morbidity will be discussed below.
    In the Chen et al. studies, which focused on mining (i.e., tin,
tungsten) and pottery cohorts, high volume area samplers collected dust
and the respirable crystalline silica concentration was determined from
those samples (2001, Document ID 0332; 2005, 0985). However, according
to the ACC, the rest of the collected dust was not assessed for
chemicals that potentially could also cause radiographic opacities
(Document ID 2307, Attachment A, pp. 132-135). Neither study expressed
reason to be concerned about the non-silica portion of the dust
samples. OSHA recognizes that uncertainty about potential unknown
exposures exists in retrospective studies, which describes most
epidemiological research. However, OSHA emphasizes that the risk values
derived from the Chen et al. studies do not differ remarkably from
other silicosis morbidity studies used in the risk assessment (Document
ID 0306, 1052, 0451). Therefore, OSHA concludes that it is unlikely
that an unknown compound significantly impacted the exposure-response
relationships reported in both Chen studies.
    The study on gold miners (Steenland and Brown, 1995b, Document ID
0451), which found that cumulative exposure was the best disease
predictor, followed by duration of exposure and average exposure, was
also criticized by the ACC, which alleged that the exposure assessment
suffered from ``enormous uncertainty'' (Document ID 2307, Attachment A,
pp. 146-147). The ACC noted that exposure measurements were not
available for the years prior to 1937 or after 1975 and that this
limitation of the exposure information may have resulted in an
underestimation of exposures (Document ID 2307, Attachment A, pp. 124-
126). OSHA agrees that these are potential sources of uncertainty in
the exposure estimates, but recognizes exposure uncertainty to be a
common occurrence in occupational epidemiology studies. OSHA believes
that the authors used the best measurement data available to them in
their study.
    The ACC also took issue with Steenland and Brown's conversion
factor for converting particle count to respirable silica mass (10
mppcf = 100 [mu]g/m\3\), which was somewhat higher than that used in
the Vermont granite worker studies (10 mppcf = 75 [mu]g/m\3\) (Document
ID 2307, Attachment A, p. 126). OSHA notes that the study's reasoning
for adopting that specific particle count conversion factor was to
address the higher percentage of silica found in the gold mine samples
applicable to their cohort in comparison to the Vermont granite study
(Document ID 0451, p. 1373). OSHA finds this decision, which was based
on the specific known exposure conditions of this cohort, to be
reasonable.
    With respect to the Hnizdo and Sluis-Cremer (1993, Document ID
1052)

study, which found that silicosis risk increased exponentially with
cumulative exposure to respirable dust (Document ID 1052, p. 447), the
ACC questioned three assumptions the study made about exposures. First,
exposures were assumed to be static from the 1930s to the 1960s, based
on measurements from the late 1950s to mid-1960s, an assumption that,
according to the ACC, might underestimate exposure for workers employed
before the late 1950s (Document ID 2307, Attachment A, pp. 117-119).
Second, although respirable dust, by definition, includes particles up
to 10 [mu]m, the study only considered particles sized between 0.5 and
5 [mu]m in diameter (Document ID 1052, p. 449). The ACC contends this
exclusion may have resulted in underestimated exposure and
overestimated risk (Document ID 2307, Attachment A, p. 119). OSHA
agrees that uncertainty in exposure estimates is an important issue in
the silica risk assessment, and generally discusses the issue of
exposure measurement uncertainty in depth in a quantitative uncertainty
analysis described in Section V.K, Comments and Responses Concerning
Exposure Estimation Error and ToxaChemica's Uncertainty Analysis. As
discussed there, after accounting for the likely effects of exposure
measurement uncertainty in the risk assessment, OSHA affirms the
conclusion of the risk assessment that there is significant risk of
silicosis to workers exposed at the previous PELs.
    Thirdly, the ACC challenged the authors' estimate of the quartz
content of the dust as 30 percent when it should have been 54 percent
(Document ID 1052, p. 450; 2307, Attachment A, p. 120). According to
the ACC, the 30 percent estimate was based on an incorrect assumption
that the samples had been acid-washed (resulting in a reduction in
silica content) before the quartz content was measured (Document ID
2307, Attachment A, pp. 120-122). This assumption would greatly
underestimate the exposures of the cohort and the exposures needed to
cause adverse effects, thus overestimating actual risk (Document ID
2307, Attachment A, pp. 121-122). The ACC recommended that the quartz
content in the Hnizdo and Sluis-Cremer study be increased from 30 to 54
percent, based on the Gibbs and Du Toit study (2002, Document ID 1025,
p. 602).
    OSHA considered this issue in the Preliminary QRA (Document ID
1711, p. 332). OSHA noted that the California Environmental Protection
Agency's Office of Environmental Health Hazard Assessment reviewed the
source data for Hnizdo and Sluis-Cremer, located in the Page-Shipp and
Harris (1972, Document ID 0583) study, and compared them to the quartz
exposures calculated by Hnizdo and Sluis-Cremer (OEHHA, 2005, Document
ID 1322, p. 29). OEHHA concluded after analyzing the data that the
samples likely were not acid-washed and that the Hnizdo and Sluis-
Cremer paper erred in describing that aspect of the samples.
Additionally, OEHHA reported data that suggests that the 30 percent
quartz concentration may actually overestimate the exposure. It noted
that recent investigations found the quartz content of respirable dust
in South African gold mines to be less than 30 percent (Document ID
1322). In summary, OSHA concludes that no meaningful evidence was
submitted to the rulemaking record that changes OSHA's original
decision to include the Hnizdo and Sluis-Cremer study in its risk
assessment.
    Despite the uncertainties inherent in estimating the exposures of
occupational cohorts in silicosis morbidity studies, the resulting
estimates of risk for the previous general industry PEL of 100 [mu]g/
m\3\ are in reasonable agreement and indicate that lifetime risks of
silicosis morbidity at this level, and, by extension, risks at the
higher previous PELs for maritime and construction (see section VI,
Final Quantitative Risk Assessment and Significance of Risk) are in the
range of hundreds of cases per 1,000 workers. Even in the unlikely
event that exposure estimates underlying all of these studies were
systematically understated by several fold, the magnitude of resulting
risks would likely still be such that OSHA would determine them to be
significant.
3. Conclusion
    After carefully considering all of the comments on the studies
relied on by OSHA to estimate silicosis and NMRD mortality and
silicosis morbidity risks, OSHA concludes that the scientific evidence
used in its quantitative risk assessment substantially supports the
Agency's finding of significant risk for silicosis and non-malignant
respiratory disease. In its risk estimates in the Preliminary QRA, OSHA
acknowledged the uncertainties raised by the ACC and other commenters,
but the Agency nevertheless concluded that the assessment was
sufficient for evaluating the significance of the risk. After
evaluating the evidence in the record on this topic, OSHA continues to
conclude that its risk assessment (see Final Quantitative Risk
Assessment in Section VI.C of this preamble) provides a reasonable and
well-supported estimate of the risk faced by workers who are exposed to
respirable crystalline silica.

E. Comments and Responses Concerning Surveillance Data on Silicosis
Morbidity and Mortality

    As discussed above in this preamble, OSHA has relied on
epidemiological studies to assess the risk of silicosis, a debilitating
and potentially fatal occupationally-related lung disease caused by
exposure to respirable crystalline silica. In the proposed rule (78 FR
56273, 56298; also Document ID 1711, pp. 31-49), OSHA also discussed
data from silicosis surveillance programs that provide some information
about the number of silicosis-associated deaths or the extent of
silicosis morbidity in the U.S. (78 FR at 56298). However, as OSHA
explained, the surveillance data are not sufficient for estimating the
risks of health effects associated with exposure to silica, nor are
they sufficient for estimating the benefits of any potential regulatory
action. This is because silicosis-related surveillance data are only
available from a few states and do not provide exposure data that can
be matched to surveillance data. Consequently, there is no way of
knowing how much silica a person was exposed to before developing fatal
silicosis (78 FR at 56298).
    In addition, the available data likely understate the resulting
death and disease rates in U.S. workers exposed to crystalline silica
(78 FR 56298). This understatement is due in large part to: (1) The
passive nature of these surveillance systems, which rely on healthcare
providers' awareness of a reporting requirement and submission of the
appropriate information on standardized forms to health departments;
(2) the long latency period of silicosis; (3) incomplete occupational
exposure histories, and (4) other factors that result in a lack of
recognition of silicosis by healthcare providers, including the low
sensitivity, or ability of chest x-rays to identify cases of silicosis
(78 FR 56298). Specific to death certificate data, information on usual
industry and occupation are available from only 26 states for the
period 1985 to 1999, and those codes are not verifiable (Document ID
1711). Added to these limitations is the ``lagging'' nature of
surveillance data; it often takes years for cases to be reported,
confirmed, and recorded. Furthermore, in many cases, the available
surveillance systems lack information about actual exposures or even
information about the usual occupation or industry of the deceased
individual, which could provide some information about occupational

exposure (see 78 FR at 56298). Therefore, the Agency did not use these
surveillance data to estimate the risk of silicosis for the purpose of
meeting its legal requirements to prove a significant risk of material
impairment of health (see 29 U.S.C. 655(b)(5); Benzene, 448 U.S. 607,
642 (1980)).
    Comments and testimony focusing on the silicosis surveillance data
alleged that OSHA should have used the surveillance data in its risk
estimates. Stakeholders argued that the declining numbers of reported
silicosis deaths prove the lack of necessity for a new silica standard.
Commenters also claimed that the surveillance data prove that OSHA
overestimated both the risks at the former permissible exposure limits
(PELs) and the benefits of the new rule.
    After reviewing the rulemaking record, OSHA maintains its view that
these silicosis surveillance data, although useful for providing
context and an illustration of a significant general trend in the
reduction of deaths associated with silicosis over the past 4-5
decades, are not sufficient for estimating the magnitude of the risk or
the expected benefits. In the case of silicosis, surveillance data are
useful for describing general trends nationally and a few states have
the ability to use the data at the local or state level to identify
``sentinel events'' that would justify initiating an inspection of a
workplace, for example. The overall data, however, are inadequate and
inappropriate for estimating risks or benefits associated with various
exposure levels, as is required of OSHA's regulatory process, in part
because they significantly understate the extent of silicosis in
workers in the United States and because they lack information about
exposure levels, exposure sources (e.g., type of job), controls, and
health effects that is necessary to examine the effects of lowering the
PEL. Thus, for these reasons and the ones discussed below, OSHA has
continued to rely on epidemiological data to meet its burden of
demonstrating that workers exposed to respirable crystalline silica at
the previous PELs face a significant risk of developing silicosis and
that risk will be reduced when the new limit is fully implemented.
Another related concern identified by stakeholders is the apparent
inconsistency between surveillance data and risk and benefits estimates
derived from modeling epidemiological data (Document ID 4194, pp. 7-10;
4209, pp. 3-4). However, this difference is not an inconsistency, but
the result of comparing two distinctly different items. Surveillance
data, primarily death certificate data, are known to be under-reported
and lack associated exposure data necessary to model relationships
between various exposure levels and observance of health effects. For
these reasons, OSHA relied on epidemiologic studies with detailed
exposure-response relationships to evaluate the significance of risk at
the preceding and new PELs. Thus, the silicosis mortality data derived
from death certificates and estimates of silica-related mortality risks
derived from well-conducted epidemiologic studies cannot be directly
compared in any meaningful way. With respect to silicosis morbidity,
OSHA notes that the estimates by Rosenman et al. (2003, Document ID
0420) of the number of cases of silicosis estimated to occur in the
U.S. (between 2,700 and 5,475 estimated to be in OSHA's jurisdiction
(i.e., excluding miners)) each year is in reasonable agreement with the
estimates derived from epidemiologic studies, assuming either a 13-year
or 45-year working life (see Chapter VII, Table VII-2 of the FEA).
1. Surveillance Data on Silicosis Mortality
    The principal source of data on annual silicosis mortality in the
U.S. is the National Institute for Occupational Safety and Health
(NIOSH) Work-Related Lung Disease (WoRLD) Surveillance System (e.g.,
NIOSH, 2008c, Document ID 1308), which compiles cause-of-death data
from death certificates reported to state vital statistics offices and
collected by the National Center for Health Statistics (NCHS). Paper
copies were published in 2003 and 2008 (Document ID 1307; 1308) and
data are updated periodically in the electronic version on the CDC Web
site (http://www.cdc.gov/eworld). NIOSH also developed and manages the
National Occupational Respiratory Mortality System (NORMS), a data-
storage and interactive data retrieval system that reflects death
certificate data compiled by NCHS (http://webappa.cdc.gov/ords/norms.html).
    From 1968 to 2002, silicosis was recorded as an underlying or
contributing cause of death on 16,305 death certificates; of these, a
total of 15,944 (98 percent) deaths occurred in males (CDC, 2005,
Document ID 0319). Over time, silicosis-related mortality has declined
in the U.S., but has not been eliminated. Based on the death
certificate data, the number of recognized and coded deaths for which
silicosis was an underlying or contributing cause decreased from 1,157
in 1968 to 161 in 2005, corresponding to an 86-percent decline
(Document ID 1711, p. 33; 1308, p. 55) (http://wwwn.cdc.gov/eworld).
The crude mortality rate, expressed as the number of silicosis deaths
per 1,000,000 general population (age 15 and higher) fell from about
8.9 per million to about 0.5 per million over that same time frame, a
decline of 94 percent (Document ID 1711, p. 33; 1308, p. 55) (http://wwwn.cdc.gov/eworld).
    OSHA's Review of Health Effects Literature and Preliminary QRA
included death certificate statistics for silicosis up to and including
2005 (Document ID 1711, p. 33). OSHA has since reviewed the more recent
NORMS and NCHS data, up to and including 2013, which appear to show a
general downward trend in mortality, as presented in Table V-1.

[GRAPHIC] [TIFF OMITTED] TR25MR16.003

    However, more detailed examination of the most recent data
collected through NCHS (Table V-2) indicates that the decline in the
number of deaths with silicosis as an underlying or contributing cause
has leveled off in more recent years, suggesting that the number of
silicosis deaths being recorded and captured by death certificates may
be stabilizing after 30 or more years of decline.
[GRAPHIC] [TIFF OMITTED] TR25MR16.004

    Robert Cohen, M.D., representing the American Thoracic Society,
noted this apparent plateau effect, testifying that ``[t]he data from
the NIOSH work-related lung disease surveillance report and others show
a plateau in silicosis

mortality since the 1990s, and we are concerned that that has been the
same without any further reduction for more than 20 years. So we think
that we still have work to do'' (Document ID 3577, p. 775).
    Some commenters raised the question about whether decedents who
died more recently were exposed to high levels of silica (pre-1970s)
and therefore wouldn't necessarily reflect mortalities relevant to the
current OSHA standard (Document ID 4194, p. 9; 4209, pp. 7-8). OSHA has
no information on the age of these decedents, or the timing of their
exposure to silica. If we assume that workers born in 1940-1950 would
have started working around 1960, at the earliest, and into the 1970's,
and life expectancy in general of 70 years, or 60-70 years to account
for years of life lost due to silicosis, most of these workers' working
life would have been spent after the 1971 PEL went into effect. It is
likely that some of the more recent decedents were exposed to silica
prior to 1971; however, it is less likely that all were exposed prior
to 1971. At the end of the day, there is no actual exposure information
on these decedents, and this generalization does not account for
overexposures, which have persisted over time.
2. Surveillance Data on Silicosis Morbidity
    There is no nation-wide system for collecting silicosis morbidity
case data. The data available are from three sources: (1) The National
Hospital Discharge Survey (Document ID 1711, p. 40-43); (2) the Agency
for Healthcare Research and Quality's (AHRQ) Nationwide Inpatient
Survey (Document ID 3425, p. 2; https://www.hcup-us.ahrq.gov/nisoverview.jsp); and (3) states that administer silicosis and/or
pneumoconiosis disease surveillance (see Document ID 1711, p. 40-43;
http://www.cdc.gov/niosh/topics/surveillance/ords/StateBasedSurveillance/stateprograms.html).
    Both of the first two sources of data on silicosis morbidity cases
are surveys that provide estimates of hospital discharges. The first is
the National Hospital Discharge Survey (NHDS), which was conducted
annually from 1965-2010. The NHDS was a national probability survey
designed to meet the need for information on characteristics of
inpatients discharged from non-Federal short-stay hospitals in the
United States (see http://www.cdc.gov/nchs/nhds.htm). Estimates of
silicosis listed as a diagnosis on hospital discharge records are
available from the NHDS for the years 1985 to 2010 (see http://www.cdc.gov/nchs/nhds.htm). National estimates were rounded to the
nearest 1,000, and the NHDS has consistently reported approximately
1,000 discharges/hospitalizations annually since 1980 (e.g., Document
ID 1307; 1308). The second survey, the National (Nationwide) Inpatient
Sample (NIS), is conducted annually by the AHRQ. Dr. Kenneth Rosenman,
Division Chief and Professor of Medicine at Michigan State University
and who oversees one of the few occupational disease surveillance
systems in the U.S., testified that data from the NIS indicated that
the nationwide number of hospitalizations where silicosis was one of
the discharge diagnoses has remained constant, with 2,028
hospitalizations reported in 1993 and 2,082 in 2011 (Document ID 3425,
p. 2).
    Morbidity data are also available from the states that administer
silicosis and/or pneumoconiosis disease surveillance. These programs
rely primarily on hospital discharge records and also may get some
reports of cases from the medical community and workers' compensation
programs. Currently, NIOSH funds the State-Based Occupational Safety
and Health Surveillance cooperative agreements (Document ID 1711, p.
40-41; http://www.cdc.gov/niosh/topics/surveillance/ords/StateBasedSurveillance.html). All states funded under a cooperative
agreement conduct population-based surveillance for pneumoconiosis
(hospitalizations and mortality), and a few states (currently Michigan
and New Jersey) have expanded surveillance specifically for silicosis
(Document ID 1711, p. 40-42; http://www.cdc.gov/niosh/topics/surveillance/ords/StateBasedSurveillance/stateprograms.html).
    State-based hospital discharge data are a useful population-based
surveillance data source for quantifying pneumoconiosis (including
silicosis), even though only a small number of individuals with
pneumoconiosis are hospitalized for that condition (Document ID 0996),
and the data refer to hospitalizations with a diagnosis of silicosis,
and not specific people. In addition to mortality data, NIOSH has
updated its WoRLD Surveillance System with some state-based morbidity
case data (http://wwwn.cdc.gov/eworld/Grouping/Silicosis/94). State-
based surveillance systems can provide more detailed information on a
few cases of silicosis.
    NIOSH has published aggregated state case data in its WoRLD Reports
(Document ID 1308; 1307) for two ten-year periods that overlap, 1989 to
1998 and 1993 to 2002. State morbidity case data are compiled and
evaluated by variables such as ascertainment source, primary industry,
and occupations. For the time period 1989 to 1998, Michigan reported
589 cases of silicosis, New Jersey 191 cases, and Ohio 400 cases
(Document ID 1307, p. 69). In its last published report, for the later
and partially overlapping time period 1993 to 2002, Michigan reported
465 cases, New Jersey 135, and Ohio 279 (Document ID 1308, p. 72). Data
for the years 2003 to 2011, from the CDC/NIOSH electronic report,
eWoRld, show a modest decline in the number of cases of silicosis in
these three states; however, decreases are not nearly as substantial as
are those seen in the mortality rates (see Table V-3). Annual averages
for the two ten-year periods and the nine-year time period were
calculated by OSHA solely for the purpose of comparing cases of
silicosis reported over time.
[GRAPHIC] [TIFF OMITTED] TR25MR16.005

3. Critical Comments Received on Surveillance Data
    Industry representatives, including ACC's Crystalline Silica Panel
and Dr. Jonathan Borak, representing the Chamber of Commerce (Chamber),
contended that the steep decline seen in the number and rate of
silicosis deaths since 1968 proves that OSHA cannot meet its burden of
demonstrating that a more protective standard is necessary (e.g.,
Document ID 4209, p. 10; 2376, p. 8; 4016, p. 9). Similarly, other
commenters, such as the American Petroleum Institute, the Independent
Petroleum Association of America, the National Mining Association, the
American Foundry Society (AFS), the National Utility & Excavating
Contractors Association, Acme Brick, the National Ready Mixed Concrete
Association, and the Small Business Administration's Office of Advocacy
stated that surveillance data demonstrate that the previous OSHA PEL
was sufficiently effective in reducing the number of deaths from
silicosis (Document ID 3589, Tr. 4041; 4122; 2301, pp. 3, 7-9; 2211, p.
2; 2379, pp. 23-25; 2171, p. 1; 3730, p. 5; 3586, Tr. 3358-3360; 3589,
Tr. 4311; 2349, pp. 3-4). Industry commenters also argued that the
number of recorded silicosis-related deaths in recent years, as
reflected in the surveillance data, is far lower than the number of
lives that OSHA projected would be saved by a more stringent rule,
indicating that OSHA's risk assessment is flawed (e.g., Document ID
3578, Tr. 1074-1075; 4209, p. 3-4).
    The Chamber, along with others, declared that OSHA ignored steep
declines in silicosis mortality, which in its view indicates that there
is no further need to reduce the PEL (Document ID 4194, pp. 7-8). OSHA
has not ignored the fact that the available surveillance data indicate
a decline in silicosis mortality. As discussed above and in the
proposal, the Agency has acknowledged that the available surveillance
data do show a decline in the silicosis mortality since 1968.
Furthermore, OSHA has no information on whether underreporting has
increased or decreased over time, and does not believe that differing
rates of reporting and underreporting of silicosis on death
certificates explains the observed decline in silicosis mortality. OSHA
believes that the reductions in deaths attributable to silicosis are
real, and not a statistical artifact. However, OSHA disagrees with
commenters' argument that this trend shows the lack of a need for this
new rule. First, as explained above, there is strong evidence that the
death certificate data do not capture the entirety of silicosis
mortality that actually exists, due to underreporting of silicosis as a
cause of death. Second, the stakeholders' argument assumes that
mortality will continue to decline, even in the absence of a stronger
silica standard, and that OSHA and workers should wait for this decline
to hit bottom (e.g., Document ID 4209, p. 7). However, testimony in the
record suggests that the decline in the number of deaths has leveled
off since 2000, probably because of the deaths of those historically
exposed to higher levels of silica occurred before then (e.g., Document
ID 3577, p. 775).
    Third, the decline in silicosis deaths recorded over the past
several decades cannot be solely explained by improved working
conditions, but also reflects the decline in employment in industries
that historically were associated with high workplace exposures to
crystalline silica. One of OSHA's peer reviewers for the Review of
Health Effects Literature and Preliminary QRA, Bruce Allen, commented
that the observed decline in mortality ``. . . in no way adjusts for
the declining employment in jobs with silica exposure,'' making ``its
interpretation problematic. To emphasize the contribution of historic
declines in exposure as the underlying cause is spurious; no
information is given to allow one to account for declining employment''
(Document ID 3574, p. 7). The CDC/NIOSH also identified declining
employment in heavy industries where silica exposure was prevalent as a
``major factor'' in the reduction over time in silicosis mortality
(Document ID 0319, p. 2). As discussed below, however, some silica-
generating operations or industries are new or becoming more prevalent.
    In his written testimony, Dr. Rosenman pointed out that there are
``two aspects to the frequency of occurrence of disease (1) . . . the
risk of disease based on the level of exposure and (2) the number of
individuals at risk'' (Document ID 3425, pp. 3-4). Dr. Rosenman
estimated the decline in the number of workers in Michigan foundries
(75 percent) and the number of abrasive blasting companies in Michigan
(71 percent), and then compared these percentages to the percentage
decline in the number of recorded silicosis deaths (80 percent) over a
similar time period. The similarities in these values led him to
attribute ``almost all'' of the decrease in silicosis deaths to a
decrease in the population at risk (Document ID 3425, pp. 3-4).
    Finally, OSHA's reliance on epidemiological data for its risk
assessment purposes does not suggest that the Agency ignored the
available surveillance data. As discussed above, the data are
inadequate and inappropriate for estimating risks or benefits
associated with various exposure levels, as is required of OSHA's
regulatory process. Even in the limited cases where surveillance data
are available, OSHA generally relies on epidemiological data, to the
extent they include sufficiently detailed information on exposures,
exposure sources (e.g., type of job), and health effects, to satisfy
its statutory requirement to use the best available evidence to
evaluate the significance of risk associated with exposure to hazardous
substances.
    Some stakeholders provided comments to the rulemaking record
consistent with OSHA's assessment. For example, Dr. Borak stated that
the surveillance data ``provide little or no basis'' (Document ID 2376,
p. 8) for OSHA to evaluate the protectiveness of the previous PELs.
Similarly, NIOSH asserted that relying on the surveillance data to show
that there is no need for a lower PEL or that there is no significant
risk at 100 [mu]g/m\3\ would be ``a misuse of surveillance data''
(Document ID 3579, Tr. 167). NIOSH also added that, because the
surveillance data do not include information about exposures, it is not
the kind of data that could be used for a quantitative risk assessment.
NIOSH concluded that surveillance data are, in fact, ``really not
germane to the risk assessment'' (Document ID 3579, Tr. 248). OSHA
agrees with both Dr. Borak and NIOSH that the surveillance data cannot
and do not inform the Agency on the need for a lower PEL, nor is there
a role for surveillance data in making its significant risk findings.
Therefore, for its findings of significant risk at the current PEL, the
Agency relied on evidence derived from detailed exposure-response
relationships from well-conducted epidemiologic studies, and not
surveillance data, which have no associated exposure information. In
this case, epidemiologic data provided the best available evidence.
    In its testimony, the AFL-CIO pointed out that a recent U.S.
Government Accountability Office (GAO) report on the Mine Safety and
Health Administration's (MSHA) proposed coal dust standard references
the National Academy of Sciences (NAS) conclusion that risk assessments
based on epidemiological data, not surveillance data, were an
appropriate means to assess risk for coal-dust exposures (Document ID
4204, p. 21; 4072, Attachment 48, pp. 7-8). The NAS

emphasized that the surveillance data available to MSHA did not include
individual miners' levels of exposure to coal mine dust and, therefore,
could not be used for the purpose of estimating disease risk for
miners. ``Based on principles of epidemiology and statistical modeling,
measures of past exposures to coal mine dust are critical to assessing
the relationship between miners' cumulative coal mine dust exposure and
their risk of developing [pneumoconiosis]'' (Document ID 4072,
Attachment 48, p. 8). The same rationale applies here. Thus, OSHA's
decision to rely on epidemiological data is well supported by the
record.
    Commenters from companies and industry groups also argued that they
had no knowledge of workers acquiring silicosis in their companies or
industry (e.g., Document ID 2384, p. 2; 2338, p. 3; 2365, p. 2; 2185,
p. 3; 2426, p. 1). OSHA received similar comments as part of a letter
campaign in which over 100 letters from brick industry representatives
claimed there to be little or no silicosis observed in the industry
despite historical exposures above the PEL (e.g., Document ID 2009).
OSHA considered these comments and believes that many companies,
including companies in the brick industry, may not have active medical
surveillance programs for silicosis. Silicosis may not develop until
after retirement as a result of its long latency period. In addition,
silica exposures in some workplaces may be well below the final PEL as
a result of the environment in which workers operate, including
existing controls. Thus, OSHA believes that it is difficult to draw
conclusions about the rate of silicosis morbidity in specific
workplaces without having detailed information on medical surveillance,
silica exposures, and follow-up. This is why OSHA relies heavily on
epidemiological studies with detailed exposure data and extended
follow-up, and uses these data to evaluate exposure-response
relationships to assess health risks at the preceding and new PELs.
    Commenters also argued that, due to the long latency of the
disease, silicosis cases diagnosed today are the result of exposures
that occurred before the former PELs were adopted, and thus reflect
exposures considerably higher than the previous PELs (e.g., Document ID
2376, p. 3; 2307, p. 12; 4194, p. 9; 3582, Tr. 1935). OSHA notes that
the evidence shows that the declining trend in silicosis mortality does
not provide a complete picture with regard to silicosis trends in the
United States. Although many silicosis deaths reported today are likely
the result of higher exposures (both magnitude and duration), some of
which may have occurred before OSHA adopted the previous PELs,
silicosis cases continue to occur today--some in occupations and
industries where exposures are new and/or increasing. For example, five
states reported cases of silicosis in dental technicians for the years
1994 to 2000 (CDC, MMWR Weekly, 2004, 53(09), pp. 195-197), for the
first time. For the patients described in this report, the only
identified source of crystalline silica exposure was their work as
dental technicians. Exposure to respirable crystalline silica in dental
laboratories can occur during procedures that generate airborne dust
(e.g., mixing powders, removing castings from molds, grinding and
polishing castings and porcelain, and using silica sand for abrasive
blasting). In 2015, the CDC reported the first case of silicosis
(progressive massive fibrosis) associated with exposure to quartz
surfacing materials (countertop fabrication and installation) in the
U.S. The patient was exposed to dust for 10 years from working with
conglomerate or quartz surfacing materials containing 70%-90%
crystalline silica. Cases had previously been reported in Israel, Italy
and Spain (MMWR, 2015, 64(05); 129-130). Recently, hazardous silica
exposures have been newly documented during hydraulic fracturing of gas
and oil wells (Bang et al., MMWR, 2015, 64(05); 117-120).
    Dr. Rosenman's testimony provides support for this point. He
testified that newer industries with high silica exposures may also be
under-recognized because workers in those industries have not yet begun
to be diagnosed with silicosis due to the latency period (Document ID
3577, p. 858). Dr. Rosenman submitted to the record a study by Valiante
et al. (2004, Document ID 3926) that identified newly exposed
construction workers in the growing industry of roadway repair, which
began using current methods for repair in the 1980s. These methods use
quick-setting concrete that generates dust containing silica above the
OSHA PEL when workers perform jackhammering, and sawing and milling
concrete operations. State surveillance systems identified 576
confirmed silicosis cases in New Jersey, Michigan, and Ohio that were
reported to NIOSH for the years 1993 through 1997. Of these, 45 (8
percent) cases were in construction workers, three of which had been
engaged in highway repair.
    Sample results for this study indicated a significant risk of
overexposure to crystalline silica for workers who performed the five
highway repair tasks involving concrete. Sample results in excess of
the OSHA PEL were found for operating a jackhammer (88 percent of
samples), sawing concrete and milling concrete tasks (100 percent of
samples); cleaning up concrete tasks (67 percent of samples); and
drilling dowels (100 percent of samples). No measured exposures in
excess of the PEL were found for milling asphalt and cleaning up
asphalt; however, of the eight samples collected for milling asphalt,
six (55 percent) results approached the OSHA PEL, and one was at 92
percent of the PEL. No dust-control measures were in place during the
sampling of these highway repair operations.
    The authors pointed out that surveillance systems such as those
implemented by these states are limited in their ability to detect
diseases with long latencies in highway repair working populations
because of the relatively short period of time that modern repair
methods had been in use when the study was conducted. Nevertheless, a
few cases were identified, although the authors explain that the work
histories of these cases were incomplete, and the authors recommended
ongoing research to evaluate the silicosis disease potential among this
growing worker population (Document ID 3926, pp. 876-880). In
construction, use of equipment such as blades used on handheld saws to
dry-cut masonry materials have increased both efficiency and silica
exposures for workers over the past few decades (Document ID 4223, p.
11-13). Exposure data collected by OSHA as part of its technological
feasibility analysis demonstrates that exposures frequently exceed
previous exposure limits for these operations when no dust controls are
used (see Chapter IV of the FEA). Another operation seeing new and
increasing exposures to respirable crystalline silica is hydraulic
fracturing in the oil and gas industry (Document ID 3588, p. 3773).
Information in the record from medical professionals noted that lung
diseases caused by silica exposures are ``not relics of the past,'' and
that they continue to see cases of silicosis and other related
diseases, even among younger workers who entered the workforce after
the former PEL was enacted (see Document ID 3577, Tr. 773).
    Furthermore, the general declining trend seen in the death
certificate data is considerably more modest in silicosis morbidity
data. In his written testimony, Dr. Rosenman stated that the nationwide
number of hospitalizations where silicosis was one of the discharge
diagnoses has remained constant, with 2,028 hospitalizations reported
in 1993

and 2,082 in 2011 (Document ID 3425, p. 2). It is the opinion of
medical professionals including the American Thoracic Society and the
American College of Chest Physicians that these hospitalizations likely
represent ``the tip of the iceberg'' (of silicosis cases) since milder
cases are not likely to be admitted to the hospital (Document ID 2175,
p. 3). Again, this evidence shows that the declining trend observed in
silicosis mortality statistics does not provide a complete picture with
regard to silicosis trends in the United States. While silicosis
mortality has decreased substantially since records were first
available in 1968, the number of silicosis related deaths appears to
have leveled off (see Table V-2; Document ID 3577, Tr. 775). Workers
are still dying from silicosis today, and new cases are being
identified by surveillance systems, where they exist.
    Based on the testimony and evidence described above, OSHA finds
that the surveillance data describing trends in silicosis mortality and
morbidity provide useful evidence of a continuing problem, but are not
suitable for evaluating either the adequacy of the previous PELs or
whether a more protective standard is needed. In fact, it would not be
possible to derive estimates of risk at various exposure levels from
the available surveillance data for silica. OSHA therefore
appropriately continues to rely on epidemiological data and its
quantitative risk assessment to support the need to reduce the previous
PELs in its final rule.
    Commenters also argued that OSHA has failed to prove that a new
standard is necessary because silica-associated deaths are due to
existing exposures in excess of the previous PELs; therefore, the
Agency should focus on better enforcing the previous PELs, rather than
enacting a new standard (e.g., Document ID 2376, p. 8; 2307, p. 12;
4016, pp. 9-10; 3582, Tr. 1936). OSHA does not find this argument
persuasive. First, many of the commenters used OSHA's targeted
enforcement data to make this point. These data were obtained during
inspections where OSHA suspected that exposures would be above the
previous PELs. Consequently, the data by their very nature are skewed
in the direction of exceeding the previous PELs, and such enforcement
serves a deterrence function, encouraging future compliance with the
PEL.
    Second, not all commenters agreed that overexposures were
``widespread.'' A few other commenters (e.g., AFS) thought that OSHA
substantially overstated the number of workers occupationally exposed
above 100 [mu]g/m\3\ in its PEA (Document ID 2379, p. 25). However
OSHA's risk analyses evaluated various exposure levels in determining
risks to workers, and did not rely on surveillance data, which rarely
have associated exposure data. Although OSHA relied on exposure data
from inspections to assess technological feasibility, it did not rely
on inspection data for its risk assessment because these exposure data
are not tied to specific health outcomes. Instead, the exposure data
used for risk assessment purposes is found in the scientific studies
discussed throughout this preamble section.
    The surveillance data are also not comparable to OSHA's estimate of
deaths avoided by the final rule because, as is broadly acknowledged,
silicosis is underreported as a cause of death on death certificates.
Thus, the surveillance data capture only a portion of the actual
silicosis mortality. This point was raised by several rulemaking
participants, including Dr. Rosenman; Dr. James Cone, MD, MPH,
Occupational Medicine Physician at the New York City Department of
Health, the AFL-CIO; and the American Thoracic Society (ATS) (Document
ID 3425, p. 2; 3577, Tr. 855, 867; 4204, p. 17; 2175, p. 3; 3577, Tr.
772).
    The rulemaking record includes one study that evaluated
underreporting of silicosis mortality. Goodwin et al. (2003, Document
ID 1030) estimated, through radiological confirmation, the prevalence
of unrecognized silicosis in a group of decedents presumed to be
occupationally exposed to silica, but whose causes of death were
identified as respiratory diseases other than silicosis. In order to
assess whether silicosis had been overlooked and under-diagnosed by
physicians, the authors looked at x-rays of decedents whose underlying
cause of death was listed as tuberculosis, cor pulmonale, chronic
bronchitis, emphysema, or chronic airway obstruction, and whose usual
industry was listed as mining, construction, plastics, soaps, glass,
cement, concrete, structural clay, pottery, miscellaneous mineral/
stone, blast furnaces, foundries, primary metals, or shipbuilding and
repair.
    Any decedent found to have evidence of silicosis on chest x-ray
with a profusion score of 1/0 was considered to be a missed diagnosis.
Of the 177 individuals who met study criteria, radiographic evidence of
silicosis was found in 15 (8.5 percent). The authors concluded that
silicosis goes undetected even when the state administers a case-based
surveillance system. Goodwin et al. (2003, Document ID 1030) also cites
mortality studies of Davis et al. (1983, Document ID 0999) and Hughes
(1982, Document ID 0362) who reported finding decedents with past chest
x-ray records showing evidence of silicosis but no mention of silicosis
on the death certificate.
    The Goodwin et al. (2003) study illustrates the importance of
information about the decedent's usual occupation and usual industry on
death certificates. Yet for the years 1985 to 1999, only 26 states
coded this information for inclusion on death certificates. If no
occupational information is available, recognizing exposure to silica,
which is necessary to diagnose silicosis, becomes even more difficult,
further contributing to possible underreporting.
    Dr. Rosenman, a physician, epidemiologist and B-reader, testified
that in his research he found silicosis recorded on only 14 percent of
the death certificates of individuals with confirmed silicosis
(Document ID 3425, p. 2; 3577, Tr. 854; see also 3756, Attachment 11).
This means that as much as 86 percent of deaths related to silicosis
are missing from the NIOSH WoRLD database, substantially compromising
the accuracy of the surveillance information. Dr. Rosenman also found
that silicosis is listed as the cause of death in a small percentage of
individuals who have an advanced stage of silicosis; 18 percent in
those with progressive massive fibrosis (PMF) and 10 percent in those
with category 3 profusion.
    As noted above, factors that contribute to underreporting by health
care providers include lack of information about exposure histories and
difficulty recognizing occupational illnesses that have long latency
periods, like silicosis (e.g., Document ID 4214, p. 13; 3584, Tr.
2557). Dr. Rosenman's testimony indicated that many physicians are
unfamiliar with silicosis and this lack of recognition is one factor
that contributes to the low recording rate for silicosis on death
certificates (Document ID 3577, Tr. 855). In order to identify cases of
silicosis, a health care provider must be informed of the patient's
history of occupational exposure to dust containing respirable silica,
a critical piece of information in identifying and reporting cases of
silicosis. However, information on a decedent's usual occupation and/or
industry is often not available at the time of death or is too general
to be useful. If the physician completing the death certificate is
unaware of the decedent's occupational exposure history to crystalline
silica, and does not have that information available to her/him on a
medical record, a diagnosis of silicosis on the death certificate is

unlikely. According to a study submitted by the Laborers' Health and
Safety Fund of North America, (Wexelman et al., 2010), a sample of
physician residents surveyed in New York City did not believe that
cause of death reporting is accurate; this was a general finding, and
not specific to silicosis (Document ID 3756, Attachment 7).
    The ATS and the American College of Chest Physicians commented that
physicians often fail to recognize or misdiagnose silicosis as another
lung disease on the death certificate, leading to under-reporting on
death certificates (3577, Tr. 821, 826-827) and under-recognize and
underreport cases of silicosis (Document ID 2175, p. 3). As Dr.
Weissman from NIOSH responded:

    . . . it's well known that death certificates don't capture all
of the people that have a condition when they pass away, and so
there would be many that probably would not be captured if the
silicosis didn't directly contribute to the death and depending on
who filled out the death certificate, and the conditions of the
death and all those kinds of things. So it's an under-representation
of people who die with the condition . . . . (Document ID 3579, pp.
166-167).

    Although there is little empirical evidence describing the extent
to which silicosis is underreported as a cause of death, OSHA finds,
based on this evidence as well as on testimony in the record, that the
available silicosis surveillance data are likely to significantly
understate the number of deaths that occur in the U.S. where silicosis
is an underlying or contributing cause. This is in large part due to
physicians and medical residents who record causes of death not being
familiar or having access to the patient's work or medical history (see
Wexelman et al., 2010, Document ID 3756, Attachment 7; Al-Samarri et
al., Prev. Chronic Dis. 10:120210,2013). According to Goodwin et al.
(2003, Document ID 1030, p. 310), most primary care physicians do not
take occupational histories, nor do they receive formal training in
occupational disease. They further stated that, since it is likely that
a person would not retain the same health care provider over many
years, even if the presence of silicosis in a patient might have been
known by a physician who cared for them, it would not necessarily be
known by another physician or resident who recorded cause of death
years or decades later and who did not have access to the patient's
medical or work history. OSHA finds the testimony of Dr. Rosenman
compelling, who found that silicosis was not recorded as an underlying
or contributing cause of death even where there was chest x-ray
evidence of progressive massive fibrosis related to exposure to
crystalline silica.
    Some commenters stated that the decline in silicosis mortality
demonstrates that there is a threshold for silicosis above the prior
PEL of 100 [mu]g/m\3\ (Document ID 4224, p. 2-5; 3582, Tr. 1951-1963).
OSHA finds this argument irrelevant as the threshold concept does not
apply to historical surveillance data. As noted above and discussed in
Section V.I, Comments and Responses Concerning Threshold for Silica-
Related Diseases, OSHA believes that surveillance data should not be
used for quantitative risk analysis (including determination of
threshold effects) because it lacks an exposure characterization based
on sampling. Thus, the surveillance data cannot demonstrate the
existence of a population threshold.
    There is also evidence in the record that silicosis morbidity
statistics reviewed earlier in this section are underreported. This can
be due, in part, to the relative insensitivity of chest roentgenograms
for detecting lung fibrosis. Hnizdo et al. (1993) evaluated the
sensitivity, specificity and predictive value of radiography by
correlating radiological and pathological (autopsy) findings of
silicosis. ``Sensitivity'' and ``specificity'' refer to the ability of
a test to correctly identify those with the disease (true positive
rate), and those without the disease (true negative). Because
pathological findings are the most definitive for silicosis, findings
on biopsy and autopsy provide the best comparison for determining
sensitivity and specificity of chest imaging.
    The study used three readers and defined a profusion score of 1/1
as positive for silicosis. Sensitivity was defined as the probability
of a positive radiological reading (ILO category >1/1) given that
silicotic nodules were found in the lungs at autopsy. Specificity was
defined as the probability of a negative radiological reading (ILO
category <1/1) given that no, or only an insignificant number of
silicotic nodules were found at autopsy. The average sensitivity values
were low for each of the three readers (0.39, 0.37, and 0.24), whereas
the average specificity values were high (0.99, 0.97, and 0.98). For
all readers, the proportion of true positive readings (i.e., the
sensitivity) increased with the extent of silicosis found at autopsy
(Document ID 1050).
    In the only published study that quantified the extent of
underreporting of silicosis mortality and morbidity, Rosenman et al.
estimated the number of new cases of silicosis occurring annually in
the U.S. at between 3,600 and 7,300 based on the ratio of living to
deceased persons identified and confirmed as silicotics in the Michigan
surveillance data and extrapolating that ratio using the number of
deaths due to silicosis for the U.S. as a whole (2003, Document ID
0420). OSHA reviewed the study in its Review of the Health Effects
Literature (Document ID 1711, p. 48). Patrick Hessel, Ph.D., criticized
the methods used by Dr. Rosenman, and deemed the resulting estimates
unreliable, stating that the actual number of new silicosis cases
arising each year is likely to be lower than the authors estimated
(Document ID 2332, p. 2; 3576, Tr. 323-331).
    OSHA disagrees with the criticisms that Dr. Hessel, commenting on
behalf of the Chamber, offered on the study by Rosenman et al. (2003,
Document ID 0420). Specifically, Dr. Hessel argued: (1) That the
silicosis-related deaths used by Rosenman et al. occurred during the
period 1987 through 1996, and do not reflect the declining numbers
after that time period; (2) that the Michigan surveillance system
relied on a single B-reader who was biased toward finding silicosis in
patients who were brought to his attention for suspected silicosis; and
(3) that the Michigan population was not representative of the rest of
the country, since about 80 percent of the workers diagnosed with
silicosis worked in foundries, which are not prevalent in most other
states. Finally, in his hearing testimony, Dr. Hessel criticized the
capture-recapture analysis used by Rosenman et al. to estimate the
extent of underreporting of cases, stating that a number of underlying
assumptions used in the analysis were not met (Document ID 3576, Tr.
323-332).
    Dr. Rosenman addressed many of these criticisms in the study and at
the rulemaking hearing. Regarding the fact that the number of
silicosis-related deaths does not reflect the decline in deaths after
1996, Dr. Rosenman testified that, although the number of recorded
silicosis deaths have declined since then, the ratio of cases to deaths
has increased because the number of cases has not declined. ``The
living to dead ratio that we reported in our published study in 2003
was 6.44. This ratio has actually increased in recent years to 15.2. A
similar ratio . . . [was] found in the New Jersey surveillance data,
which went from 5.97 to 11.5 times'' (Document ID 3577, Tr. 854). If
one were to apply the more recent ratio from Michigan (more than double
the ratio used by Rosenman et al.) to the more recent number of deaths
in the country (about half that recorded in the mid-1990s; see Table V-
1) to extrapolate

the number of silicosis cases for the U.S. overall, the result would be
even greater than the estimate in Rosenman et al. (2003).
    At the hearing, Dr. Rosenman testified that he was the sole B-
reader of lung x-rays for the study, and that he received the x-ray
films from other radiologists who suspected but did not confirm the
presence of silicosis (Document ID 3577, Tr. 877-878). Dr. Rosenman,
while acknowledging that there could be differences between readers in
scoring x-ray films, argued that such differences in scoring--for
example, whether a film is scored a 3/3, 3/2, or 2/3--did not affect
this study since the study design only required that a case be
identified and confirmed (diagnosis requires a chest radiograph
interpretation showing rounded opacities of 1/0 or greater profusion)
(Document ID 3577, Tr. 877-878; 0420, p. 142).
    Dr. Rosenman also addressed the criticism that Michigan's worker
population with silica exposure is significantly different from the
rest of the country. In the study, Rosenman et al. reported that the
ratio of cases to deaths was about the same for Ohio as for Michigan
and, during the public hearing, Dr. Rosenman testified that the ratio
of cases to deaths for New Jersey was also similar to Michigan's (11.5
vs. 15.2) (Document ID 0420, p. 146; 3577, Tr. 854). This similarity
was despite the fact that New Jersey had a different industrial mix,
with fewer foundries (Document ID 3577, Tr. 878). Furthermore, the
estimates made by Rosenman et al. depended on the ratio of cases to
deaths in Michigan, rather than just the number of cases in that state.
The authors believed that the ratio would be unaffected by the level of
industrialization in Michigan (Document ID 0420, p. 146).
    Finally, regarding the capture-recapture analysis, OSHA notes that
Dr. Hessel acknowledged that this technique has been used in
epidemiology to estimate sizes of populations identified from multiple
overlapping sources (Document ID 2332, p. 2), which is the purpose for
which Rosenman et al. used the approach. In addition, the Rosenman et
al. study noted that the assumptions used in capture-recapture analysis
could not be fully met in most epidemiological study designs, but that
the effect of violating these assumptions was either negligible or was
evaluated using interaction terms in the regression models employed.
The investigators also reported that the capture-recapture analysis
used on Ohio state surveillance data found that the total number of
cases estimated for the state was between 3.03 and 3.18 times the
number of cases identified, a result that is comparable to that for
Michigan (Document ID 0420, pp. 146-147). After considering Dr.
Hessel's written testimony, Dr. Rosenman testified that ``. . . overall
I don't think his comments make a difference in my data'' (Document ID
3577, Tr. 877).
    OSHA finds all of Dr. Rosenman's responses to Dr. Hessel's
criticisms to be reasonable. And based on Dr. Rosenman's comments and
testimony, OSHA continues to believe that the Rosenman et al. (2003)
analysis and resulting estimates of the number of new silicosis cases
that arise each year are reasonable. Additionally, Dr. Rosenman, in
updating his data for his testimony for this rulemaking, found that the
ratio had increased from 6.44 in the published study to 15.2 times in
more recent years (Document ID 3577, Tr. 854). The study supports
OSHA's hypothesis that silicosis is a much more widespread problem than
the surveillance data suggest and that OSHA's estimates of the non-
fatal illnesses that will be avoided as a result of this new silica
standard are not unreasonable. Regardless, even assuming commenters'
criticisms have merit, they do not significantly affect OSHA's own
estimates from the epidemiological evidence of the risks of silicosis.
    Accordingly, after careful consideration of the available
surveillance data, stakeholders' comments and testimony, and the
remainder of the record as a whole, OSHA has determined that the
available silicosis surveillance data are useful for providing context
and an illustration of a significant general trend in the reduction of
deaths associated with silicosis over the past four to five decades. As
discussed above, and in large part because the data themselves are
limited and incomplete, OSHA believes reliance upon them for the
purpose of estimating the magnitude of the risk would be inappropriate.
The Agency has chosen instead to follow its well-established practice
of relying on epidemiological data to meet its burden of demonstrating
that workers exposed to respirable crystalline silica at the previous
PELs face a significant risk of developing silicosis and that such risk
will be reduced when the new limit is fully implemented.

F. Comments and Responses Concerning Lung Cancer Mortality

    OSHA received numerous comments regarding the carcinogenic
potential of crystalline silica as well as the studies of lung cancer
mortality that the Agency relied upon in the Preliminary Quantitative
Risk Assessment (QRA). Many of these comments, particularly from the
ACC, asserted that (1) OSHA should have relied upon additional
epidemiological studies, and (2) the studies that the Agency did rely
upon (Steenland et al., 2001a, as re-analyzed in ToxaChemica, 2004;
Rice et al., 2001; Attfield and Costello, 2004; Hughes et al., 2001;
and Miller and MacCalman, 2009) were flawed or biased. In this section,
OSHA presents these comments and its responses to them.
1. Carcinogenicity of Crystalline Silica
    As discussed in the Review of Health Effects Literature and
Preliminary QRA (Document ID 1711, pp. 76-77), in 1997, the World
Health Organization's International Agency for Research on Cancer
(IARC) conducted a thorough expert committee review of the peer-
reviewed scientific literature and classified crystalline silica dust,
in the form of quartz or cristobalite, as Group 1, ``carcinogenic to
humans'' (Document ID 2258, Attachment 8, p. 211). IARC's overall
finding for silica was based on studies of nine occupational cohorts
that it considered to be the least influenced by confounding factors
(Document ID 1711, p. 76). In March of 2009, 27 scientists from eight
countries participated in an additional IARC review of the scientific
literature and subsequently, in 2012, IARC reaffirmed that respirable
crystalline silica dust is a Group 1 human carcinogen that causes lung
cancer (Document ID 1473, p. 396). Additionally, in 2000, the National
Toxicology Program (NTP) of HHS concluded that respirable crystalline
silica is a known human carcinogen (Document ID 1164, p. 1).
    The ACC, in its pre-hearing comments, questioned the carcinogenic
potential of crystalline silica, asserting that IARC's 1996
recommendation that crystalline silica be classified as a Group 1
carcinogen was controversial (Document ID 2307, Attachment A, p. 29).
The ACC cited Dr. Patrick Hessel's 2005 review of epidemiological
studies, published after the initial IARC determination, in which he
concluded that ``the silica-lung cancer hypothesis remained
questionable'' (Document ID 2307, Attachment A, p. 31). The ACC
reasserted this position in its post-hearing brief, contending that
``epidemiological studies have been negative as often as they have been
positive'' (Document ID 4209, pp. 33-34).
    After the publication of Dr. Hessel's 2005 review article, IARC
reaffirmed in 2012 its earlier Group 1 classification for crystalline
silica dust (Document ID 1473). As pointed out by Steenland and

Ward, IARC is one of ``2 agencies that are usually considered to be
authoritative regarding whether a substance causes cancer in humans,''
the other being the NTP, which has also determined crystalline silica
to be carcinogenic on two separate occasions (2013, article included in
Document ID 2340, p. 5). David Goldsmith, Ph.D., who coauthored one of
the first published articles linking silica exposure to lung cancer,
echoed Steenland and Ward:

    It is important to recognize that evidence for silica's
carcinogenicity has been reviewed three times by the International
Agency for Research on Cancer, once in 1987, 1997, and 2012. It has
been evaluated by California's Proposition 65 in 1988, by the
National Toxicology Program in 2000 and reaffirmed in 2011, and by
the National Institute for Occupational Safety and Health in 2002
(Document ID 3577, Tr. 861-862).

    Multiple organizations with great expertise in this area, including
the American Cancer Society, submitted comments supporting the thorough
and authoritative nature of IARC's findings regarding silica's
carcinogenicity (e.g., Document ID 1171; 1878). OSHA likewise places
great weight on the IARC and NTP classifications and, based on their
findings, concludes that the carcinogenic nature of crystalline silica
dust has been well established. Further support for this finding is
discussed in Section V.L, Comments and Responses Concerning Causation.
2. Silicosis and Lung Cancer
    In addition to debating the conclusions of IARC, Peter Morfeld, Dr.
rer. medic, testifying on behalf of the ACC Crystalline Silica Panel,
concluded that OSHA's risk estimates for lung cancer are ``unreliable''
because they ``ignore threshold effects and the apparent mediating role
of silicosis'' (Document ID 2307, Attachment 2, p. 16). Dr. Morfeld
argued that silicosis is a necessary prerequisite for silica-related
lung cancer. Commenters' arguments about silicosis being a prerequisite
for lung cancer and silicosis having a threshold are linked; if it were
shown both that silicosis requires a certain threshold of exposure and
that only persons with silicosis get lung cancer, then silica-related
lung cancer would also have an exposure threshold. As discussed in
Section V.I, Comments and Responses Concerning Thresholds for Silica-
Related Diseases, commenters claimed that there is a threshold for
silicosis above the previous PEL for general industry, which would make
any threshold for lung cancer above that level as well. OSHA discusses
these comments in detail in that section, and has determined that even
if lung cancer does not occur in the absence of silicosis, the record
strongly supports the conclusion that workers exposed to respirable
crystalline silica would still be at risk of developing lung cancer as
a result of their exposure because silicosis can develop among workers
whose average and cumulative exposures are below the levels permitted
by the previous PELs.
    OSHA received comments from other stakeholders, including Robert
Glenn, representing the Brick Industry Association, and the AFS on the
possible mediating role of silicosis in the development of lung cancer
(Document ID 2307, pp. 29-35; 2343, Attachment 1, pp. 42-45; 2379,
Attachment 2, pp. 24-25). The ACC cited several review articles in
support of its claim that ``silica exposures have not been shown to
increase the risk of lung cancer in the absence of silicosis''
(Document ID 2307, Attachment A, pp. 29, 32, 35). These articles
included: A 2004 review of studies by Kurihara and Wada that found that
while silicosis is a risk factor for lung cancer, exposure to silica
itself may not be a risk factor (Document ID 1084); a 2006 review by
Pelucchi et al. that determined that the issue of whether silica itself
increases lung cancer risk in the absence of silicosis has not been
resolved (Document ID 0408); and a 2011 review by Erren et al. that
concluded it is unclear whether silica causes lung cancer in persons
who do not already have silicosis (Document ID 3873). Similarly, the
AFS cited a review by the Health and Safety Executive (2003) that
concluded that increased risks of lung cancer are restricted to those
groups with the highest cumulative exposures, with evidence tending to
show that excess lung cancer mortality is restricted to those with
silicosis (Document ID 2379, Attachment 2, pp. 24-25). Having reviewed
the studies cited by commenters, OSHA has come to the conclusion that
none of the cited studies demonstrates that silicosis is a necessary
precursor to lung cancer, but acknowledges that uncertainty remains
about what percentage of lung cancers in silica-exposed workers are
independent of silicosis.
    Similarly, the ACC stated that none of the studies of lung cancer
mortality that OSHA relied upon in the Preliminary QRA demonstrates
that silica exposure causes lung cancer in the absence of silicosis
(Document ID 2307, Attachment A, p. 66). During the rulemaking hearing,
NIOSH scientists addressed the issue of whether silicosis is a
necessary precursor to the development of lung cancer. They stated that
it is a difficult issue to resolve because the two diseases may have a
similar pathway, such that they can develop independently but still
appear correlated. Mr. Robert Park also added that:

    [S]ilicosis isn't detectable until there's splotches on the lung
that are visible in x-rays. So prior to that point, somebody could
have [been] developing lung disease and you just can't see it. So,
of course, people that have silicosis are going to have higher lung
cancer, and it's going to look like a threshold because you didn't
see the silicosis in other people that have lower lung cancer risk.
To really separate those two, you'd have to do a really big study.
You'd have to have some measures, independent measures of lung
physiological pathology, and see what's going on with silicosis as a
necessary condition for development of lung cancer (Document ID
3579, Tr. 245-247).

    Similarly, David Weissman, MD, concurred that ``there's quite a bit
of reason as Bob [Park] said to think that the two processes
[development of silicosis and development of lung cancer] don't require
each other, and it would be extraordinarily difficult to sort things
out in human data'' (Document ID 3579, Tr. 247). Indeed, Checkoway and
Franzblau (2000) reviewed the epidemiological literature addressing
this topic, and found that the ``limitations of existing epidemiologic
literature that bears on the question at hand suggest that prospects
for a conclusive answer are bleak'' (Document ID 0323, p. 257). The
authors concluded that silicosis and lung cancer should be treated in
risk assessments as ``separate entities whose cause/effect relations
are not necessarily linked'' (Document ID 0323, p. 257). Brian Miller,
Ph.D., a peer reviewer of OSHA's Review of Health Effects Literature
and Preliminary QRA, likewise wrote in his post-hearing comments, ``I
consider this issue unanswerable, given that we cannot investigate for
early fibrotic lesions in the living, but must rely on radiographs''
(Document ID 3574, p. 31).
    During the public rulemaking hearing, several stakeholders pointed
to a recent study of Chinese pottery workers and miners by Liu et al.
(2013, article included in Document ID 2340) as evidence that exposure
to crystalline silica is associated with lung cancer even in the
absence of silicosis (Document ID 3580, Tr. 1232-1235; 3577, Tr. 803-
804, 862-863). In this study, the authors excluded 15 percent of the
cohort (including 119 lung cancer deaths) with radiographic evidence of
silicosis and found that the risk of lung cancer mortality still
increased with cumulative exposure to crystalline silica, suggesting
that clinically-

apparent silicosis is not a prerequisite for silica-related lung cancer
(article included in Document ID 2340, pp. 3, 7).
    The ACC argued that it is ``premature to draw that conclusion,''
stating that the Liu study's conclusions are not supported by the data
and raising questions about uncertainty in the exposure estimates,
modeling and statistics, confounding, and the silicosis status of
cohort members (Document ID 2307, Attachment A, p. 48; 4027, pp. 35-36;
4209, pp. 40-51). With regard to exposure estimates, the ACC had a
number of concerns, including that conversion factors determined by
side-by-side sampling in 1988-1989 were used to convert Chinese total
dust concentrations to respirable crystalline silica exposures
(Document ID 4209, pp. 40-41). Dr. Cox expressed concern that these
conversion factors from 1988-1989 might not have been applicable to
other time periods, as particle size distributions could change over
time (Document ID 4027, p. 32). OSHA acknowledges this concern, but
given the ``insufficient historical particle size data . . . to analyze
whether there were changes in particle size distributions from the
1950s to the 1990s,'' believes that the authors were justified in
making their exposure assumptions (Document ID 4027, p. 32). Dr. Cox's
concerns involving modeling and statistics (see Document ID 4027, pp.
33-36) in the study, including the absence of model diagnostics, the
use of inappropriate or misspecified models, the lack of a discussion
of residual confounding and model uncertainty, and the use of
inappropriate data adjustments and transformations, are discussed in
detail in Section V.J, Comments and Responses Concerning Biases in Key
Studies.
    On the issue of confounding, the ACC noted that Liu et al. (2013)
used a subcohort of 34,018 participants from 6 tungsten mines, 1 iron
mine, and 4 potteries derived from a total cohort of 74,040
participants from 29 mines and pottery factories studied previously by
Chen et al. (2007, Document ID 1469; 2307, Attachment A, pp. 48-50).
Liu et al. (2013) excluded participants in the original cohort if
detailed information on work history or smoking was not available, or
if they worked in copper mines or tin mines where the analysis could be
confounded by other exposures, namely radon and carcinogenic polycyclic
aromatic hydrocarbons (PAHs) in the former and arsenic in the latter
(article included in Document ID 2340, p. 2). The ACC's main concern
was that Liu et al. (2013) did not adjust for these confounders in
their analyses, but rather claimed that there were no confounding
exposures in their smaller cohort on the basis of the exclusion
criteria (Document ID 2307, Attachment A, p. 49).
    The ACC also noted that Chen et al. (2007) stated that the Chinese
pottery workers were exposed to PAHs, and some of the iron-copper
miners were exposed to PAHs and radon progeny (Document ID 2307,
Attachment A, p. 49). Chen et al. (2007) initially found an association
between respirable silica and lung cancer mortality in the pottery
workers and iron-copper miners, but it disappeared after adjusting for
PAH exposures (Document ID 1469). In the tungsten miners, Chen et al.
(2007) found no significant association for lung cancer mortality,
while Liu et al. (2013) did. Similarly, the ACC pointed out that a
subsequent study by Chen et al. (2012, article included in Document ID
2340) also failed to find a statistically significant increase in the
hazard ratio for lung cancer, meaning that there was no significant
positive exposure-response relationship between cumulative silica
exposure and lung cancer mortality (Document ID 4209, p. 45). Dr.
Morfeld concluded, ``Unless and until these issues are resolved, Liu et
al. (2013) should not be used to draw conclusions regarding exposure-
response relationships between RCS [respirable crystalline silica],
silicosis and lung cancer risk'' (Document ID 2307, Attachment 2, pp.
15-16).
    During the public hearing, counsel to the ACC asked Dr. Steenland,
a co-author on the Liu et al. (2013) study, if he would provide
measurement data on the PAH exposures in the potteries, as well as
present the data from the Liu et al. (2013) study separately for
pottery factories and tungsten mines, as they were in Chen et al.
(2007, Document ID 1469) (Document ID 3580, Tr. 1237-1240). Dr.
Steenland subsequently provided the requested data for inclusion in the
rulemaking record (Document ID 3954).
    With respect to the PAH data for the potteries, Dr. Weihong Chen,
the study's first author, reported that, in measurements in 1987-1988
in the four potteries that were excluded from the Liu et al. (2013)
analysis, the mean total PAHs was 38.9 [micro]g/m\3\ and the mean
carcinogenic PAHs was 4.7 [micro]g/m\3\. In the four potteries that
were included in the Liu et al. (2013) analysis, the mean total and
carcinogenic PAHs, as measured in 1987-1988, were substantially lower
at 11.6 and 2.5 [micro]g/m\3\, respectively. When the measurements were
repeated in 2006, the mean total and carcinogenic PAHs in the four
potteries included in the analysis were still lower, at 2.2 and 0.08
[micro]g/m\3\, levels that were ``not much higher than environmental
PAH in many [Chinese] cities'' (Document ID 3954, p. 2). Dr. Chen also
reported that, when comparing levels within six job titles, there was
no significant correlation between total or carcinogenic PAHs (based on
the 2006 measurements) and respirable silica dust. When the results
were presented separately for the mines and potteries, in analyses
using continuous cumulative exposure, the relationship between silica
exposure and lung cancer mortality remained significant for the pottery
factories, but not the metal mines. In the categorical analyses using
quartiles of cumulative exposure, the results were mixed: The
association between silica exposure and lung cancer mortality was
statistically significant in some exposure quartiles for both metal
mines and pottery factories (Document ID 3954, p. 2).
    Based upon these subsequent data, the ACC concluded that PAHs were
likely present in the potteries but not in the mines (Document ID 4209,
p. 45). OSHA believes this conclusion, although plausible, to be
speculative. What is known is that the potteries that were excluded had
a higher average level of PAHs, and that a significant association
between cumulative silica exposure and lung cancer mortality remained
in the included potteries even after the analysis was separated by
potteries and mines. However, the association was less clear in the
metal mines.
    The ACC also raised concerns about the silicosis status of lung
cancer cases in the Liu cohort, asserting that some workers may not
have had post-employment radiography given that social health insurance
only recently began to pay for it. As such, the ACC asserted that some
workers who developed lung cancer post-employment may have also had
undiagnosed silicosis (Document ID 4209, pp. 49-50). OSHA acknowledges
the limitations of the study, as with any retrospective study, but also
notes that no evidence was put forth to indicate that workers with
silicosis were misclassified in the study as workers without silicosis.
Further, Dr. Goldsmith testified that the method used by Liu et al. for
excluding workers with silicosis (x-ray findings) was ``very eminently
reasonable,'' given that the only foolproof means of proving the
absence of silicosis--autopsy--was not available for this particular
cohort (Document ID 3577, Tr. 874-875).
    Thus, OSHA concludes that the Liu et al. (2013) study preliminarily
suggests

that silicosis is not required for the development of lung cancer;
however, no one study will settle the question of the role of silicosis
in the carcinogenicity of crystalline silica. As acknowledged by Dr.
Cox, the Agency did not rely upon the Liu et al. (2013) study in its
preliminary or final QRA (Document ID 2307, Attachment 4, p. 37).
    Overall, after giving lengthy consideration to all evidence in the
record regarding whether silicosis is a necessary precursor to the
development of lung cancer, including the Liu study, the NIOSH
testimony, and the mechanistic evidence for the carcinogenicity of
crystalline silica discussed in Section V.H, Mechanisms of Silica-
Induced Adverse Health Effects, OSHA concludes that the mediating role
of silicosis in the development of lung cancer is not ``apparent,'' as
suggested by Dr. Morfeld and the ACC (Document ID 2307, Attachment 2,
p. 16). As such, OSHA continues to believe that substantial evidence
supports the Agency's decision to consider lung cancer as a separate,
independent health endpoint in its risk analysis. The Agency also notes
that even if lung cancer does not occur in the absence of silicosis,
the record strongly supports the conclusion that workers exposed to
respirable crystalline silica would still be at risk of developing lung
cancer as a result of their exposure because silicosis can develop from
average and cumulative exposures below the levels allowed at the
previous PEL (see Section V.I, Comments and Responses Concerning
Thresholds for Silica-Related Diseases.)
3. Additional Studies
    Stakeholders also suggested several additional studies that they
believe OSHA should include in its QRA on lung cancer. The AFS
commented that OSHA's Preliminary QRA overlooked a 2003 report by the
Health and Safety Executive (HSE, Document ID 1057), asserting that
over 40 percent of the references cited by HSE were omitted in OSHA's
review (Document ID 4035, p. 2). OSHA disagrees with this assessment of
overlooking the report, noting that the Agency reviewed and referenced
the HSE report in its Review of Health Effects Literature and
Preliminary QRA (Document ID 1711, p. 77). As discussed in Section V.C,
Summary of the Review of Health Effects Literature and Preliminary QRA,
OSHA used a weight-of-evidence approach to evaluate the scientific
studies in the literature to determine their overall quality. In so
doing, OSHA thoroughly reviewed approximately 60 published, peer-
reviewed primary epidemiological studies covering more than 30
occupational cohorts in over a dozen industrial sectors, as well as the
IARC pooled study and several meta-analyses (Document ID 1711, pp. 75-
172).
    The AFS also submitted a 2011 review of 30 foundry epidemiology
studies by the Industrial Industries Advisory Council (IIAC) and noted
that only 7 of those 30 studies were included in OSHA's Review of
Health Effects Literature and Preliminary QRA (Document ID 2379, p.
24). AFS wrote:

    The PQRA largely dismisses the foundry epidemiology studies,
based on assertions of positive confounding. However, a study
showing that there is no adverse effect despite a positive
confounder is not only still relevant to the question, but should be
more persuasive than a study without positive confounders because
the data then show that even with an additive risk, there is no
increase in effect at the reported exposure levels (Document ID
2379, p. 24).

    In response to this comment, OSHA gathered the remaining 23 foundry
studies cited in the submitted report and placed them in the rulemaking
docket during the post-hearing comment period. OSHA notes, in the first
instance, that most of these studies were not designed to study the
effects of silica exposure on foundry workers, and did not even attempt
to do so; rather, their purpose was to examine lung cancer mortality
and/or morbidity in foundry work, which involves many toxic and
otherwise harmful substances besides silica. Therefore, OSHA would
likely be unable to suitably use these studies as a basis for a
quantitative risk assessment regarding respirable crystalline silica by
itself.
    With respect to AFS's assertions of studies showing ``no adverse
effect,'' OSHA notes that the summary section of the IIAC review
report, submitted as evidence by AFS, stated that, ``The cohort
mortality studies and two morbidity studies suggest an increased risk
of lung cancer in foundry workers when considered overall, but do not
support a doubling of risk. . . . Findings in the case-control studies,
the majority of which adjust for the effects of smoking . . . tend to
support those of the cohort studies'' (Document ID 3991, p. 5). As
such, this review of 30 foundry epidemiology studies showed an
increased excess risk of lung cancer from foundry work; the fact that
the excess risk was not increased by a factor of two is irrelevant to
the current proceedings. The factor of two appears to be used by the
IIAC in determining whether monetary benefits should be paid to foundry
workers in Great Britain and is completely unrelated to OSHA's
statutory requirements for determining whether workers exposed to
silica are at a significant risk of material impairment of health.
Given that excess lung cancer was observed in many of these studies,
OSHA rejects the AFS's assertion that, even with positive confounding,
there was no increase in adverse effect (i.e., lung cancer).
    OSHA also notes that the IIAC's finding of an elevated risk of lung
cancer in foundries is not surprising. As Dr. Mirer stated during his
testimony, IARC categorized foundry work as Group 1, carcinogenic to
humans, in 1987 based on observed lung cancer (Document ID 2257,
Attachment 3, p. 5). IARC reaffirmed its Group 1 classification for
foundry work in 2012 (Document ID 4130). However, as noted by OSHA in
its Review of Health Effects Literature, the foundry epidemiology
studies were profoundly confounded by the presence of exposures to
other carcinogens, including PAHs, aromatic amines, and metals
(Document ID 1711, p. 264). Because of this confounding, as well as the
fact that most of these studies did not specifically study the effects
of silica exposure on foundry workers, OSHA has decided not to include
them in its QRA.
    The ACC likewise cited several individual studies that it believed
found no relationship between silica exposure and lung cancer risk
(Document ID 2307, Attachment A, pp. 33-35). These included studies by:
(1) Yu et al. (2007), which found no consistent exposure-response
relationship between silica exposure and lung cancer death in workers
with silicosis in Hong Kong (Document ID 3872); (2) Chen et al. (2007),
which found, as mentioned in relation to the Liu et al. (2013) study,
no relationship between silica exposure and lung cancer after adjusting
for confounders in a study of Chinese tungsten miners, tin miners,
iron-copper miners, and pottery workers (Document ID 1469); (3) Birk et
al. (2009), which found the standardized mortality ratio (SMR) for lung
cancer was not elevated in a subgroup of men who worked in areas of
German porcelain plants with the highest likely silica exposures
(Document ID 1468); (4) Mundt et al. (2011), which found, in a
subsequent analysis of the German porcelain industry, that cumulative
silica exposure was not associated with lung cancer mortality,
mortality from kidney cancer, or any other cause of death other than
silicosis (Document ID 1478); and (5) Westberg et al. (2013), which
found that cumulative silica exposure was not associated with lung
cancer morbidity (Document ID 4054).

    Briefly, Chen et al. (2007) examined a cohort of male workers in 29
Chinese mines and factories, and initially found a significant trend
between cumulative silica exposure and lung cancer mortality in pottery
workers and tin miners; this trend was no longer significant after
adjustment for occupational confounders (carcinogenic PAHs in
potteries, arsenic in tin mines) (Document ID 1469, pp. 320, 323-324).
On the contrary, Liu et al. (2013) demonstrated a statistically
significant association between cumulative silica exposure and lung
cancer mortality after excluding mines and factories with confounding
exposures (article included in Document ID 2340). As noted previously,
there are questions of how confounding exposures to radon, PAHs, and
arsenic were handled in both the Chen et al. (2007) and Liu et al.
(2013) studies. One important difference between the two studies,
however, was the follow-up time. While Chen et al. (2007) had follow-up
to 1994 and identified 511 lung cancer deaths in a cohort of 47,108
workers (Document ID 1469, pp. 321-322), Liu et al. (2013) had follow-
up to 2003 and identified 546 lung cancer deaths in a cohort of 34,018
workers (article included in Document ID 2340, pp. 2-4).
    OSHA discussed the Birk et al. (2009, Document ID 1468) and Mundt
et al. (2011, Document ID 1478) studies of the German porcelain
industry in its Supplemental Literature Review, noting several
limitations that are applicable to both studies and might preclude the
conclusion that there was no association between silica exposure and
lung cancer (Document ID 1711, Attachment 1, pp. 6-12). One such
limitation was the mean age of subjects--35 years--at the start of
follow-up, making this a relatively young cohort in which to observe
lung cancer. The mean follow-up period of 19 years per subject was also
a limitation, given the long latency for lung cancer and the young age
of the cohort at the start of follow-up; only 9.2 percent of the cohort
was deceased by the end of the follow-up period. OSHA noted that Mundt
et al. (2011) acknowledged that additional follow-up of the cohort may
be valuable (Document ID 1711, Attachment 1, pp. 10-11; 1478, p. 288).
In addition, Mundt et al. (2011) had only 74 male lung cancer deaths,
some of whom had possible or probable prior silica exposure that could
have resulted in cumulative exposure misclassification (Document ID
1478, pp. 285, 288). The authors also reported statistically
significantly elevated lung cancer hazard ratios for some categories of
average silica exposure, but did not present any trend analysis data
(Document ID 1478, p. 285). It also does not appear that Mundt et al.
performed any lagged analyses for lung cancer to account for the
latency period of lung cancer.
    Following the ACC's citation of the Yu et al. (2007) and Westberg
et al. (2013) studies in its pre-hearing comments, OSHA obtained and
reviewed these studies, and added them to the rulemaking docket
(Document ID 3872; 4054). Yu et al. (2007) followed a cohort of 2,789
workers in Hong Kong diagnosed with silicosis between 1981 and 1998.
The average follow-up time was 9 years, with 30.6 percent of the cohort
deceased when the study ended in 1999. The SMR for lung cancer was not
statistically significantly elevated following indirect adjustment for
cigarette smoking; similarly, the authors did not find a significant
exposure-response relationship between cumulative silica exposure and
lung cancer mortality (Document ID 3872). Westberg et al. (2013)
studied a group of 3,045 male Swedish foundry workers to determine lung
cancer incidence and morbidity. Although the lung cancer incidence was
statistically significantly elevated, the authors did not find a
significant exposure-response relationship with cumulative quartz
exposure (Document ID 4054, p. 499).
    Regarding these studies, OSHA notes that the Westberg et al. (2013)
study, like other foundry studies, is confounded by other carcinogenic
substances present in foundries, including, as the authors pointed out,
phenol, formaldehyde, furfuryl alcohols, PAHs, carbon black,
isocyanates, and asbestos (Document ID 4054, p. 499). The Yu et al.
(2007) study had an average follow-up period of only 9 years (Document
ID 3872, p. 1058, Table 1), which is a short follow-up period when
considering the latency period for the development of cancer. In
addition, the Yu et al. study (2007), as described in the earlier Tse
et al. (2007) study, used a job exposure matrix developed from expert
opinion to assign estimated past levels of silica exposure to
individuals based on self-reported work history; changes in exposure
intensity with calendar year were not considered because of limited
data (Document ID 3841, p. 88; 3872, p. 1057). OSHA notes that this
exposure estimation may have included considerable misclassification
due to inaccuracies in self-reported work history, the use of expert
opinion to estimate past exposure levels rather than actual
measurements for the subjects under study, and the failure to
incorporate any changes in exposure levels over calendar time into the
exposure estimates. Although these exposure estimates were used in an
analysis that found a significant exposure-response for NMRD mortality
among workers with silicosis (Tse et al., 2007, Document ID 3841), an
exposure-response for lung cancer mortality may not be as strong and
may be harder to detect, requiring more accurate exposure information.
OSHA also notes that NMRD mortality is likely to be a competing cause
of death with lung cancer, such that some workers may have died from
NMRD before developing lung cancer. The workers with silicosis in this
study also had high exposures (mean cumulative exposure of 10.89 mg/
m\3\-yrs) (Document ID 3872, p. 1058), possibly making it difficult to
detect an exposure-response for lung cancer when exposures are
relatively homogenous and high. Selection effects would have been
extreme in these highly-exposed workers, whose all-cause mortality was
double what would be expected (853 deaths observed, 406 expected) in
the general population of males in Hong Kong and whose respiratory
disease mortality was an astounding six times the expected level (445
deaths observed, 75 expected) (Document ID 3872, p. 1059).
    OSHA acknowledges that not every study reaches the same results and
conclusions. This is typically true in epidemiology, as there are
different cohorts, measurements, study designs, and analytical methods,
among other factors. As a result, scientists critically examine the
studies, both individually and overall, in the body of literature to
draw weight-of-evidence conclusions. IARC noted, with respect to its
1997 carcinogenicity determination:

    [N]ot all studies reviewed demonstrated an excess of cancer of
the lung and, given the wide range of populations and exposure
circumstances studied, some non-uniformity of results had been
expected. However, overall, the epidemiological findings at the time
supported an association between cancer of the lung and inhaled
crystalline silica ([alpha]-quartz and cristobalite) resulting from
occupational exposure (Document ID 1473, p. 370).

    Given IARC's re-affirmation of this finding in 2012, OSHA does not
believe that the individual studies mentioned above fundamentally
change the weight of evidence in the body of literature supporting the
carcinogenicity of crystalline silica. The best available evidence in
the rulemaking record continues to indicate that exposure to respirable
crystalline silica causes lung cancer. OSHA acknowledges, however, that
there is some uncertainty with respect to the exact magnitude of the

lung cancer risk, as each of the key studies relied upon provides
slightly different risk estimates, as indicated in Table VI-1.
    Further, the ACC focused extensively on and advocated for a study
by Vacek et al. (2011) that found no significant association between
respirable silica exposure and lung cancer mortality in a cohort of
Vermont granite workers (Document ID 1486, pp. 75-81). Included in the
rulemaking docket are the peer-reviewed published version of the study
(Document ID 1486) and the earlier Final Report to the ACC, whose
Crystalline Silica Panel funded the study (Document ID 2307, Attachment
6), as well as comments from two of the authors of Vacek et al. (2011)
responding to OSHA's treatment of the study in its Supplemental
Literature Review (Document ID 1804). The ACC stated:

    Perhaps of most interest and relevance for present purposes--
because the cohort has been studied so extensively in the past and
because the present PEL is based indirectly on experience in the
Vermont granite industry--is the mortality study of Vermont granite
workers published in 2011. While the Vermont granite workers cohort
has been studied on a number of previous occasions, this is the most
comprehensive mortality study of Vermont granite workers to date
(Document ID 2307, Attachment A, p. 36).

    The ACC criticized OSHA for rejecting the Vacek et al. (2011) study
in its Supplemental Literature Review and instead relying upon the
Attfield and Costello (2004, Document ID 0284) study of Vermont granite
workers (Document ID 2307, Attachment A, pp. 36-47; 4209, pp. 34-36).
The ACC asserted several differences between the studies. First, while
Attfield and Costello had 5,414 workers (201 lung cancer deaths) in the
cohort, Vacek et al. had 7,052 workers (356 lung cancer deaths) as they
extended the follow-up period by 10 years to 2004. Vacek et al. also
claimed to have more complete mortality data, finding that ``162
workers, whom Attfield assumed were alive in 1994, had died before that
time and some decades earlier'' (Document ID 2307, Attachment A, p.
38). In addition, Vacek et al. used exposure measurements and raw data
not used by Attfield and Costello; for example, Vacek et al. used
pension records and interviews from other studies to account for gaps
in employment and changes in jobs, while Attfield and Costello assumed
that a person remained in the same job between chest x-rays at the
Vermont Department of Industrial Health surveillance program. Different
conversion factors to estimate gravimetric concentrations from particle
count data were also used: Attfield and Costello used a factor of 10
mppcf = 75 [micro]g/m\3\ while Vacek et al. used a factor of 10 mppcf =
100 [micro]g/m\3\ (Document ID 2307, Attachment A, pp. 36-39; 1804, p.
3). OSHA notes that this discrepancy in gravimetric conversion factors
should not affect the detection of an exposure-response relationship,
as all exposures would differ by a constant factor.
    The ACC also pointed out that Attfield and Costello's exposure
estimate for sandblasters was 60 [micro]g/m\3\ prior to 1940, 50
[micro]g/m\3\ from 1940-1950, and 40 [micro]g/m\3\ after 1950,
maintaining these numbers were too low compared to Vacek et al.'s
estimates of 240, 160, and 70 [micro]g/m\3\, respectively (Document ID
2307, Attachment A, p. 39; 1486, p. 313). Attfield and Costello took
these estimates for sand blasters from the Davis et al. (1983, Document
ID 0999) study, discussed in detail below; the estimates were based on
six published industrial hygiene measurement studies.
    Lastly, the ACC posited that Attfield and Costello inappropriately
excluded the highest exposure group, stating:

    Vacek et al. used all their data in evaluating potential E-R
[exposure-response] trends with increasing exposure. Attfield and
Costello did not. Instead, on a post hoc basis, they excluded the
highest exposure category from their analysis when they discovered
that the E-R trend for lung cancer was not significant if that group
was included (even though the trends for non-malignant respiratory
diseases were significant when all the data were used). This is an
example of both data selection bias and confirmation bias (Document
ID 2307, Attachment A, p. 40).

    Based upon these assertions, the ACC concluded, ``In sum, when
judged without a result-oriented confirmation bias, the larger, more
recent, more comprehensive, and more detailed study by Vacek et al.
(2011) must be deemed to supersede Attfield and Costello (2004) as the
basis for evaluating potential silica-related lung cancer risks in the
Vermont granite industry'' (Document ID 2307, Attachment A, p. 41).
    OSHA initially discussed some issues surrounding the Vacek et al.
(2011) study in its Supplemental Literature Review (Document ID 1711,
Attachment 1, pp. 2-5). Specifically, OSHA noted that (1) the
cumulative exposure quintiles used in the Vacek et al. (2011) analysis
were higher than the values used in the Attfield and Costello (2004)
analysis; (2) the regression models used in the Vacek et al. (2011)
study exhibited signs of uncontrolled confounding, as workers in the
second lowest cumulative exposure stratum in the models (except for
silicosis) exhibited a lower risk than those in the lowest stratum,
while all outcomes (except NMRD) in the highest exposure stratum showed
a decline in the odds ratio (a measure of the association between
silica exposure and health outcome) compared to the next lower stratum;
and (3) Vacek et al. (2011) found a statistically significant excess of
lung cancer (SMR = 1.37, with almost 100 excess lung cancer deaths) in
the cohort when compared to U.S. white males (Document ID 1486, p.
315). Regarding the excess lung cancer deaths, although they were
unable to obtain information on smoking for many of the cohort members,
Vacek et al. suggested that the elevated SMR for lung cancer was due,
at least in part, to the differences between the smoking habits of the
cohort and reference populations (Document ID 1486, p. 317). OSHA noted
that although the SMR for other NMRD was elevated, there was no
significant SMR elevation for other smoking-associated diseases,
including cancers of the digestive organs, larynx, and bladder, as well
as bronchitis, emphysema, and asthma (Document ID 1711, Attachment 1,
p. 5). Elevated SMRs for these diseases would be expected if workers in
the study population smoked more than those in the reference
population; in fact, for all heart disease, the mortality in the study
population (SMR = 0.89) was statistically significantly lower than the
reference population (Document ID 1486, p. 315). These data do not
support Vacek et al.'s assertion that smoking was responsible for the
increased lung cancer SMR in the cohort. In addition, Davis et al.
(1983) noted that granite shed workers employed during the 1970's
smoked only slightly more than U.S. white males (Document ID 0999, p.
717). OSHA also pointed out that the SMR may have been understated, as
Vacek et al. did not account for a healthy worker effect (HWE).
    The ACC did not agree with OSHA's review of the Vacek et al. study,
noting that OSHA ``rejects Vacek et al. (2011) on grounds that are
confusing and unfounded'' (Document ID 2307, Attachment A, p. 41). The
ACC argued that the quintiles of cumulative exposure used by Vacek et
al. were not higher than typical values for lung cancer, and that OSHA,
in its Supplemental Literature Review, compared the Vacek et al.
quintiles of cumulative exposure for silicosis with the Attfield and
Costello groups used for both silicosis and lung cancer (Document ID
2307, Attachment A, pp. 41-42). OSHA acknowledges this discrepancy and,
given that Vacek et al.

used quintiles of cumulative exposure that differed for each health
endpoint, agrees that the quintiles for lung cancer used by Vacek et
al. were not appreciably higher than the exposure groups used by
Attfield and Costello, though the Agency recognizes that there may be
alternative explanations for the patterns observed in the Vacek et al.
data. Regarding uncontrolled confounding, the ACC stated that ``The
Vermont granite worker cohort, after all, supposedly is free of
confounding exposures,'' (Document ID 2307, Attachment A, p. 43 (citing
Attfield and Costello, 2004, 0284)). Vacek et al. also pointed out that
although the odds ratios for the second lowest exposure stratums were
lower than those for the lowest categories for each of the diseases,
they were not statistically significantly lower (Document ID 1804, pp.
1-2).
    Although OSHA notes that this latter phenomenon, in which the odds
ratio for the second lowest exposure stratum is lower than that for the
lowest stratum, is commonly observed and often attributable to some
form of selection confounding, the Agency recognizes that there may be
alternative explanations for the patterns observed in the Vacek et al.
data. One such explanation for the decreased odds ratios in the highest
exposure group is potential attenuation resulting from a HWE.
    The HWE, as defined by Stayner et al. (2003), has two components:
(1) A healthy initial hire effect, in which bias is ``introduced by the
initial selection of workers healthy enough to work . . . and the use
of general population rates for the comparison group, which includes
people who are not healthy enough to work,'' and (2) a healthy worker
survivor effect, referring ``to the tendency of workers with ill health
to drop from the workforce and the effect this dropout may have on
exposure-response relationships in which cumulative exposure is the
measure of interest'' (Document ID 1484, p. 318). Thus, the healthy
initial hire effect occurs in the scenario in which the death rate in a
worker group is compared to that in the general population; because the
general population has many people who are sick, the death rate for
workers may be lower, such that a direct comparison of the two death
rates results in a bias. The healthy worker survivor effect occurs in
the scenario in which less healthy workers transfer out of certain jobs
into less labor-intensive jobs due to decreased physical fitness or
illness, or leave the workforce early due to exposure-related illness
prior to the start of follow-up in the study. As a result, the
healthier workers accumulate the highest exposures such that the risk
of disease at higher exposures may appear to be constant or decrease.
    OSHA disagrees with the ACC's statement that ``the possibility of a
potential HWE in this cohort could not have affected the E-R analyses''
in Vacek et al. (2011) (Document ID 2307, Attachment A, p. 46), and
with the similar statement by study authors Pamela Vacek, Ph.D. and
Peter Callas, Ph.D., both of the University of Vermont, who asserted
that the HWE could not have impacted their exposure-response analyses
``because they were not based on an external reference population''
(Document ID 1804, p. 2). This explanation only considers one component
of the HWE, the healthy initial hire effect. An internal control
analysis, such as that performed by Vacek et al., will generally
minimize the healthy initial hire effect but does not address the
healthy worker survivor effect (see Document ID 1484, p. 318 (Stayner
et al. (2003)). Thus, the statement by the ACC that there could be no
HWE in the internal case control analysis of Vacek et al. (2011) is
incorrect, as it considered only the healthy initial hire effect and
not the healthy worker survivor bias.
    In contrast, Attfield and Costello's stated rationale for excluding
the highest exposure group is related to the healthy worker survivor
effect:

    We do know that this group is distinctive in entering the cohort
with substantial exposures--83% had worked for 20 years or more in
the high dust levels prevalent prior to controls. They were,
therefore, a highly selected healthy worker group. A further reason
may be that in the days when tuberculosis and silicosis were the
main health concerns in these workers, lung cancer may have been
obscured in this group as a cause of death in some cases'' (Document
ID 0284, p. 136).

    Support for Attfield and Costello's reasoning is provided by a
study by Applebaum et al. (2007), which re-analyzed the data from the
Attfield and Costello (2004) paper and concluded that there was a
healthy worker survivor effect present (study cited by Vacek et al.,
2009, Document ID 2307, Attachment 6, p. 3). Applebaum et al. (2007)
split the cohort of Vermont granite workers into two groups: (1) Those
that began working before the start of the study follow-up, i.e.,
prevalent hires; and (2) those that began working after the start of
the study follow-up, i.e., incident hires. The rationale for splitting
the cohort into these two groups was to examine if a healthy worker
survivor effect was more likely in the prevalent hire group, as this
group would be affected by workers that were more susceptible to health
effects and left the industry workforce prior to the start of the study
follow-up (Applebaum et al., 2007, pp. 681-682). Using spline models to
examine exposure-response relationships without forcing a particular
form (e.g., linear, linear-quadratic) on the observed data, the authors
found that the inclusion of prevalent hires in the analysis weakened
the association between cumulative silica exposure and lung cancer
because of bias from the healthy worker survivor effect. The bias can
be reduced by including only incident hires, or keeping the date of
hire close to the start of follow-up (Applebaum et al., 2007, pp. 685-
686). An alternative explanation for this trend offered by Applebaum et
al. may be that, assuming that there was more measurement error in the
older data, the prevalent hires had more exposure misclassification
(2007, p. 686); in such a case, however, the inclusion of prevalent
hires would still bias the results towards the null. Given the findings
of the Applebaum et al. (2007) study, OSHA believes that Attfield and
Costello (2004) had good reasons for removing the highest exposure
group, which was composed mostly of prevalent workers (83 percent of
workers in the highest exposure group had worked at least 20 years
prior to the start of the follow-up period) (Document ID 0284, p. 136).
    Vacek et al. (2011), on the other hand, excluded 609 workers in the
design of their study cohort due to insufficient information. However,
the majority of the workers excluded from the cohort were incident
hires who began work after 1950 (Document ID 2307, Attachment 6, p. 12;
1486, p. 314). The final Vacek et al. (2011) cohort included 2,851
prevalent hires (began employment before 1950) compared to 4,201
incident hires (began employment in or after 1950) (Document ID 2307,
Attachment 6, p. 12; 1486, p. 314). By composing about 40 percent of
their cohort with prevalent hires and excluding many incident hires,
Vacek et al. (2011) may have introduced additional healthy worker
survivor effect bias into their study. Interestingly, Vacek et al.
described the Applebaum et al. (2007) results in their 2009 report,
stating, ``They [Applebaum et al.] found that decreasing the relative
proportion of prevalent to incident hires [in the data used by Attfield
and Costello] resulted in a stronger association between cumulative
silica exposure and lung cancer mortality'' (Document ID

2307, Attachment 6, p. 3). Despite their acknowledgement of the
Applebaum et al. (2007) findings, Vacek et al. (2011) did not conduct
any analysis of only the incident hires, or use statistical methods to
better determine the presence and effect of a healthy worker survivor
effect in their study.
    The ACC also commented on Vacek et al.'s suggestion that the
elevated SMR observed for lung cancer in the cohort (when compared to a
reference population of U.S. white males) was due to differences in the
smoking habits of the cohort and reference population, which OSHA
criticized in its Supplemental Literature Review (Document ID 1486, p.
317; 1711, Attachment 1, p. 5). The ACC stated, ``OSHA suggests that
the lack of complete smoking data for the cohort is a problem and
contends that smoking could not explain the elevated SMR for lung
cancer. This criticism, as Dr. Vacek explains, is overstated, and, in
any event, does not detract from the study's findings regarding the
absence of an association between silica exposure and lung cancer''
(Document ID 2307, Attachment A, pp. 46-47; 1804, p. 2).
    Vacek et al. (2011) estimated the relative smoking prevalence in
the cohort to be 1.35 times that in the reference population; using
this estimated relative smoking prevalence, the authors estimated that
``the expected number of lung cancer deaths in the cohort after
adjusting the reference rates for smoking would be 353, yielding a
[non-significant] SMR of 1.02'' (Document ID 1486, p. 317). OSHA notes
that this method used by Vacek et al. to adjust the SMR for smoking
neglects the healthy worker survivor effect (i.e., smokers may leave
the workforce sooner than nonsmokers because smoking is a risk factor
for poor health). Absent control for the healthy worker survivor
effect, smoking would (and perhaps did) become a negative confounder
because long duration--high cumulative exposure--workers would tend
toward lower smoking attributes. The method used by Vacek et al. is
also inconsistent with the frequently cited Axelson (1978) method,
which is used to adjust the SMR when the exposed population has a
higher percentage of smokers than the reference population (Checkoway
et al. 1997, Document ID 0326; Chan et al. 2000, 0983). As a result,
Vacek et al. (2011) likely overestimated the confounding effect of
smoking in this cohort.
    In addition, as previously noted by OSHA, the SMRs for cancers
largely attributable to smoking, such as those of the buccal cavity and
pharynx (SMR = 1.01), larynx (SMR = 0.99), and esophagus (SMR = 1.15)
were not significant in the Vacek et al. study (Document ID 1486, p.
315; 2307, Attachment 6, p. 14). The SMR of 0.94 for bronchitis,
emphysema, and asthma also was not significant. If smoking were truly
responsible for the highly statistically significant SMR (1.37)
observed for lung cancer, the SMRs for these other diseases should be
significant as well. OSHA likewise notes that other studies have found
that smoking does not have a substantial impact on the association
between crystalline silica exposure and lung cancer mortality (e.g.,
Checkoway et al., 1997, Document ID 0326; Steenland et al., 2001a,
0452, p. 781) and that crystalline silica is a risk factor for lung
cancer independent of smoking (Kachuri et al., 2014, Document ID 3907,
p. 138; Preller et al., 2010, 4055, p. 657).
    OSHA is also concerned about some features of the study design and
exposure assessment in Vacek et al. (2011). Regarding the study design,
in their nested case-control analyses, Vacek et al. sorted cases into
risk sets based on year of birth and year of death, and then matched
three controls to each risk set; from the data presented in Table 5 of
the study, the actual number of controls per lung cancer case can be
calculated as 2.64 (Document ID 1486, p. 316). Vacek et al.'s decision
to use such a small number of controls per case was unnecessarily
restrictive, as there were additional cohort members who could have
been used as controls for the lung cancer deaths. Typically, if the
relevant information is available, four or more (or all eligible)
controls are used per case to increase study power to detect an
association. OSHA notes that Steenland et al. (2001a), in their nested
case-control pooled analysis, used 100 controls per case (Document ID
0452, p. 777).
    In addition, Vacek et al. stated that for the categorical analysis,
cut points on cumulative exposure were based on quintiles of the
combined distribution for cases and controls (Document ID 1486, p.
314). Therefore, there should be an approximately equal total number of
subjects (cases plus controls) in each group (or quintile). OSHA's
examination of Table 5 in the Vacek et al. (2011) study shows that
there is an approximately equal distribution of subjects for all
endpoints except lung cancer; for example, the silicosis groups each
had 43-44 subjects, the NMRD groups each had 125-130 subjects, the
kidney cancer groups each had 22-23 subjects, and the kidney disease
groups each had 25 subjects. However, the lung cancer groups, ranging
from the lowest to the highest exposure, had 325, 232, 297, 241, and
202 subjects (Document ID 1486, p. 316). OSHA could find no explanation
for this discrepancy in the text of the Vacek et al. (2011) study, and
questions how the lung cancer groups were composed.
    With respect to the different job exposure matrices, OSHA has
reason to believe that the exposure data reported in the Attfield and
Costello study are more accurate than the data Vacek et al. used. OSHA
is particularly concerned that Vacek et al.'s pre-1940 exposure
estimate of 150 [micro]g/m\3\ for one job (channel bar operator) was
much lower than Attfield and Costello's estimate, from the Davis et al.
(1983) matrix, of 1070 [micro]g/m\3\ (Document ID 1486, p. 313; 0284,
p. 131). As NIOSH observed in its post-hearing comments, changing the
exposure estimate for channel bar operators could have ``major
consequences'' on the exposure-response analysis, as the job occurred
frequently (Document ID 4233, p. 22). NIOSH then pointed out that the
Attfield and Costello (2004) exposure estimate for channel bar
operators was based on multiple exposure measurements conducted by
Davis et al. (1983), whereas Vacek et al. based their exposure estimate
``on only three dust measurements'' in which ``only wet drilling was
used. Thus, their study used not only very limited sampling data but
also values that were biased towards low levels, since the samples were
taken when water was being used to control dust,'' a practice that was
not typically used for this occupation at the time (Document ID 4233,
p. 22). In fact, photographs from Hosey et al. (1957) showed channel
bar drilling in 1936 and 1937 with and without dust control; the
caption for the photo without dust control states that the ``operator
in background is barely visible through dust cloud'' (Document ID 4233,
p. 24, citing 3998, Attachment 14b). As NIOSH explained,

    If there is a true [linear] relationship between exposure to
silica dust and lung cancer mortality, classifying highly exposed
workers incorrectly as low-exposed shifts the elevated risks to the
low exposure range. The impact is to spuriously elevate risks at low
exposures and lower them at high exposures, resulting in the
exposure-response trend being flattened or even obscured.
Ultimately, the true relationship may not be evident, or if it is,
may be attenuated (Document ID 4233, p. 22, n. 1).

    Vacek et al. reported in their study that they conducted a
sensitivity analysis that did not change the exposure-response
relationship between silica exposure and lung cancer risk,

even when Attfield and Costello's pre-1940 exposure estimates were used
for channel bar operators (Document ID 2340, pp. 317-318; 2307,
Attachment 6, p. 31). Part of the problem may be the way that channel
bar operators were defined by Vacek et al. As noted by NIOSH, ``Leyner
driller and channel bar operator or driller are synonyms'' (Document ID
4233, p. 22, n. 3). Attfield and Costello defined channel bar operators
in that way, with a pre-1940 exposure estimate of 1070 [micro]g/m\3\
(Document ID 0284, p. 131). Vacek et al., on the contrary, assigned
channel bar operators to a category called ``channel bar (wet)'' and
assigned a pre-1940 exposure estimate of 150 [micro]g/m\3\ (Document ID
2307, Attachment 6, Appendix B, pp. 7, 15). They included Leyner
drillers under a general category called ``driller'' with a pre-1940
exposure estimate of 1070 [micro]g/m\3\ (Document ID 2307, Attachment
6, Appendix B, pp. 7, 15). Included in the Vacek et al. (2009) category
of ``drillers'' were plug drillers (Document ID 2307, Attachment 6,
Appendix B, p. 15); OSHA notes that Attfield and Costello used a lower
pre-1940 exposure estimate of 650 [micro]g/m\3\ for plug drillers, as
defined by Davis et al. (1983). OSHA believes that Vacek et al.
underestimated the exposures of some channel bar operators, and
overestimated the exposures of plug drillers, which may have
contributed to the lack of association, and that the categorization
used by Attfield and Costello, with the synonymous channel bar
operators and Leyner drillers in one category, and plug drillers in a
separate category, was more appropriate. Thus, even in Vacek et al's
sensitivity analysis, in which they used Attfield and Costello's
exposure estimate of 1070 [micro]g/m\3\ for channel bar operators and
drillers, the plug drillers would still have had a higher exposure
estimate (1070 [micro]g/m\3\ versus Attfield and Costello's 650
[micro]g/m\3\), making the analysis different from that of Attfield and
Costello.
    For the reasons discussed herein, OSHA has decided not to reject
the Attfield and Costello (2004) study in favor of the Vacek et al.
(2011) study as a basis for risk assessment. OSHA maintains that it has
performed an objective analysis of the Attfield and Costello (2004) and
Vacek et al. (2011) studies. OSHA agrees with some of the ACC's
criticisms regarding the Agency's initial evaluation of the exposure
groupings and confounding in the Vacek et al. (2011) study. OSHA is
concerned, however, as discussed above, about several aspects of Vacek
et al. (2011), including a potential bias from the healthy worker
survivor effect, which was shown to exist in this cohort (see Applebaum
et al., 2007, cited in Document ID 2307, Attachment 6, p. 3), as well
as about job categorization that may have resulted in exposure
misclassification for certain job categories (e.g., the synonymous
channel bar operators and Leyner drillers). Despite its concerns with
the Vacek et al. study, OSHA acknowledges that comprehensive studies,
such as Attfield and Costello (2004) and Vacek et al. (2011), in the
Vermont granite industry have shown conflicting results with respect to
lung cancer mortality (Document ID 0284; 1486). As discussed earlier,
conflicting results are often observed in epidemiological studies due
to differences in study designs, analytical methods, exposure
assessments, populations, and other factors. In addition, the exposure-
response relationship between silica and lung cancer may be easily
obscured by bias, as crystalline silica is a comparably weaker
carcinogen (i.e., the increase in risk per unit exposure is smaller)
than other well-studied, more potent carcinogens such as hexavalent
chromium (Steenland et al., 2001, Document ID 0452, p. 781). Although
OSHA believes that the Attfield and Costello (2004) study is the most
appropriate Vermont granite study to use in its QRA, the Agency notes
that, even in the absence of the Attfield and Costello (2004) study,
the risk estimates for lung cancer mortality based on other studies
still provide substantial evidence that respirable crystalline silica
poses a significant risk of serious health conditions to exposed
workers.
4. Comments on Specific Studies Relied Upon by OSHA in Its QRA
a. Attfield and Costello (2004)
    As stated above, OSHA disagrees with the ACC's contention that
Vacek et al. provides a more reliable scientific basis for estimating
risk than Attfield and Costello. While it is true that the final risk
estimate (54 deaths per 1,000 workers) derived from the Attfield and
Costello study for an exposure level of 100 [micro]g/m\3\ is the
highest when compared to the other studies, it is not true that the
final risk estimate (22 deaths per 1,000 workers) derived from the
Attfield and Costello study is the highest for the final rule's PEL of
50 [micro]g/m\3\. In fact, it is within the range of risk estimates
derived from the ToxaChemica (2004) pooled analysis of 16 to 23 deaths
per 1,000 workers at the final PEL. Thus OSHA has decided to retain its
reliance on the Attfield and Costello (2004) study and, again, notes
that, even without the Attfield and Costello (2004) study, all of the
other studies in the Final QRA demonstrate a clearly significant risk
of lung cancer mortality (11 to 54 deaths per 1,000 workers) at an
exposure level of 100 [micro]g/m\3\, with a reduced, albeit still
significant, risk (5 to 23 deaths per 1,000 workers) at an exposure
level of 50 [micro]g/m\3\ (see Table VI-1 in Section VI, Final
Quantitative Risk Assessment and Significance of Risk). Excluding
Attfield and Costello (2004), in other words, would not change OSHA's
final conclusion regarding the risk of death from lung cancer.
b. Miller and MacCalman (2009)
    According to the ACC, OSHA's risk estimates based on the Miller and
MacCalman (2009, Document ID 1306) study are ``more credible than the
others--because [the study] involved a very large cohort and was of
higher quality in terms of design, conduct, and detail of exposure
measurements,'' and also adjusted for smoking histories (Document ID
2307, Attachment A, p. 73). Although the risk estimates generated from
the Miller and MacCalman data were the lowest of the lung cancer
mortality estimates, the ACC next asserted that they were biased
upwards for several reasons. First, the ACC stated that exposure
information was lacking for cohort members after the mines closed in
the mid-1980's, and quoted OSHA as stating, ``Not accounting for this
exposure, if there were any, would bias the risk estimates upwards''
(Document ID 2307, Attachment A, p. 74 (quoting 1711, p. 289)). OSHA,
however, does not believe there to have been additional substantial
quartz exposures. As the study authors wrote, ``Because of the steep
decline of the British coal industry, the opportunities for further
extensive coal mine exposure were vanishingly small'' (Document ID
1306, p. 11). Thus OSHA believes it to be unlikely that the risk
estimates are biased upwards to any meaningful degree based on lack of
exposure information at the end of the study period.
    The ACC also stated that the unrestricted smoking of cohort members
after the closure of the mines would have resulted in risk estimates
that were biased upwards (Document ID 2307, Attachment A, p. 74). OSHA
has no reason to believe, nor did the ACC submit any evidence in
support of its contention, that unrestricted smoking occurred, however,
and notes that the authors stated that the period after the mines
closed was one of ``greater anti-

smoking health promotion campaigns'' (Document ID 1306, p. 11).
    Finally, the ACC noted that Miller and MacCalman did not adjust
significance levels for the multiple comparisons bias with respect to
lag selection that Dr. Cox alleged affected their study (Document ID
2307, Attachment A, p. 74). Dr. Cox claimed that trying multiple
comparisons of alternative approaches, such as different lag periods,
and then selecting a final choice based on the results of these
multiple comparisons, leads to a multiple comparisons bias that could
result in false-positive associations (Document ID 2307, Attachment 4,
p. 28; see Section V.J, Comments and Responses Concerning Biases in Key
Studies). He argued that the authors should have reduced the
significance level (typically p = 0.05) at which a result is considered
to be significant. ``Lag'' refers to the exclusion of the more recent
years of exposure (e.g., 10-year lag, 15-year lag) to account for the
fact that diseases like cancer often have a long latency period (i.e.,
that the cancer may not be detected until years after the initiating
exposure, and exposures experienced shortly before detection probably
did not contribute to the development of disease). ``Lag selection,''
therefore, refers to the choice of an appropriate lag period. As
addressed later in the Section V.J, Comments and Responses Concerning
Biases in Key Studies, OSHA does not necessarily believe such an
adjustment of significance levels to be appropriate, based upon the
testimony of Mr. Park of NIOSH, nor is it typically performed in the
occupational epidemiology literature (Document ID 3579, Tr. 151-152).
Similarly, the ACC stated that the confidence intervals are overly
narrow because they ignore model uncertainty, and that multiple
imputation of uncertain exposure values should have been performed
(Document ID 2307, Attachment A, p. 75). OSHA rejects this assertion on
the grounds that the authors used detailed exposure estimates that the
ACC recognized raised the credibility of the study; the ACC wrote,
regarding the study, ``it involved a very large cohort and was of
higher quality in terms of design, conduct, and detail of exposure
measurements'' (Document ID 2307, Attachment A, p. 73). Lastly, the ACC
argued that an exposure threshold should have been examined (Document
ID 2307, Attachment A, p. 75). OSHA discusses at length this issue of
thresholds, and the difficulty in ruling them in or out at low
exposures, in Section V.I, Comments and Responses Concerning Thresholds
for Silica-Related Diseases.
    In summary, OSHA notes that the ACC has not provided any non-
speculative evidence to support its claims that the risk estimates
derived from the Miller and MacCalman (2009) study are biased upwards.
As stated in the Review of Health Effects Literature and Preliminary
QRA, and acknowledged by the ACC (Document ID 2307, p. 73), OSHA
believes these risk estimates to be very credible, as the study was
based on well-defined union membership rolls with good reporting, had
over 17,000 participants with nearly 30 years of follow-up, and had
detailed exposure measurements of both dust and quartz, as well as
smoking histories (Document ID 1711, pp. 288-289).
c. Steenland (2001a) and ToxaChemica (2004)
    OSHA also received several comments on the ToxaChemica (2004,
Document ID 0469) analysis, which was based on the Steenland et al.
(2001a, Document ID 0452) pooled analysis. First, the ACC claimed that
there is significant heterogeneity in the exposure-response
coefficients, derived from the individual studies. Because the risk
estimates based on these coefficients differ by almost two orders of
magnitude, the ACC suggested that these models are misspecified for the
data (Document ID 2307, Attachment A, pp. 75-76). Essentially, the ACC
claimed that the exposure-response coefficients differ too much among
the individual studies, and asserted that it is therefore inappropriate
to use the pooled models. Dr. Cox wrote: ``Steenland et al. did not
address the heterogeneity, but artificially suppressed it by
unjustifiably applying a log transformation. This is not a valid