL or below. For this portion of the analysis,
OSHA relied on information and exposure measurements from many
different sources, including OSHA's inspection database (OSHA
Information System (OIS)), OSHA inspection reports, National Institute
of Occupational Safety and Health (NIOSH) reports, site visits by NIOSH
and OSHA's contractor, Eastern Research Group, Inc. (ERG), and
materials from other federal agencies, state agencies, labor
organizations, industry associations, and other groups. In addition,
OSHA reviewed studies from the published literature that evaluated the
effectiveness of engineering controls and work practices in order to
estimate the reductions from current, baseline exposures to silica that
can be achieved through wider or improved implementation of such
controls. Finally, OSHA considered the extensive testimony and numerous
comments regarding the feasibility of implementing engineering and work
practice controls, including circumstances that preclude the use of
controls in certain situations. In total, OSHA's feasibility analysis
is based on hundreds of sources of information in the record,
constituting one of the largest databases of information OSHA has used
to evaluate the feasibility of a health standard.
The technological feasibility chapter of the FEA describes the
industry sectors and application groups affected by the rule, and
identifies the sources of exposure to respirable crystalline silica for
each affected job category or task. The technological feasibility
analysis subdivides the general industry and maritime workplaces into
24 industry sectors.\21\ General industry sectors are identified
primarily based on the type of product manufactured (e.g., concrete
products, pottery, glass) or type of process used (e.g., foundries,
mineral processing, refractory repair). Where sufficiently detailed
information was available, the Agency further divided general industry
sectors into specific job categories on the basis of common factors
such as materials, work processes, equipment, and available exposure
control methods. OSHA notes that these job categories are intended to
represent job functions; actual job titles and responsibilities might
differ depending on the facility or industry practice.
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\21\ OSHA's technological feasibility analysis in the FEA is
divided into 22 sections, one for each of the general industry and
maritime sectors. However, separate technological feasibility
findings are made for three different foundry sectors (ferrous,
nonferrous, and non-sand casting foundries), making a total of 24
sectors for which separate analyses and findings are made (see Table
VII-8).
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For the construction industry, OSHA identified application groups
based on construction activities, tasks, or equipment that are commonly
recognized to create silica exposures; these tasks involve the use of
power tools (e.g., saws, drills, jackhammers) or larger equipment that
generates silica-containing dust (e.g., milling machines, rock and
concrete crushers, heavy equipment used in demolition or earthmoving).
The technological feasibility analysis for the construction industry
addresses 12 different application groups, defined by common
construction tasks or activities. OSHA organized construction workers
by application groups, rather than by industry sector or job titles,
because construction workers often perform multiple activities and job
titles do not always coincide with the sources of exposure; likewise,
the same equipment, tool or task may be called by different names throughout
construction and its various subspecialties. By organizing construction
activities this way, OSHA was able to create exposure profiles for employees
who perform the same activities in any segment of the construction
industry.
OSHA developed exposure profiles for each sector and application
group in order to characterize the baseline exposures and conditions
for each operation or task (see sections 4 and 5 of Chapter IV of the
FEA). The sample results included in the exposure profiles presented in
the Preliminary Economic Analysis (PEA) were obtained primarily from
OSHA compliance inspection reports and from NIOSH Health Hazard
Evaluation and control technology assessments. Samples were also
obtained from state plan case files, contractor site visits, published
literature and other sources. To ensure the exposure profiles were
based on the best available data, the exposure profiles were updated by
removing samples collected prior to 1990 (n = 290), leaving 2,512
samples from exposure profiles presented in the PEA from 1990 through
2007. More recent samples submitted by commenters during the rulemaking
(n = 153), primarily from 2009 through 2014, and samples obtained from
the OIS database (n = 699) from OSHA compliance inspections from 2011
to 2014 were added to exposure profiles, resulting in a total of 3,364
samples (2,483 for general industry and 881 for construction) in the
final exposure profiles. In total, these were obtained from 683 source
documents (see Table VII-6).
The exposure profiles characterize what OSHA considers to be the
baseline, or current, exposures for each job category or application
group. Where sufficient information on control measures was available,
the exposure profiles were subdivided into sample results with and
without controls and the controls were discussed in the baseline
conditions section. OSHA also discusses the sampling results associated
with specific controls in the baseline conditions section. In these
cases, the exposure profiles include exposures associated with a range
of controlled and uncontrolled exposure scenarios.
The exposure profiles include silica exposure data only for
employees in the United States. Information on international exposure
levels is occasionally referenced for perspective or in discussions of
control options. The rule covers three major polymorphs of crystalline
silica (i.e., quartz, cristobalite, and tridymite). However, the vast
majority of crystalline silica encountered by employees in the United
States is in the quartz form, and the terms crystalline silica and
quartz are often used interchangeably. Unless specifically indicated
otherwise, all silica exposure data, samples, and results discussed in
the technological feasibility analysis refer to personal breathing zone
(PBZ) measurements of respirable crystalline silica.
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\22\ OSHA silica Special Emphasis Program (SEP) inspection
reports are from inspections conducted by OSHA compliance safety and
health officers (CSHOs) under the silica National Emphasis Program
between 1993 and 2000.
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In general industry and maritime, the exposure profiles in the
technological feasibility analysis consist mainly of full-shift
samples, collected over periods of 360 minutes or more (see
Table IV-02-G in the FEA). By using this criterion, OSHA ensured that
the samples included in the exposure profiles were collected for at
least three-quarters of a typical 8-hour shift and therefore captured
most activities involving exposure to silica at which the employee
spends a substantial amount of time (Document ID 0845, pp. 38-40; see
Table IV-02-G in the FEA). Due to the routine nature of most job
activities in general industry, OSHA assumed that, for the partial
shift samples of less than 480 minutes, the same level of exposure as
measured during the sampled portion of the shift continued during the
smaller, unsampled portion. OSHA considers the 6-hour (360-minute)
sampling duration to be a reasonable criterion for including a sample
because it limits the extent of uncertainty about general industry/
maritime employees' true exposures, as no more than 25 percent of an 8-
hour shift would be unsampled. The sample result is therefore assumed
to be representative of an 8-hour time-weighted average (TWA).
Moreover, by relying primarily on sampling results 360 minutes or
greater, OSHA minimized the number of results included in the profiles
reported as below the limit of detection (LOD). The LOD for an
analytical method refers to the smallest mass of silica that can be
detected on the filter used to collect the air sample. Many
laboratories currently report an LOD of 10 [mu]g or lower for quartz
samples (Document ID 0666). As discussed in the Methodology section of
Chapter IV of the FEA, relying primarily on samples with a duration of
360 minutes or greater allows OSHA to draw the conclusion that any
sample results reported as non-detect for silica are at most 16 [mu]g/
m\3\, and well below the action level of 25 [mu]g/m\3\.
In the construction industry, approximately 43 percent of the
sampling data used in the exposure profiles also consisted of samples
collected over periods of 360 minutes or more. Most of the samples
(approximately 70%, or an additional 27%) in the construction industry
exposure profiles were collected over periods of 240 minutes or more
(see Table IV-02-G in the FEA). This allows OSHA to draw the conclusion
that any sample results reported as non-detect are below the action
level of 25 [mu]g/m\3\ (see Table IV-2-F in the FEA). Construction
workers typically spend their shifts working at multiple discrete tasks
and do not normally engage in any one task for the entire duration of a
shift; these varied tasks can include tasks that generate exposure to
respirable crystalline silica (Document ID 0677). Consequently, for
construction, OSHA assumed zero exposure during the unsampled portion
of the employee's shift unless there was evidence that silica exposures
continued for the entire shift. For example, if a sample measured an
average of 100 [mu]g/m\3\ over 240 minutes (4 hours), the result would
be recorded as 50 [mu]g/m\3\ TWA for a full 8-hour shift (480 minutes).
The Construction Industry Safety Coalition (CISC), comprised of 25
trade associations, was critical of several aspects of OSHA's
feasibility analysis. CISC objected to the assumption of zero exposure
for the unsampled portion of the work shift when calculating 8-hour
TWAs for the construction exposure profiles. It claimed that assuming
zero exposure underestimated TWA exposure levels when compared with the
alternative assumption used for general industry that the exposure
level measured during the sampled time period remained at the same
level during the unsampled period (Document ID 2319, pp. 21-25). While
there would be some uncertainty whichever assumption OSHA used, OSHA
concludes that the no-exposure assumption for unsampled portions of a
shift produces a more accurate result than the assumption of continued
exposure at the same level because of the widely-recognized differences
in work patterns between general industry and construction operations.
In general industry, most operations are at a fixed location and
involve manufacturing processes that remain relatively constant over a
work shift. Also, most of the sample durations in general industry were
360 minutes or longer, and therefore were more likely to be
representative of 8-hour TWA exposures. In contrast, construction work
is much more variable with respect to the location of the work site,
the number of different tasks performed, and the duration of tasks
performed. As stated above, tasks that generate exposure to respirable
crystalline silica in construction are often performed on an
intermittent basis (e.g., Document ID 0677).
OSHA's conclusion that the variability in sample durations for the
samples taken by OSHA in the construction industry more accurately
reflects the variability in exposure duration for these activities thus
comports with empirical experience. An assumption that exposure levels
during short-term tasks continued for the entire work shift would
substantially overestimate the actual 8-hour TWA exposures. The
Building and Construction Trades Department, AFL-CIO (BCTD) supported
OSHA's assumptions on work patterns, stating "OSHA correctly treated
the unsampled time as having `zero exposure' in its technological
feasibility assessment" (Document ID 4223, pp. 16-17). Its conclusion
was based on research performed by The Center to Protect Workers'
Rights, which developed a task-based exposure assessment model for the
construction industry that combines air sampling with task observations
and task durations in order to assess construction workers' exposure to
workplace hazards (Susi, et al., 2000, Document ID 4073, Attachment
8c). This model, when applied to masonry job sites, found that
employees spent much of their shifts performing non-silica-generating
tasks, both before and after the task involving silica exposure
(Document ID 4223, p. 16; 4073, Attachment 3a, pp. 1-2). BCTD indicated
that it was reasonable to assume these types of work patterns would be
similar for other construction tasks (Document ID 4223, pp. 16-17).
CISC also commented that OSHA did not account for the varying
amounts of crystalline silica that could exist in materials being
disturbed by employees, and that OSHA did not account for differences
in exposure results "due solely to what part of the country the
activity took place in" (Document ID 2319, pp. 26-27). OSHA has
determined that the sampling data relied on to establish baseline
silica exposures are representative of the range of silica content in
materials worked on by construction workers. Information on the percent
silica content of the respirable dust sampled was available for 588 of
the 881 samples used in the exposure profiles for construction tasks.
The silica content in these samples ranged from less than 1 percent
(non-detect) to 50 percent, with an average silica content of 9.1
percent. Thus, the sample results in the exposure profiles reflect the
range in the silica content of the respirable dust sampled by OSHA at
construction work sites. Similarly, the exposure profiles contain
exposure results from many different construction tasks taken in a
variety of locations around the country under different weather
conditions. Therefore, OSHA concludes that the exposure data used in
the exposure profiles are the best available evidence of actual
exposures in construction representing nationwide weather patterns, and
that these data reflect the broad range of silica exposures experienced
by employees in the construction industry.
Each section in the technical feasibility analysis presented in
Chapter IV of the FEA begins with descriptions of the manufacturing or
industrial process or construction activity that has potential exposure
to respirable crystalline silica, each job category or construction
task with exposure, and the major activities and sources of exposure.
Exposure profiles based on the available sampling information are then
presented and used to characterize the baseline exposures and
conditions for each operation or task (including exposure controls
currently in use). Based on the profile of baseline exposures, each
section next includes a description of additional engineering and work
practice controls that can be implemented to reduce employee exposures
to at least the rule's PEL. In addition, comments and other evidence in
the record relating to the description of the industry sector or
application group, the exposure profile and baseline conditions, and
the need for additional controls are discussed in each section.
Finally, based on the exposure profile and assessment of available
controls and other pertinent evidence in the record, each section
includes a feasibility determination for each operation, task, or
activity, including an overall feasibility determination where more
than one operation, task, or activity is addressed in the section.
In particular, OSHA evaluated information and testimony from the
record on the effectiveness of engineering and work practice controls
and either: (1) Identified controls that have been demonstrated to
reduce exposures to 50 [mu]g/m\3\ or below; or (2) evaluated the extent
to which baseline exposures would be reduced to 50 [mu]g/m\3\ or below
after applying the percent reduction in respirable silica or dust
exposure that has been demonstrated for a given control in the
operation or task under consideration or, in some cases, in analogous
circumstances. In some cases, the evidence demonstrates that most
exposures are already below the PEL. OSHA considers the evidence relied
on in making its feasibility determinations to be the best available
evidence on these issues.
For general industry and maritime, the additional engineering
controls and work practices identified by OSHA consist of equipment and
approaches that are widely available and are already used in many
applications. In some cases, the same technology can be transferred or
adapted to similar operations in other industry sectors covered under
the scope of this rule. Such controls and work practices include
implementing and maintaining local exhaust ventilation (LEV) systems
with dust collection systems (such as integrated material transfer
stations); enclosing a conveyor of silica-containing material or other
containment systems; worker isolation; process modifications; dust
suppression, systems such as water sprays; and housekeeping. In many
cases, a combination of controls is necessary to control exposures to
silica. In general industry, enclosed and ventilated equipment is often
already in use. For example, most paint and coating production
operations have switched from manual transfer of raw materials
containing crystalline silica to integrated bag dumping stations
equipped with well-ventilated enclosures and bag compactors (e.g.,
Document ID 0199, pp. 9-10; 0943, p. 87; 1607 p. 10-19; 1720, p. IV-
237). Where the evidence shows that a type of control like the material
transfer system is already being used in a sector covered by the rule,
OSHA is able to conclude that it can be used more widely in that sector
as an additional control or can be adapted to other industry sectors
for use during similar operations (see sections IV-15 Paint and
Coatings, IV-16 Porcelain Enameling, IV-11 Glass, and IV-05 Concrete
Products, of the FEA for additional information).
For construction, the exposure controls contained in Table 1 of the
rule consist primarily of water-based dust suppression systems, and LEV
systems that are integrated into hand tools and heavier equipment. As
shown in Chapter IV of the FEA, such systems are commercially available
from several vendors. In addition, equipment such as filtered,
ventilated booths or cabs and water-based systems for suppressing
fugitive dust generated by crushers and heavy equipment are available
to control exposures of construction workers to respirable crystalline
silica.
OSHA received numerous comments that disputed OSHA's preliminary
conclusion in the Notice of Proposed Rulemaking (NPRM) that a PEL of 50
[mu]g/m\3\ TWA was technologically feasible. These comments addressed
two general areas of concern: (1) Whether sampling and analytical
methods are sufficiently accurate to reliably measure respirable
crystalline silica concentrations at levels around the PEL and action
level; and (2) whether engineering and work practice controls can
reduce exposures from current levels to the lower levels required to
comply with the new standards. These issues and OSHA's technological
feasibility findings are discussed in the sections that follow. Much
more detail can be found in Chapter IV of the FEA.
2. Feasibility Determination for Sampling and Analytical Methods
As explained in Pertinent Legal Authority (Section II of this
preamble to the final rule), a finding that a standard is
technologically feasible requires that "provisions such as exposure
measurement requirements must also be technologically feasible" (see
Forging Indust. Ass'n v. Sec'y of Labor, 773 F.2d 1436, 1453 (4th Cir.
1985)). Thus, part of OSHA's technological feasibility assessment of a
new or revised health standard includes examining whether available
methods for measuring worker exposures have sufficient sensitivity and
precision to ensure that employers can evaluate compliance with the
standard and that workers have accurate information regarding their
exposure to hazardous substances. Consistent with the Supreme Court's
definition of "feasibility", OSHA finds that it is feasible to
measure worker exposures to a hazardous substance if achieving a
reasonable degree of sensitivity and precision with sampling and
analytical methods is "capable of being done" (Am. Textile Mfrs.
Inst., Inc. v. Donovan, 452 U.S. 490, 509-510 (1981)). OSHA also notes
that its analysis of the technological feasibility of the sampling and
analysis of respirable crystalline silica must be performed in
recognition of the fact that, as recognized by federal courts of
appeals, measurement error is inherent to sampling (Nat'l Min. Assoc.
v. Sec'y, U.S. Dep't of Labor, Nos. 14-11942, 14-12163, slip op. at 55
(11th Cir. Jan. 25, 2016); Am. Mining Cong. v. Marshall, 671 F.2d 1251,
1256 (10th Cir. 1982)). "Since there is no perfect sampling method,
the Secretary has discretion to adopt any sampling method that
approximates exposure with reasonable accuracy." Am. Mining Cong. v.
Marshall, 671 F.2d at 1256.
Since the late 1960s, exposures to respirable crystalline silica
(hereinafter referred to as "silica") have typically been measured
using personal respirable dust samplers coupled with laboratory
analysis of the crystalline silica content of the collected airborne
dust. The laboratory analysis is usually performed using X-ray
diffraction (XRD) or infrared spectroscopy (IR). A colorimetric method
of analysis that was used by a few laboratories has now been phased out
(Harper et al., 2014, Document ID 3998, Attachment 8, p. 1). OSHA has
successfully used XRD analysis since the early 1970s to enforce its
previous PELs for crystalline silica, which, for general industry, were
approximately equivalent to 100 micrograms per cubic meter ([mu]g/m\3\)
for quartz and 50 [mu]g/m\3\ for cristobalite and tridymite
(and within the range of about 250 [mu]g/m\3\ to 500 [mu]g/m\3\ for quartz in construction).
There are no other generally accepted methods for measuring
worker exposure to respirable crystalline silica.
The ability of current sampling and analytical methods to
accurately measure worker exposures to respirable crystalline silica
was a subject of much comment in the rulemaking record. In particular,
the Chamber of Commerce (Chamber) and American Chemistry Council (ACC)
submitted comments and testimony maintaining that existing methods do
not measure respirable crystalline silica exposures with sufficient
accuracy to support OSHA's proposal in the Notice of Proposed
Rulemaking to reduce the PEL to 50 [mu]g/m\3\ and establish the 25
[mu]g/m\3\ action level (Document ID 2285; 2288, pp. 17-21; 2307,
Attachment A, pp. 198-227; 4209, pp. 129-155; 3436, p. 8; 3456, pp. 18-
19; 3460; 3461; 3462; 4194, pp. 17-21). Similar views were expressed by
several other rulemaking participants (e.g., Document ID 2056, p. 1;
2085, p. 3; 2174; 2185, pp. 5-6; 2195, Attachment 1, p. 37; 2276, pp.
4-5; 2317, p. 2; 2379, Comments, pp. 28-30; 4224, pp. 11-14; 4232,
Attachment 1, pp. 3-24). Specifically, these commenters argue that, due
to several asserted sources of error, current sampling and analytical
methods do not meet the NIOSH accuracy criterion of 25
percent (NIOSH Manual of Analytical Methods, http://www.cdc.gov/niosh/docs/95-117/). Their arguments include: (1) That there is sampling
error attributed to bias against the particle-size selection criteria
that defines the performance of the samplers and variation in
performance between sampling devices; (2) that the accuracy and
precision of the analytical method at the low levels of silica that
would be collected at the revised PEL and action level is less than
that in the range of the previous PELs for silica, particularly in the
presence of interfering substances; and (3) variation between
laboratories analyzing comparable samples adds an unacceptable degree
of uncertainty. After considering all of the testimony and evidence in
the record, OSHA rejects these arguments and, as discussed below,
concludes that it is feasible to obtain measurements of respirable
crystalline silica at the final rule's PEL and action level with
reasonable accuracy.
OSHA is basing its conclusions on the following findings, which are
described in detail in this section. First, although there is variation
in the performance of respirable dust samplers, studies have
demonstrated that, for the majority of work settings, samplers will
perform with an acceptable level of bias (as defined by international
standards) as measured against internationally recognized particle-size
selection criteria that define respirable dust samplers. This means
that the respirable dust mass collected by the sampler will be
reasonably close to the mass that would be collected by an ideal
sampler that exactly matches the particle-size selection criteria. In
addition, OSHA finds that the measure of precision of the analytical
methods for samples collected at crystalline silica concentrations
equal to the revised PEL and action level is only somewhat higher
(i.e., somewhat less precise) than that for samples collected at
concentrations equal to the previous, higher PELs. Further, the
analytical methods can account for interferences such that, with few
exceptions, the sensitivity and precision of the method are not
significantly compromised. Studies of measurement variability between
laboratories, as determined by proficiency testing, have demonstrated a
significant decline in inter-laboratory variability in recent years.
Improvements in inter-laboratory variability have been attributed to
changes in proficiency test procedures as well as greater
standardization of analytical procedures among laboratories. Finally,
although measurement variability increases at low sample loads compared
to sample loads in the range of the former PELs, OSHA finds, based on
these studies, that the magnitude of this increase has also declined in
recent years.
Several rulemaking participants commented that OSHA's analysis of
the feasibility of sampling and analytical methods for crystalline
silica was well supported and sound (Document ID 2080, pp. 3-4; 2244,
p. 3; 2371, Attachment 1, p. 5; 3578, Tr. 941; 3586, Tr. 3284; 3577,
Tr. 851-852; 4214, pp. 12-13; 4223, pp. 30-33). Gregory Siwinski, CIH,
and Dr. Michael Lax, Medical Director of Upstate Medical University, an
occupational health clinical center, commented that current laboratory
methods can measure respirable crystalline silica at the 50 [mu]g/m\3\
PEL and 25 [mu]g/m\3\ action level, and that they have measured
exposures below the action level (Document ID 2244, p. 3). Dr. Celeste
Montforton of the George Washington School of Public Health testified
that "[i]ndustrial hygienists, company safety personnel, consultants,
and government inspectors have been conducting for decades workplace
sampling for respirable silica..." and that some governments, such
as Manitoba and British Columbia, are successfully collecting and
analyzing samples to determine compliance with their occupational
exposure limits of 25 [mu]g/m\3\ (Document ID 3577, Tr. 851-852). Dr.
Frank Mirer of the CUNY School of Public Health, formerly with the UAW
and on behalf of the AFL-CIO, stated that "[a]ir sampling is feasible
at 25 [mu]g/m\3\ and below for [a] full shift and even for part shift.
It was dealt with adequately in the OSHA proposal" (Document ID 3578,
Tr. 941).
The ACC, Chamber, and others base their argument that sampling and
analytical methods for respirable crystalline silica are insufficiently
precise on strict adherence to NIOSH's accuracy criterion of 25 percent at a 95-percent confidence level for chemical sampling
and analysis methods (http://www.cdc.gov/niosh/docs/95-117/). The ACC
pointed out that "OSHA standards typically reflect the NIOSH Accuracy
Criterion by requiring employers to use a method of monitoring and
analysis that has an accuracy of plus or minus 25 percent...," and
cited a number of OSHA standards where the Agency has included such
requirements (benzene, 29 CFR 1910.1028; lead (which requires a method
accuracy of 20%), 29 CFR 1910.1025; cadmium, 29 CFR
1910.1027; chromium (VI), 29 CFR 1910.1026) (Document ID 4209, p. 129).
However, the NIOSH accuracy criterion is not a hard, bright-line rule
in the sense that a sampling and analytical method must be rejected if
it fails to meet this level of accuracy, but is rather a goal or target
to be used in methods development. Where evidence has shown that a
method does not meet the accuracy criterion at the PEL or action level,
OSHA has stipulated a less rigorous level of accuracy to be achieved.
For example, OSHA's acrylonitrile standard requires use of a method
that is accurate to 35 percent at the PEL and 50 percent at the action level (29 CFR 1910.1045), and several
OSHA standards require that 35 percent accuracy be obtained
at the action level (arsenic, 29 CFR 1910.1018; ethylene oxide, 29 CFR
1910.1047; formaldehyde, 29 CFR 1910.1048; 1,3-butadiene, 29 CFR
1910.1051; methylene chloride, 29 CFR 1910.1052). As discussed below,
the precision of the sampling and analytical method for crystalline
silica, as currently implemented using OSHA Method ID-142 for X-ray
diffraction, is about 21 percent for quartz and
cristobalite.
In the remainder of this section, OSHA first describes available
respirable dust sampling methods and addresses comments and testimony
related to the performance and accuracy of respirable dust samplers.
Following that discussion, OSHA summarizes available analytical methods
for measuring crystalline silica in respirable dust samples and addresses
comments and evidence regarding analytical method precision, the presence
of interfering materials, and reported variability between laboratories
analyzing comparable samples.
a. Respirable Dust Sampling Devices
Respirable dust comprises particles small enough that, when
inhaled, they are capable of reaching the pulmonary region of the lung
where gas exchange takes place. Measurement of respirable dusts
requires the separation of particles by size to assess exposures to the
respirable fraction of airborne dusts. A variety of different
industrial hygiene sampling devices, such as cyclones and elutriators,
have been developed to separate the respirable fraction of airborne
dust from the non-respirable fraction. Cyclones are the most commonly
used size-selective sampling devices, or "samplers," for assessing
personal exposures to respirable dusts such as crystalline silica. The
current OSHA (ID-142, revised December 1996, Document ID 0946) and
NIOSH (Method 7500, Document ID 0901; Method 7602, 0903; Method 7603,
http://www.cdc.gov/niosh/docs/2003-154/pdfs/7603.pdf) methods for
sampling and analysis of crystalline silica specify the use of
cyclones.
Although respirable dust commonly refers to dust particles having
an aerodynamic diameter of 10 [mu]m (micrometer) or less, it is more
precisely defined by the collection efficiency of the respiratory
system as described by a particle collection efficiency model. These
models are often depicted by particle collection efficiency curves that
describe, for each particle size range, the mass fraction of particles
deposited in various parts of the respiratory system. These curves
serve as the "yardsticks" against which the performance of cyclone
samplers should be compared (Vincent, 2007, Document ID 1456). Figure
VII-1 below shows particle collection efficiency curves for two
particle size selection criteria: The criteria specified in the 1968
American Conference of Governmental Industrial Hygienists (ACGIH)
Threshold Limit Value (TLV) for respirable dust, which was the basis
for the prior OSHA general industry silica PEL, and an international
specification by the International Organization for Standardization
(ISO) and the Comit[eacute] Europ[eacute]en de Normalisation (CEN)
known as the ISO/CEN convention, which was adopted by ACGIH in 1994 and
is the basis for the definition of respirable crystalline silica in the
final rule. In addition to the curves, which cover the full range of
particle sizes that comprise respirable dust, particle size collection
criteria are also often described by their 50-percent respirable "cut
size" or "cut point." This is the aerodynamic diameter at which 50
percent of the particle mass is collected, i.e., the particle size that
the sampler can collect with 50-percent efficiency. Particles with a
diameter smaller than the 50-percent cut point are collected with an
efficiency greater than 50 percent, while larger-diameter particles are
collected with an efficiency less than 50 percent. The cut point for
the 1968 ACGIH specification is 3.5 [mu]m and for the ISO/CEN
convention is 4.0 [mu]m (Lippman, 2001, Document ID 1446, pp. 107,
113).
For most workplace conditions, the change in the criteria for
respirable dust in the final rule would theoretically increase the mass
of respirable dust collected over that measured under the previous
criteria by an amount that depends on the size distribution of airborne
particles in the workplace. Soderholm (1991, Document ID 1661) examined
these differences based on 31 aerosol size distributions measured in
various industrial workplaces (e.g., coal mine, lead smelter, brass
foundry, bakery, shielded metal arc [SMA] welding, spray painting,
pistol range) and determined the percentage increase in the mass of
respirable dust that would be collected under the ISO/CEN convention
over that which would be collected under the 1968 ACGIH criteria.
Soderholm concluded that, for all but three of the 31 size
distributions that were evaluated, the increased respirable dust mass
that would be collected using the ISO/CEN convention for respirable
dust instead of the 1968 ACGIH criteria would be less than 30 percent,
with most size distributions (25 out of the 31 examined, or 80 percent)
resulting in a difference of between 0 and 20 percent (Document ID
1661, pp. 248-249, Figure 1). In the PEA, OSHA stated its belief that
the magnitude of this effect does not outweigh the advantages of
adopting the ISO/CEN convention. In particular, most respirable dust
samplers on the market today are designed and calibrated to perform in
a manner that closely conforms to the international ISO/CEN convention.
Incorporating the ISO/CEN convention in the definition of
respirable crystalline silica will permit employers to use any sampling
device that conforms to the ISO/CEN convention. There are a variety of
these cyclone samplers on the market, such as the Dorr-Oliver, Higgins-
Dewell (HD), GK2.69, SIMPEDS, and SKC aluminum. In the PEA, OSHA
reviewed several studies demonstrating that these samplers collect
respirable particles with efficiencies that closely match the ISO/CEN
convention (Document ID 1720, pp. IV-21--IV-24). In addition to cyclone
samplers, there are also personal impactors available for use at flow
rates from 2 to 8 L/min that have been shown to conform closely with
the ISO/CEN convention (Document ID 1834, Attachment 1). Cyclones and
impactors both separate particles by size based on inertia. When an
airstream containing particles changes direction, smaller particles
remain suspended in the airstream and larger ones impact a surface and
are removed from the airstream. Cyclones employ a vortex to separate
particles centrifugally, while impactors use a laminar airflow around a
flat surface such that particles in the desired size range impact onto
the surface.
The current OSHA sampling method for crystalline silica, ID-142, is
the method used by OSHA to enforce the silica PELs and is used by some
employers as well. It specifies that a respirable sample be collected
by drawing air at 1.7 0.2 liters/minute (L/min) through a
Dorr-Oliver 10 millimeter (mm) nylon cyclone attached to a cassette
containing a 5-[mu]m pore-size, 37-mm diameter polyvinyl chloride (PVC)
filter (Document ID 0946). NIOSH sampling and analysis methods for
crystalline silica (Method 7500, Method 7602, Method 7603) have also
adopted the ISO/CEN convention with flow rate specifications of 1.7 L/
min for the Dorr-Oliver 10-mm nylon cyclone and 2.2 L/min for the HD
cyclone (Document ID 0901; 0903). Method 7500 also allows for the use
of an aluminum cyclone at 2.5 L/min. NIOSH is revising its respirable
dust method to include any sampler designed to meet the ISO/CEN
criteria (Document ID 3579, Tr. 218).
The devices discussed above, when used at the appropriate flow
rates, are capable of collecting a quantity of respirable crystalline
silica that exceeds the quantitative detection limit for quartz (the
principle form of crystalline silica) of 10 [mu]g for OSHA's XRD method
(Document ID 0946). For several scenarios based on using various
devices and sampling times (8-hour, 4-hour, and 1-hour samples), OSHA
calculated the amount of respirable quartz that would be collected at
quartz concentrations equal to the existing general industry PEL, the
proposed (and now final) rule's PEL, and the proposed (and now final)
rule's action level. As seen in Table IV.3-A, computations show that
the 10-mm nylon Dorr-Oliver operated at an optimized flow rate of 1.7
L/min, the aluminum cyclone operated at 2.5 L/min, the HD cyclone
operated at 2.2 L/min, and the GK2.69 operated at 4.2 L/min will all
collect enough quartz during an 8-hour or 4-hour sampling period to
meet or exceed the 10 [micro]g quartz limit of quantification for OSHA
Method ID-142. Therefore, each of the commercially available cyclones
is capable of collecting a sufficient quantity of quartz to exceed the
limit of quantification when airborne concentrations are at or below
the action level, provided that at least 4-hour air samples are taken.
Table VII-7 also shows that the samplers can collect enough silica to
meet the limit of quantification when the airborne respirable silica
concentration is below the action level of 25 [mu]g/m\3\, in one case
as low as 5 [mu]g/m\3\.
A comment from the National Rural Electric Cooperative Association
(NRECA) stated that the current OSHA and NIOSH analytical methods
require sampling to collect a minimum of 400 liters of air, and that at
the flow rates specified for current samplers, sampling would have to
be performed for approximately 2.5 to 4 hours; however, this is
considerably longer than most construction tasks performed in
electrical transmission and distribution work, which tend to last 2
hours or less (Document ID 2365, pp. 2, 6-7). OSHA does not view this
discrepancy to be a problem. The minimum sampling times indicated in
the OSHA and NIOSH methods contemplate that exposure occurs over most
of the work shift. Construction operations frequently involve shorter-
term tasks after which there is no further exposure to respirable
crystalline silica. In those situations, OSHA often does not itself
continue sampling during inspections and does not expect employers to
continue sampling when there is no exposure to silica, and considers
the sampling result that is obtained from shorter-term task sampling to
be sufficient to represent a worker's 8-hour time-weighted-average
(TWA) exposure, which can be calculated assuming no exposure for the
period of the shift that is not sampled. If the airborne concentration
of silica for the task is low, the sampling result would likely be
below the limit of quantification. In that case, it would be safe for
the employer to assume that the exposure is below the action level.
Transition to ISO-CEN Criteria for Samplers
In the final rule, OSHA is adopting the ISO/CEN particle size-
selective criteria for respirable dust samplers used to measure
exposures to respirable crystalline silica. Under the ISO/CEN
convention, samplers should collect 50 percent of the mass of particles
that are 4 [mu]m in diameter (referred to as the cut point), with
smaller particles being collected at higher efficiency and larger
particles being collected at lower efficiency. Particles greater than
10 [mu]m in diameter, which are not considered to be respirable, are to
be excluded from the sample based on the ISO/CEN convention (Document
ID 1446, pp. 112-113).
Several rulemaking participants supported OSHA's proposed adoption
of the ISO/CEN criteria for respirable dust samplers (Document ID 1730;
1969; 3576, Tr. 290; 3579, Tr. 218-219; 4233, p. 4). For example, a
representative of SKC, Inc., which manufactures samplers used to
collect respirable crystalline silica, stated that:
Adoption of the ISO/CEN performance standard for respirable dust
samplers by OSHA will bring the U.S. regulatory standards in line
with standards/guidelines established by other occupational health
and safety agencies, regulatory bodies, and scientific consensus
organizations around the world. It will also align OSHA performance
criteria for respirable dust samplers to that of NIOSH (Document ID
1730, pp. 1-2).
As discussed above, OSHA's previous (and currently enforceable)
general industry PEL for crystalline silica was based on a 1968 ACGIH
definition, which specified a model with a cut point of 3.5 [mu]m.
Based on available studies conducted over 40 years ago, the Dorr-Oliver
10-mm cyclone was thought to perform closely to this specification. As
such, it is the sampling device specified in OSHA's respirable dust
sampling and analytical methods, including Method ID-142 for respirable
crystalline silica (Document ID 0946). For most sizes of respirable
particles, the ISO/CEN convention specifies a greater efficiency in
particle collection than does the 1968 ACGIH model; consequently,
samplers designed to meet the ISO/CEN convention will capture somewhat
greater mass of airborne particle than would a sampler designed to the
1968 ACGIH model, with the magnitude of the increased mass dependent on
the distribution of particle sizes in the air. For most particle size
distributions encountered in workplaces, the increase in dust mass
theoretically collected under the ISO/CEN convention compared to the
ACGIH model would be 25 percent or less (Soderholm, 1991, Document ID
1661).
Several rulemaking participants commented that moving from the 1968
ACGIH model to the ISO/CEN convention effectively decreased the PEL and
action level below the levels intended, since more dust would be
collected by samplers that conform to the ISO/CEN convention than by
those that conform to the 1968 ACGIH model
(Document ID 2174; 2195, p. 30; 2285, pp. 3-4; 2307, Attachments
10, p. 19, and 12, p. 3; 2317, p. 2; 3456, p. 10; 4194, pp. 15-16). For
example, the Chamber commented that adopting the ISO/CEN specification
"can result in citations for over exposure to quartz dust where none
would have been issued prior to the adoption of this convention"
(Document ID 2288, p. 16). OSHA disagrees with this assessment because,
based on more recent evaluations (Bartley et al., 1994, Document ID
1438, Attachment 2; Lee et al., 2010, 3616; 2012, 3615), the Dorr-
Oliver 10-mm cyclone that has been used by the Agency for enforcement
of respirable dust standards for decades has been found to perform
reasonably closely (i.e., with an acceptable level of bias) to the ISO/
CEN specification when operated at the 1.7 L/min flow rate specified by
OSHA's existing method. Consequently, OSHA and employers can continue
to use the Dorr-Oliver cyclone to evaluate compliance against the final
PEL of 50 [mu]g/m\3\ without having to change equipment or procedures,
and thus would not be collecting a greater quantity of dust than
before. Furthermore, OSHA notes that other ISO/CEN-compliant samplers,
such as the SKC 10-mm aluminum cyclone and the HD cyclone specified in
the NIOSH Method 7500, are already widely used by investigators and
employers to evaluate exposures to respirable crystalline silica
against benchmark standards. Therefore, the change from the ACGIH
convention to the ISO/CEN convention is more a continuation of the
status quo than a drastic change from prior practice.
Other rulemaking participants argued that moving to the ISO/CEN
convention effectively invalidates OSHA's risk and feasibility analyses
since the exposure data that underlie these analyses were obtained
using devices conforming to the 1968 ACGIH specification. For example,
Thomas Hall, testifying for the Chamber, stated that moving to the ISO/
CEN convention "would produce a difference in [current] exposure
results from...historical measurements that have been used in the
risk assessments" (Document ID 3576, Tr. 435). Similarly, in its pre-
hearing comments, the ACC argued that:
When OSHA conducted technological feasibility studies for
attaining the proposed 50 [mu]g/m\3\ PEL, the Agency based its
decisions on samples collected using the current ACGIH method, not
the proposed ISO/CEN method. Thus, the switch to the ISO/CEN
definition will have two impacts on feasibility. First, it will add
uncertainty regarding OSHA's technological feasibility determination
because greater reductions in exposure will be required to achieve a
50 [mu]g/m\3\ PEL measured by the ISO/CEN definition than by the
ACGIH definition that OSHA applied. Second, OSHA's use of the ACGIH
definition to estimate compliance costs causes the Agency to
underestimate the costs of achieving the 50 [mu]g/m\3\ PEL because
OSHA did not account for the additional workers whose exposures
would exceed the proposed PEL under the ISO/CEN definition but who
would be exposed below the proposed PEL if measured under the ACGIH
definition (Document ID 2307, Attachment 8, p. 9).
OSHA rejects these arguments for the following reasons. First, with
respect to the risk information relied on by the Agency, exposure data
used in the various studies were collected from employer records
reflecting use of several different methods. Some studies estimated
worker exposures to silica from particle counts, for which the sampling
method using impingers does not strictly conform to either the ACGIH or
ISO/CEN conventions (e.g., Rice et al., Document ID 1118; Park et al.,
Document ID 0405; Attfield and Costello, Document ID 0285; Hughes et
al., Document ID 1060). Other studies used measurements taken using
cyclone samplers and modern gravimetric methods of silica analysis
(e.g., Rice et al. and Park et al., data obtained from cyclone pre-
separator up through 1988, Document ID 1118, 0405; Hughes et al., data
from 10-mm nylon cyclone through 1998, Document ID 1060). OSHA believes
it likely that exposure data collected using cyclones in these studies
likely conformed to the ISO/CEN specification since flow rates
recommended in the OSHA and NIOSH methods were most likely used. The
studies by Miller and MacCalman (Document ID 1097) and by Buchanan et
al. (Document ID 0306) used exposure measurements made with the MRE
113A dust sampler, which does conform reasonably well with the ISO/CEN
specification (Gorner et al., Document ID 1457, p. 47). The studies by
Chen et al. (2001, Document ID 0332; 2005, Document ID 0985) estimated
worker exposures to silica from total dust measurements that were
converted to respirable silica measurements from side-by-side
comparisons of the total dust sampling method with samples taken using
a Dorr-Oliver cyclone operated at 1.7 L/min, which is consistent with
the ISO/CEN convention (see Section V, Health Effects, of this preamble
and OSHA's Preliminary Review of Health Effects Literature and
Preliminary Quantitative Risk Assessment, Document ID 1711). Thus, it
is simply not the case that the exposure assessments conducted for
these studies necessarily reflect results from dust samples collected
with a device conforming to the 1968 ACGIH particle size-selective
criteria, and OSHA finds that no adjustment of OSHA's risk estimates to
reflect exposure measurements consistent with the ISO/CEN convention is
warranted.
Second, with respect to the feasibility analysis, OSHA relied on
exposure data and constructed exposure profiles based principally on
measurements made by compliance officers using the Dorr-Oliver cyclone
operated at 1.7 L/min, as the Agency has done since Method ID-142 was
developed in 1981, well before the 1990 cut-off date for data used to
construct the exposure profiles. As explained earlier in the section,
recent research shows that the Dorr-Oliver cyclone operated at this
flow rate performs in a manner consistent with the ISO/CEN
specification. Other data relied on by OSHA comes from investigations
and studies conducted by NIOSH and others who used various cyclones
that conform to the ISO/CEN specification. Thus, OSHA finds that the
exposure profiles being relied on to evaluate feasibility and costs of
compliance do not reflect sample results obtained using the 1968 ACGIH
model. Instead, the vast majority of sample results relied upon were
collected in a manner consistent with the requirements of the final
rule. NIOSH supported this assessment, stating that, given the Dorr-
Oliver sampler operated at a flow rate of 1.7 L/min conforms closely to
the ISO/CEN convention, "there is continuation with historic exposure
data" (Document ID 4233, p. 4). For these reasons, OSHA finds that it
is appropriate to rely on the feasibility and cost analyses and
underlying exposure data without adjustment to account for the final
rule's adoption of the ISO/CEN specification for respirable dust
samplers.
Sampling Error
Several commenters raised issues concerning the accuracy of
respirable dust samplers in relation to the ISO/CEN criteria, asserting
that sampling respirable dust is uncertain and inaccurate, and that
there are numerous sources of error. Chief among these were Dr. Thomas
Hall of Industrial Hygiene Specialty Resources, LLC, testifying for the
Chamber, and Paul K. Scott of ChemRisk, testifying for the ACC.
The Chamber's witnesses and others referenced studies showing that
all samplers were biased against the ISO/CEN particle-size selection
convention. This means that the sampler would collect more or less mass
of respirable particulate than would an ideal sampler that exactly
conforms to the ISO/CEN convention. OSHA discussed this issue in the PEA,
noting that most samplers tend to over-sample smaller particles and
under-sample larger particles, compared to the ISO/CEN convention,
at their optimized flow rates. This means that, for particle size
distributions dominated by smaller particles, the sampler will collect
more mass than would be predicted from an ideal sampler that exactly
conforms to the ISO/CEN convention. For particle size distributions
dominated by larger particles in the respirable range, less
mass would be collected than predicted. In the PEA, OSHA evaluated
several studies that showed that several cyclone samplers exhibited a
bias of 10 percent or less for most particle size distributions
encountered in the workplace. Some of these studies found biases as
high as 20 percent but only for particle size distributions
having a large mass median aerodynamic diameter (MMAD) (i.e., 20
[micro]m or larger) and narrow distribution of particle sizes (i.e., a
geometric standard deviation (GSD) of 2 or less) (Document ID 1720, pp.
IV-21--IV-24). Such particle size distributions are infrequently seen
in the workplace; for well-controlled environments, Frank Hearl of
NIOSH testified that the GSD for typical particle size distributions
would be about 2 (Document ID 3579, Tr. 187). Dr. Hall (Document ID
3576, Tr. 502) testified, similarly, that it would be around 1.8 to 3
for well-controlled environments and higher for uncontrolled
environments (see also Liden and Kenny, 1993, Document ID 1450, p. 390,
Figure 5; Soderholm, 1991,1661, p. 249, Figure 1). Furthermore, a
particle size distribution with a large MMAD and small GSD would
contain only a very small percentage (< 10%) of respirable dust that
would be collected by a sampler optimized to the ISO/CEN criteria
(Soderholm, 1991, Document ID 1661, p. 249, Figure 2). According to
Liden and Kenny (1993), "samplers will perform reasonably well
providing the absolute bias in sampling is kept to within 10 percent .
. . this aim can be achieved...over the majority of size
distributions likely to be found in field sampling" (Document ID 1450,
p. 390).
Dr. Hall commented that "sampling results differ depending on the
choice of sampler used" and that published evaluations have shown that
they "have different collection efficiencies, specifically with
respect to particle collection in aerosol clouds with large [MMADs
greater than] 10 [mu]m" (Document ID 2285, p. 16). He cited the work
of Gorner et al. (2001, Document ID 1457), who noted that the cut
points achieved by different samplers varied considerably and that flow
rates were optimized to bring their respective cut points closer to the
ISO/CEN convention, as evidence that commercial samplers do not provide
consistently similar results. However, OSHA interprets the findings of
Gorner et al. as actually providing evidence of samplers' consistency
with the ISO/CEN convention for most particle size distributions
encountered in the workplace. This study, which was reviewed in OSHA's
PEA, evaluated 15 respirable dust samplers, most of them cyclones,
against 175 different aerosol size distributions and evaluated the bias
and accuracy of sampler performance against the ISO/CEN convention.\23\
Gorner et al. found that most of the samplers they tested met the
international criteria for acceptable bias and accuracy (described by
Bartley et al., 1994, Document ID 1438, Attachment 2 and Gorner et al.,
2001, 1457); under those criteria, bias is not to exceed 10 percent and
inaccuracy is not to exceed 30 percent for most of the size
distributions tested (Document ID 1457, pp. 49, 52; Document ID 1438,
Attachment 2, p. 254). Gorner et al. concluded that the samplers "are
therefore suitable for sampling aerosols within a wide range of
particle size distributions" (Document ID 1457, p. 52). Gorner et al.
also stated that sampler performance should be evaluated by examining
bias and accuracy rather than simply comparing cut points and slopes
against the ISO/CEN convention (Document ID 1457, p. 50), as Dr. Hall
did in his comments.
---------------------------------------------------------------------------
\23\ Bias means the difference in particle mass collected by a
sampler as compared to the mass that would be collected by a
hypothetical ideal sampler that exactly matched the ISO/CEN
convention. Accuracy includes bias and other sources of error
related to the testing procedure (e.g., errors in flow rate and
particle mass analysis)(Document ID 1457, p. 49).
---------------------------------------------------------------------------
The ACC's witness, Mr. Scott, noted several potential sources of
sampling error in addition to the conventional 5-percent pump flow rate
error that is included in OSHA's estimate of sampling and analytical
error (SAE, discussed further in Section IV-3.2.4--Precision of
Measurement). These included variation in performance of the same
cyclone tested multiple times (estimated at 6 percent) and variation
between different cyclones tested in the same environment (estimated at
5 percent) (Document ID 2308, Attachment 6, pp. 7-8). Based on
published estimates of the magnitude of these kinds of errors, Mr.
Scott estimated a total sampling error of 9.3 percent after factoring
in pump flow rate error, inter-sampler error, and intra-sampler error;
this would increase the SAE by 4 percent, for example, from 15 to 19
percent at 50 [mu]g/m\3\ (Document ID 2308, pp. 8-9). This means that,
if all sampler error were factored into the SAE, an employer would be
considered out of compliance with the PEL for an exposure exceeding
59.5 [micro]g/m\3\, rather than at 57.5 [micro]g/m\3\ if only pump
error were considered, a difference of only 2 [micro]g/m\3\ in silica
concentration. OSHA therefore concludes that intra- and inter-sampler
error of the types described by Mr. Scott do not materially change how
OSHA would enforce, or how employers should evaluate, compliance with
the final rule PEL.
As described above, many different respirable dust samplers have
been evaluated against the ISO/CEN convention for different particle
size distributions and, in general, these biases are small for the vast
majority of particle size distributions encountered in the workplace.
OSHA concludes that Mr. Scott's estimate likely overstates the true
total sampling error somewhat because the measurements of sampler bias
against the ISO/CEN criteria involve accurately measuring and
maintaining consistent pump flow rates during the testing of the
samplers; therefore, adding pump flow rate error to estimates of inter-
and intra-sampler measurement error is redundant. Furthermore, if an
employer relies on a single type of cyclone sampler, as is OSHA's
practice, there would be no inter-sampler variability between different
field samples. If an employer is concerned about this magnitude of
uncertainty, he or she can choose simply to use the same sampling
device as OSHA (i.e., the Dorr-Oliver cyclone operated at a flow rate
of 1.7 L/min, as specified in Method ID-142) and avoid any potential
measurement uncertainties associated with use of different sampling
devices.
The American Foundry Society (AFS) commented that the ASTM Standard
D4532 for respirable dust sampling includes errors for sampling,
weighing, and bias, none of which is included in OSHA's pump flow rate
error (Document ID 2379, p. 29). This ASTM standard describes
procedures for sampling respirable dust using a 10-mm cyclone, HD
cyclone, or aluminum cyclone in a manner identical to that prescribed
in the OSHA and NIOSH methods for sampling and analysis of silica.
Thus, the kinds of errors identified by AFS are the same as those
reflected in Mr. Scott's testimony described above, which, as OSHA has
shown, do not result in substantial uncertainties in exposure
measurement.
OSHA further observes that the kinds of sampling errors described
by rulemaking participants are independent of where the PEL is
established and are not unique to silica; these biases have existed
since OSHA began using the Dorr-Oliver cyclone to enforce the previous
PELs for crystalline silica, as well as many other respirable dust
standards, over 40 years ago. OSHA also believes that sampling error
within the range quantified by Mr. Scott would be unlikely to change
how an employer makes risk management decisions based on monitoring
results. One Chamber witness, Gerhard Knutson, President of Knutson
Ventilation, testified that the type of cyclone used to obtain exposure
measurements for crystalline silica was not typically a consideration
in designing industrial ventilation systems (Document ID 3576, Tr. 521-
522). Dr. Hall, another Chamber witness, also testified that he has
used all three sampling devices listed in the NIOSH Method 7500 and has
not historically made a distinction between them, though he might make
different decisions today based on the aerosol size distribution
encountered in a particular workplace (Document ID 3576, Tr. 522-523).
In his pre-hearing submission, Dr. Hall cited the Gorner et al. (2001,
Document ID 1457) study as recommending that "rough knowledge of the
aerosol size distribution can guide the choice of an appropriate
sampling technique" (Document ID 2285, p. 8). OSHA concludes it
unlikely that, in most instances, it is necessary to obtain such data
to minimize sampling bias for risk management purposes, given the
overall magnitude of the bias as estimated by Mr. Scott (i.e., an error
of less than 10 percent).
High Flow Samplers
OSHA's PEA also described high-flow samplers, in particular the
GK2.69 from BGI, Inc., which is run at a flow rate of 4.2 L/min in
contrast to 1.7 L/min for the Dorr-Oliver and 2.5 L/min for the
aluminum cyclone. High-flow devices such as this permit a greater
amount of dust to be collected in low-dust environments, thus improving
sensitivity and making it more likely that the amount of silica
collected will fall within the range validated by current analytical
methods. For example, a Dorr-Oliver run at 1.7 L/min where the silica
concentration is 50 [mu]g/m\3\ would collect 41 [mu]g of silica over 8
hours, compared to the GK2.69 run at 4.2 L/min, which would collect 101
[mu]g of silica (see Table IV.3-A), well within the validation range of
the OSHA method (i.e., the range over which precision is determined, 50
to 160 [mu]g) (Document ID 0946, p. 1). Several rulemaking participants
supported OSHA's proposal to permit use of high-flow samplers that
conform to the ISO/CEN convention (Document ID 2256, Attachment 3, p.
12; 3578, Tr. 941; 3586, Tr. 3286-3287; 4233, p. 4). For example,
William Walsh, representing the American Industrial Hygiene Association
(AIHA) Laboratory Accreditation Programs, stated that he could measure
concentrations of silica at the 25 [mu]g action level with sufficient
precision by using a high-flow device (Document ID 3586, Tr. 3287).
The performance of high-flow samplers has been extensively studied,
particularly by Lee et al. (2010, Document ID 3616; 2012, 3615), Stacey
et al. (2013, Document ID 3618), and Kenny and Gussman (1997, Document
ID 1444). The Kenny and Gussman study, which was reviewed in OSHA's
PEA, found the GK2.69 had good agreement with the ISO/CEN convention at
the 4.2 L/min flow rate, with a cut point of 4.2 [mu]m and a collection
efficiency curve that was steeper than the ISO/CEN (i.e., it was more
efficient for smaller particles and less so for larger particles). For
particle size distributions up to an MMAD of 25 [mu]m and GSD of 1.5 to
3.5, bias against the ISO/CEN convention was generally between +5 and -
10 percent. Bias was greater (-20 percent) for particle size
distributions having an MMAD above 10 [mu]m and a low GSD which,
according to the authors, are not likely to be encountered (Document ID
1444, p. 687, Figure 7).
The Lee et al. (2010, Document ID 3616; 2012, 3615) and Stacey
(2013, Document ID 3618) studies of high-flow sampler performance are
the product of a collaborative effort between NIOSH and the United
Kingdom's Health and Safety Executive (HSE) that examined the
performance of three high-flow samplers; these were the GK2.69, the
CIP10-R (Arelco ARC, France), and the FSP10 (GSA, Germany). The FSP10
runs at a flow rate of 10 L/min and the combination of large cyclone
and heavy-duty pump may be burdensome for workers to wear. The CIP-10
also runs at 10 L/min and is much smaller and lighter, but uses a
collection technology different from cyclones, which may be unfamiliar
to users. According to NIOSH, cyclones operating around 4 L/min "offer
a current compromise" for obtaining higher flow rates without the need
to use larger personal samplers that may be difficult for workers to
wear (Document ID 2177, Attachment B, p. 13; 3579, Tr. 163)." For this
reason, OSHA's review of these studies focuses on the performance of
the GK2.69 cyclone.
Lee et al. (2010, Document ID 3616) tested the GK2.69 against 11
sizes of monodisperse aerosol and found that, at the 4.2 L/min flow
rate, the estimated bias against the ISO/CEN convention was positive
for all particle size distributions (i.e., the sampler collected
greater mass of particulate than would be predicted from an ideal
sampler that exactly conformed to ISO/CEN), with a 10-percent
efficiency for collecting 10 [mu]m particles, compared to 1 percent for
the ISO/CEN convention. The authors estimated a bias of +40 percent for
a particle size distribution having a MMAD of 27.5 [mu]m. However,
adjustment of the flow rate to 4.4 L/min resulted in biases of less
than 20 percent for most particle size distributions and the collection
efficiency for 10 [mu]m particles was much closer to the ISO/CEN
convention (2.5 percent compared to 1 percent). The authors concluded
that, at the higher flow rate, the GK2.69 cyclone met the international
standard for sampler conformity to relevant particle collection
conventions (European Committee for Standardization, EN 13205, cited in
Lee et al., 2010, Document ID 3616), and would provide relatively
unbiased measurements of respirable crystalline silica (Document ID
3616, pp. 706, 708, Figure 5(a)).
Lee et al. (2012, Document ID 3615) performed a similar evaluation
of the same samplers using coal dust but included analysis of
crystalline silica by both XRD and IR. The GK2.69 runs at a flow rate
of 4.4 L/min collected somewhat more respirable dust and crystalline
silica than would be predicted from differences in flow rates, compared
to the 10-mm nylon cyclone, but nearly the same as the Higgins-Dewell
cyclone. The authors found that the GK2.69 "showed non-significant
difference in performance compared to the low-flow rate samplers"
(Document ID 3615, p. 422), and that "the increased mass of quartz
collected with high-flow rate samplers would provide precise analytical
results (i.e., significantly above the limit of detection and/or the
limit of quantification) compared to the mass collected with low-flow
rate samplers, especially in environments with low concentrations of
quartz..." (Document ID 3615, p. 413). Lee et al. concluded that
"[a]ll samplers met the [EN 13205] requirements for accuracy for
sampling the ISO respirable convention" (Document ID 3615, p. 424).
Stacey et al. (2013, Document ID 3618) used Arizona road dust
aerosols to evaluate the performance of high-flow samplers against the Safety In
Mines Personal Dust Sampler (SIMPEDS), which is the low-flow sampler
used to measure respirable crystalline silica in the U.K. For the
GK2.69, use of a flow rate of 4.2 L/min or 4.4 L/min made little
difference in the respirable mass collected, and there was closer
agreement between the GK2.69 and SIMPEDS sampler when comparing
respirable crystalline silica concentration than respirable dust
concentration, and the difference was not statistically significant
(Document ID 3618, p. 10). According to NIOSH, the findings by Stacey
et al. (2013) corroborate those of Lee et al. (2010 and 2012) that the
GK2.69 meets the ISO/CEN requirements for cyclone performance and that
either the 4.2 L/min or 4.4 L/min flow rate "can be used to meet the
ISO convention within acceptable limits" (Document ID 2177, p. 13).
Mr. Scott testified that the high-flow samplers (including the
GK2.69) studied by Lee et al., (2010 and 2012), "tended to have a
substantial bias towards collecting more respirable particulates than
the low-flow samplers, collecting between 12 percent and 31 percent
more mass" because high-flow samplers tend to collect a higher
proportion of larger particles (Document ID 3582, Tr. 1984). In his
written testimony, he noted that Lee et al. (2010) reported a nearly
10-fold higher collection efficiency for 10 [mu]m particles compared to
the ISO/CEN standard. However, Mr. Scott's testimony ignores Lee et
al.'s findings that the oversampling of larger particles seen at a flow
rate of 4.2 L/min was not apparent at the higher 4.4 L/min flow rate
and that Lee et al. (2010) concluded that agreement with the ISO/CEN
convention was achieved at the higher flow rate (Document ID 3616, pp.
706, 708). In addition, oversampling of larger particles at the 4.2 L/
min flow rate was not reported by Lee et al. (2012, Document 3615) or
Stacey et al. (2013, Document ID 3618).
Dr. Hall expressed a similar concern as Mr. Scott. He cited Lee et
al. (2010) as stating that the GK2.69 would collect significantly more
aerosol mass for particle size distributions having an MMAD of more
than 6 [mu]m. He also cited Lee et al. (2010 and 2012) for the finding
that the GK2.69 collects from 1.8 to 3.84 times as much aerosol mass as
the Dorr-Oliver or Higgins-Dewell cyclones (Document ID 2285, p. 12).
In his pre-hearing comment, Dr. Hall stated that "[f]or aerosol clouds
with a [MMAD] greater than 10 [mu]m, the expected absolute bias can
range be (sic) between 20 and 60%" and "the total variability for the
method SAE can be as large as 85-90%" (Document ID 2285, pp. 15-16).
OSHA notes that both Dr. Hall and Mr. Scott focus their comments
regarding the performance of high-flow samplers on environments where
the particle size distribution is characterized by larger particles and
small variance (GSD). The findings by Lee et al. (2010) show that, at a
flow rate of 4.2 L/min, under this experimental system, there were
large positive biases (>20 percent) against the ISO/CEN convention for
nearly all particle size distributions having MMAD of 5 to 10 [mu]m
(Document ID 3616, pp. 704-706, Figure 3(b)). However, when the flow
rate was adjusted to 4.4 L/min, bias exceeding 20 percent was found to
occur primarily with particle size distributions having GSDs under 2.0
and MMAD greater than 10 [mu]m (Document ID 3616, p. 707, Figure 5(a)).
As discussed above, it is rare to encounter particle size distributions
having relatively large MMADs and small GSDs, so the high variability
attributed to high-flow samplers by Dr. Hall and Mr. Scott should not
be of concern for most workplace settings. Further, sampler performance
is considered acceptable if the bias and accuracy over at least 80
percent of the remaining portion of the bias map are within acceptable
limits, which are no more than 10 and 30 percent, respectively
(Document ID 1457, pp. 49, 52). The Lee et al. studies (2010 and 2012)
concluded that the high-flow samplers tested met these international
requirements for accuracy for sampling the ISO/CEN convention, and the
Stacey et al. (2013) study found that their results compared favorably
with those of Lee et al. (2012). Therefore, OSHA finds that the
uncertainties characterized by Dr. Hall and Mr. Scott are exaggerated
for most workplace situations, and that there is substantial evidence
that high-flow samplers, in particular the GK2.69 cyclone, can be used
to collect respirable crystalline silica air samples in most workplace
settings without introducing undue bias.
Mr. Scott, testifying for the ACC, was of the opinion that,
although high-flow samplers have been evaluated by Gorner et al. (2001,
Document ID 1457) and Lee et al. (2010, Document ID 3616; 2012, 3615)
with respect to their sampling efficiencies as compared to the ISO/CEN
convention and their performance compared to low-flow samplers, none of
the studies evaluated the accuracy and precision using methods
recommended in NIOSH's Guidelines for Air Sampling and Analytical
Method Development and Evaluation (1995, http://www.cdc.gov/niosh/docs/95-117/)
(Document ID 2308, Attachment 6, p. 18). OSHA understands Mr.
Scott to contend that the sampler must be tested against a generated
atmosphere of respirable crystalline silica and that the precision of
the sampling and analytical method must be determined overall from
these generated samples.
OSHA does not agree with the implication that, until high-flow
samplers have been evaluated according to the NIOSH (1995) protocol,
the findings from the studies described above are not sufficient to
permit an assessment of sampler performance. The NIOSH Guidelines cited
by Mr. Scott state that "[a]n experimental design for the evaluation
of sampling and analytical methods has been suggested. If these
experiments are not applicable to the method under study, then a
revised experimental design should be prepared which is appropriate to
fully evaluate the method" (http://www.cdc.gov/niosh/docs/95-117/, p.
1). These guidelines contemplate the development of entirely new
sampling and analytical methods. Because the analytical portion of the
sampling and analytical method for respirable crystalline silica was
already fully evaluated before the GK2.69 was developed (Kenny and
Gussman, 1997, Document ID 1444), it was only necessary to evaluate the
performance of the GK2.69 high-flow sampler. As described above, the
studies by Lee et al. (2010, Document ID 3616; 2012, 3615) and Stacey
et al. (2013, Document ID 3618) reflect a collaborative effort between
NIOSH in the U.S. and HSE in the U.K. to evaluate the performance of
high-flow respirable dust samplers. The Lee et al. (2010, 2012) studies
were conducted by NIOSH laboratories in Morgantown, West Virginia with
peer review by HSE scientists, and the Stacey et al. (2013) study was
conducted by HSE at the Health and Safety Laboratory at Buxton in the
U.K. Both Lee et al. (2012) and Stacey et al. (2013) concluded that
high-flow samplers studied, including the GK2.69, met the EN 13205
requirements for accuracy for sampling against the ISO/CEN convention,
demonstrating that results from these two national laboratories
compared favorably. OSHA concludes these peer-reviewed studies,
performed by NIOSH and HSE scientists, meet the highest standards for
effective methods evaluation and therefore does not agree with the
suggestion that additional work following NIOSH's protocol is
necessary. Comments submitted by NIOSH indicate that the Lee et al.
(2010, 2012) and Stacy et al. (2013) studies are sufficient to
establish the GK2.69 high-flow sampler as acceptable for
sampling respirable crystalline silica under the ISO/CEN convention
(Document ID 2177, Attachment B; 4233, p. 4).
URS Corporation, on behalf of the ACC, commented that precision
will not be improved by the use of high-flow samplers because filter
loadings of interferences will increase along with the amount of
crystalline silica; this would, in URS's opinion, necessitate
additional sample handling procedures, such as acid washing, that erode
precision. URS also argued that such samples may require analysis of
multiple peaks and that overall X-ray intensity may be diminished due
to increased filter load (Document ID 2307, Attachment 12, p. 3). In
its post-hearing brief, the ACC stated that the use of high-volume
samplers "in addition to traditional Dorr-Oliver sampler" would
reduce inter-laboratory precision (i.e., the extent to which different
laboratories achieve similar results for the same sample) due to the
use of multiple sampler types (Document ID 4209, p. 154).
OSHA finds that these arguments are unsupported. Although the high-
flow sampler will collect more dust than lower-flow samplers in the
same environment, the relative proportion of any interfering materials
collected to the amount of crystalline silica collected would remain
unchanged. Thus, there should be no increased effect from the
interfering materials relative to the silica. OSHA recognizes that, to
prevent undue interference or diminished X-ray intensity, it is
important to keep the dust load on the filter within reasonable limits.
Both OSHA and NIOSH methods stipulate a maximum sample weight to be
collected (3 mg for OSHA and 2 mg for NIOSH) (Document ID 0946, p. 5;
0901, p. 3), and in the event that excess sample is collected, the
sample can be split into portions and each portion analyzed separately
(Document ID 0946, p. 5). In environments where using a high-flow
sampler is likely to collect more than the maximum sample size, use of
a lower-flow sampler is advised. In response to the concern that
permitting use of high-flow samplers will affect inter-laboratory
variability, OSHA observes that employers are already using a variety
of commercially available samplers, such as those listed in the NIOSH
Method 7500, to obtain exposure samples; not everyone uses the Dorr-
Oliver sampler. Thus, for the final rule, OSHA is permitting employers
to use any sampling device that has been designed and calibrated to
conform to the ISO/CEN convention, including higher-flow samplers such
as the GK2.69. In effect, this is a continuation of well-studied
current practice, not an untested departure from it.
b. Laboratory Analysis of Crystalline Silica
Crystalline silica is analyzed in the laboratory using either X-ray
diffraction (XRD) or infrared spectroscopy (IR). A third method,
colorimetric spectrophotometry, is no longer used (Document ID 3579,
Tr. 211; Harper et al., 2014, 3998, Attachment 8, p. 1). This section
describes crystalline silica analysis by XRD and IR and responds to
comments and testimony on the precision and accuracy of these methods
for measuring crystalline silica concentrations in the range of the
final rule's PEL and action level. As discussed below, both XRD and IR
methods can detect and quantify crystalline silica in amounts collected
below the final rule's 25 [micro]g action level.
X-Ray Diffraction
For XRD, a dust sample that has been collected by a sampler is
deposited on a silver-membrane filter and scanned by the X-ray beam,
where X-rays diffract at specific angles. A sensor detects these
diffracted X-ray beams and records each diffracted beam as a
diffraction peak. Unique X-ray diffraction patterns are created when
the diffraction peaks are plotted against the angles at which they
occur. The intensity of the diffracted X-ray beams depends on the
amount of crystalline silica present in the sample, which can be
quantified by comparing the areas of the diffraction peaks obtained
with those obtained from scanning a series of calibration standards
prepared with known quantities of an appropriate reference material.
Comparing multiple diffraction peaks obtained from the sample with
those obtained from the calibration standards permits both quantitative
and qualitative confirmation of the amount and type of crystalline
silica present in the sample (i.e., quartz or cristobalite). A major
advantage of XRD compared with the other techniques used to measure
crystalline silica is that X-ray diffraction is specific for
crystalline materials. Neither non-crystalline silica nor the amorphous
silica layer that forms on crystalline silica particles affects the
analysis. The ability of this technique to quantitatively discriminate
between different forms of crystalline silica and other crystalline or
non-crystalline materials present in the sample makes this method least
prone to interferences. Sample analysis by XRD is also non-destructive,
meaning that samples can be reanalyzed if necessary (Document ID 1720,
pp. IV-26--IV-27).
The OSHA Technical Manual lists the following substances as
potential interferences for the analysis of crystalline silica using
XRD: Aluminum phosphate, feldspars (microcline, orthoclase,
plagioclase), graphite, iron carbide, lead sulfate, micas (biotite,
muscovite), montmorillonite, potash, sillimanite, silver chloride,
talc, and zircon (https://www.osha.gov/dts/osta/otm/otm_ii/otm_ii_1.html, Chapter 1, III.K). The interference from other minerals
usually can be recognized by scanning multiple diffraction peaks
quantitatively. Diffraction peak-profiling techniques can resolve and
discriminate closely spaced peaks that might interfere with each other.
Sometimes interferences cannot be directly resolved using these
techniques. However, many interfering materials can be chemically
washed away in acids that do not dissolve the crystalline silica in the
sample. Properly performed, these acid washes can dissolve and remove
these interferences without appreciable loss of crystalline silica
(Document ID 1720, p. IV-27).
The nationally recognized analytical methods using XRD include OSHA
ID-142, NIOSH 7500, and MSHA P-2 (Document ID 0946; 0901; 1458). All
are based on the XRD of a redeposited thin-layered sample with
comparison to standard
