[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).
    ---------------------------------------------------------------------------
    
        \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).
    ---------------------------------------------------------------------------
    
        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.
    ---------------------------------------------------------------------------
    
        \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).
    ---------------------------------------------------------------------------
    
        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.).
    ---------------------------------------------------------------------------
    
        \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.
    ---------------------------------------------------------------------------
    
        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.
    ---------------------------------------------------------------------------
    
        \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.
    ---------------------------------------------------------------------------
    
        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.
    ---------------------------------------------------------------------------
    
        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.
    ---------------------------------------------------------------------------
    
        \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).
    ---------------------------------------------------------------------------
    
        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.
    ---------------------------------------------------------------------------
    
        \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).
    ---------------------------------------------------------------------------
    
        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.
    ---------------------------------------------------------------------------
    
        \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.
    ---------------------------------------------------------------------------
    
        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 standards of known concentrations (Document ID 0946, p. 
    1; 0901, p. 1; 1458, p. 1). These methods, however, differ on 
    diffraction peak confirmation strategies. The OSHA and MSHA methods 
    require at least three diffraction peaks to be scanned (Document ID 
    0946, p. 5; 1458, p. 13). The NIOSH method only requires that multiple 
    peaks be qualitatively scanned on representative bulk samples to 
    determine the presence of crystalline silica and possible 
    interferences, and quantitative analysis of air samples is based on a 
    single diffraction peak for each crystalline silica polymorph analyzed 
    (Document ID 0901, pp. 3, 5).
    Infrared Spectroscopy
        Infrared spectroscopy is based on the principle that molecules of a 
    material will absorb specific wavelengths of infrared electromagnetic 
    energy that match the resonance frequencies of the vibrations and 
    rotations of the electron bonds between the atoms making up the 
    material. The absorption of IR radiation by the sample is compared with 
    the IR absorption of calibration standards of known concentration to 
    determine the amount of crystalline silica in the sample. Using IR can 
    be efficient for routine analysis of samples that are well
    characterized with respect to mineral content, and the technique, like 
    XRD, is non-destructive, allowing samples to be reanalyzed if 
    necessary. The three principle IR analytical methods for crystalline 
    silica analyses are NIOSH 7602 (Document ID 0903), NIOSH 7603 (http://www.cdc.