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.
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    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.
[GRAPHIC] [TIFF OMITTED] TR25MR16.008

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.

[GRAPHIC] [TIFF OMITTED] TR25MR16.009

    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.

[GRAPHIC] [TIFF OMITTED] TR25MR16.010

    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