OSHA comments from the January 19, 1989 Final Rule on Air Contaminants Project extracted from 54FR2332 et. seq. This rule was remanded by the U.S. Circuit Court of Appeals and the limits are not currently in force.
CAS: 14808-60-7; Chemical Formula: None
The former OSHA limit for silica-containing dusts is a respirable dust limit expressed as the following formula:
(10 mg/m3)/(% respirable quartz + 2).
At one time, the ACGIH also expressed its silica limit in terms of this formula. However, the current ACGIH TLV is 0.1 mg/m3, measured as respirable quartz dust. OSHA proposed, and the final rule establishes, a permissible exposure limit of 0.1 mg/m3 TWA, as respirable quartz. Quartz is a colorless, odorless, noncombustible solid.
The ACGIH does not see this change in the value of its limit for occupational exposure to silica as significant; instead, the ACGIH made this change to conform its limit for this dust to its TLVs for other dusts. If the former OSHA formula is used to calculate a limit for a dust containing 100 percent quartz, the limit would be 0.098 mg/m3, a value that is not appreciably different from the ACGIH's revised limit of 0.1 mg/m3 for respirable quartz dust. For quartz dusts containing less than 100 percent free silica, the former OSHA formula would yield a limit of, for example, 0.83 mg/m3 for respirable dust containing 10 percent quartz. This result is somewhat more stringent than the ACGIH's TLV of 0.1 mg/m3. For cristobalite and tridymite, the former OSHA formula and the ACGIH limits yield approximately the same results: both are approximately one-half the limit established by these two entities for quartz dust (see the discussions below).
Occupational exposure to free silica has been known for many years to produce silicosis, a chronic, disabling lung disease characterized by the formation of silica-containing nodules of scar tissue in the lungs. Simple silicosis, in which the nodules are less than 1 cm in diameter (as measured on chest X-ray films) is generally asymptomatic but can be slowly progressive, even in the absence of continued exposure. Complicated silicosis (i.e., with nodules greater than 1 cm in diameter) is more often associated with disability and can also progress in the absence of continuing exposure.
The health basis underlying the ACGIH's limit for crystalline silica is the work of Russell et al. (1929/Ex. 1-156), which suggested that a limit of 10 mppcf would protect workers from the effects of exposure to granite dust; a study by Ayer (1969/Ex. 1-129) demonstrated that 10 mppcf of granite dust is approximately equal to 0.1 mg/m3 of respirable quartz dust (ACGIH 1986/Ex. 1-3).
NIOSH has recommended an exposure limit of 0.05 mg/m3 as respirable free silica for all crystalline forms of silica. As applied to cristobalite and tridymite, the NIOSH REL is 0.05 mg/m3, the same as the ACGIH TLV, but NIOSH's 0.05 mg/m3 REL for quartz dust is one-half the value of the ACGIH TLV for quartz dust. To support its more stringent REL for quartz dust, NIOSH cites the work of Hosey, Ashe, and Trasko (1957, as cited in ACGIH 1986/Ex. 1-3, p. 524), which reported that no new cases of silicosis occurred in workers in Vermont granite sheds who were generally exposed to 0.05 mg/m3 or less of granite dust. The recommendation was also partly based on studies by Theriault, Burgess, DiBerardinis et al. (1974/Ex. 1-94a); Theriault, Peters, and Fine (1974/Ex. 1-110); and Theriault, Peters, and Johnson (1974/Ex. 1-94b), which found that annual declines in pulmonary function and abnormal chest X-rays occurred among 192 granite shed workers exposed to an average quartz concentration of 0.05 mg/m3. NIOSH noted that the exposure estimates reported in the Theriault et al. (1974/Exs. 1-94a, 1-94b, and 1-110) studies failed to account for the higher exposures that probably occurred in the years before exposure sampling was initiated and, therefore, that the Theriault et al. (1974) exposure data may have understated average exposures to quartz. Thus, NIOSH believes that the exposures responsible for the declines in pulmonary function were actually above 0.05 mg/m3. The ACGIH (1986/Ex. 1-3) found NIOSH's reasoning unpersuasive, citing a report by Graham, O'Grady, and Dubuc (1981/Ex. 1-172), who measured the pulmonary function of the same group of workers studied by Theriault et al. (1974/Exs. 1-94a, 1-94b, and 1-110), and found, in contrast to Theriault, that these workers experienced "an overall increase in FVC and FEV" (ACGIH 1986/Ex. 1-3).
Although OSHA did not propose a significant change in the exposure limit, there were several comments that focused on two issues: (1) the adequacy of the proposed 0.1 mg/m3 respirable quartz limit in reducing the risk of silicosis; and (2) recent evidence describing the potential carcinogenicity of silica dust.
With regard to the first issue, Dr. Philip Landrigan of the Mount Sinai School of Medicine, representing the American Public Health Association, testified as follows at the informal hearing:
- Numerous epidemiologic studies have been undertaken in this century,
which have established a dose-response relationship between occupational
exposure to silica dust and the development of silicosis. These studies
have shown clearly that there is a positive dose-response relationship
between chronic silica exposure and the development of silicosis.
The most recent of these reviews which have examined that relationship is
presented in the 1986 NIOSH text on occupational respiratory diseases, a
most authoritative book in the field, widely read by medical scientists
in this country and abroad. The data which was summarized in that
chapter indicate quite clearly that the dose-response relationship
between silica exposure and silicosis is present in people with lifetime
exposure to silica below the current...standard of 100 micrograms per
cubic meter. Indeed, the data suggests that the dose-response
relationship extends downward even to levels of exposure below the
current NIOSH recommended standard of 50 micrograms per cubic meter.
And against the authoritative NIOSH review...OSHA has cited one short
three-page article...[Graham et al. 1981/Ex. 1-172] to indicate that the
dose-response relationship between silica and silicosis does not extend
downward to below 100 micrograms per cubic meter (Tr. pp. 3-277 to
Several commenters (Exs. 3-678, 3-733, 130, 138, 139, 147, 161, and 126) disagreed with Dr. Landrigan's assessment. For example, Frederick A. Renninger of the National Stone Association (Ex. 139) cited Dr. John Peters, the author of the chapter in the NIOSH reference referred to by Dr. Landrigan. In his chapter, Dr. Peters concluded as follows:
- All of the studies described in this section provide evidence for
adverse pulmonary effects at levels of exposure above 10 mppcf or 0.1
mg/m3. Some showed that foundry workers exposed to the equivalent of
0.05 mg/m3 of quartz developed silicosis while those with less
exposure did not....All the Vermont findings were seen with an average
exposure of around 0.05 mg/m3 of quartz. It is possible, however,
that since this was the average exposure, individuals whose exposure
exceeded this level accounted for the noted effects. (The "no effect"
level was probably below 0.05 mg/m3, but the available data did not
allow accurate determinations.) (Peters, J.M., "Silicosis." In:
Occupational Respiratory Diseases, p. 229, J.S. Merchant, ed. DHHS
(NIOSH) Pub. No. 86-102, NIOSH 1986b).
Mr. Renninger also points to the difficulty in equating impinger sampling results, which were used in the Vermont granite shed studies, to gravimetric (mg/m3) measures of respirable dust. He cited Dr. Peters as reporting that "gravimetric and impinger sampling are known to be poorly correlated" (Ex. 139, p. 5). Mr. Renninger also pointed out that the conversion between mppcf and mg/m3 measurements for silica will vary with the industry, thus adding another level of uncertainty in interpreting the health data.
OSHA's decision to propose a 0.1 mg/m3 PEL for respirable silica dust, rather than the NIOSH REL of 0.05 mg/m3, was partly based on the report by Dr. William Graham et al. (Graham, O'Grady, and Dubuc 1981/Ex. 1-172) discussed above. In a posthearing submission, Dr. Graham discussed the findings of Theriault and co-workers (1974/Exs. 1-94a, 1-94b, and 1-110), which heavily influenced the decision by NIOSH to issue a REL of 0.05 mg/m3 (Ex. 147). Dr. Graham discussed three limitations of the Theriault et al. (1974) studies. First, the X-ray films were interpreted by a single reader who was neither certified nor a chest physician; Dr. Peters points out that it is generally accepted that X-ray films must be read by three experienced readers. Second, there was no attempt to study workers hired after 1938 and exposed to low dust levels separately from workers exposed to higher dust levels prior to 1938. Third, there was a group of workers who were judged to have abnormal X-ray findings despite a reported lack of exposure to dust, which raises the question about the accuracy of interpretations.
Dr. Graham also interpreted his own findings of granite shed workers as showing that the loss in pulmonary function predicted to occur among these workers by Theriault et al. (1974/Exs. 1-94a, 1-94b, and 1-110) had, in fact, not occurred. One explanation offered by Dr. Graham is the possibility that technical difficulties arose during the Theriault et al. (1974) studies in the administration of spirometric tests, and may have resulted in spuriously low values for pulmonary function. Dr. Graham discussed a continuation of his own work in which he has found neither pulmonary function losses nor high prevalences of abnormal chest X-rays among granite shed workers who were employed after 1938-1940, when lower dust levels prevailed (Ex. 147, pp. 8-9). However, the analysis of quartz content in the dust samples collected has not yet been completed (Ex. 147, p. 8).
In addition to the evidence on the dose-response relationship for silicosis, rulemaking participants discussed at length recent data suggesting that silica may be carcinogenic (Exs. 147, 161, 194, 138, 3-1159, 3-1060, and 139; Tr. p. 3-94, Tr. p. 7-80, Tr. p. 11-104). NIOSH (Ex. 8-47, Table N6B) believes that the data on silica are such that the Agency should consider a separate 6(b) rulemaking for this substance. Dr. Frank Mirer, Director of the Health and Safety Department of the United Auto Workers, summarized the evidence on silica's potential carcinogenicity at the hearing:
- The most prominent study [on the health effects of silica exposure
is] by Holland and coworkers...[it] provided really clear evidence that
silica was carcinogenic in rats by inhalation. Non-malignant pulmonary
effects were also observed. There is a considerable line of other work
in rats and hamsters, in the development of both lung tumors and
lymphatic tumors from exposure to silica.
carcinogenic and that it is hazardous at levels below the proposed PEL.
The IARC monograph reviewed the data available in 1986 and described a
considerable body of evidence. Despite the methodological limitations
pointed out by IARC, the sheer number and consistency of the findings is
most persuasive (Tr. pp. 7-80 to 7-81).
Studies [exist] of workers in a variety of industries where high exposure of silica-containing dusts have revealed high lung cancer risks. These results include ten positive studies among mine workers, four in ceramics and glass industries, [and] four in the foundry industry. We also bring to your attention at least four additional studies published since the IARC criteria document was completed. These, in particular, we think create an iron-clad case for the problems presented by this material (Tr. pp. 7-80 to 7-81).
In a posthearing submission by the Refractories Institute, Dr. John Craighead of the University of Vermont reviewed the human and animal data and concluded as follows:
- I find the experimental evidence in animals, suggesting a possible
role of silica in the pathogenesis of bronchogenic carcinomas, to be
faulty and incomplete. I also conclude that the epidemiological studies
in humans provide inadequate evidence to conclude that man is at
increased risk of developing carcinoma of the lung as a result of silica
dust exposure. My comments in no way exclude from consideration silica
as a cause of bronchogenic carcinoma, but only point out the
inadequacies of the scientific information and emphasize the need for
additional, carefully designed systematic studies (Ex. 161A, p. 5).
In similar attachments to the Refractories Institute's submission, Dr. Marvin Kushner, Professor of Pathology at the State University of New York at Stony Brook, pointed to the lack of similarity between the pulmonary lesions found in exposed rats and silicosis lesions in humans; he suggested that the carcinomas seen in rats may be due to a "non-specific" effect that is not a direct result of silica inducing malignant transformation (Ex. 161C). Dr. Carl Shy, Professor of Epidemiology at the University of North Carolina, reviewed the epidemiological evidence and concluded that "the role of occupational silica exposure in causing lung cancer remains undetermined" (Ex. 161D, p. 8).
OSHA believes that the issues raised above deserve a careful and thorough scientific evaluation of the literature. The evidence that silica may present a carcinogenic hazard has been developing over the past few years and is continuing to receive considerable attention by investigators. OSHA will continue to monitor with great interest emerging developments in this area. At this time, however, OSHA believes that the record evidence leaves many questions unanswered regarding the need to reduce the PEL for silica. Therefore, in the final rule, OSHA is establishing an 8-hour TWA PEL of 0.1 mg/m3 for quartz, measured as the respirable silica fraction. This limit represents no substantial change from OSHA's former formula limit, but will simplify sampling procedures, as indicated in the NPRM.
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