Document wDezrK5qbyBkLv0zxaYgO1b63

22626 Federal Register / Vol. 51, No. 119 / Friday, June 20, 1986 / Rules and Regulations criterion. Citing a study by Samet et at., cohort, the prevalence of crepitations, can exceed parenchymal abnormalities which used a relatively large cohort, possible asbestosis, certified asbestosis, in prevalence ai long times from onset of Kilburn argued that smoking neither and small radiological opacities was exposure" (Ex. 172-B. p. 29). Similar produced the x-ray appearance of higher among heavy and ex-smokers results were obtained after pulmonary fibrosis nor contributed to compared with light smokers (1-4 standardizing for age and smoking fibrosis resulting from asbestos cigarettes per day) ar.d nonsmokers. For history. exposure. Pearle (Ex. 84-079) studied 141 shipyard workers who were referred for medical exams because of suspected asbestos-related lung disease. The shortest duration of exposure in this group was 7 years. Chest x-rays were taken on all subjects and pulmonary function data were collected, including FVC, FEVi, and diffusion capacity. Xrays were examined for pleural thickening and interstitial abnormalities consistent with asbestosis. Smoking groups were defined in terms of nonsmokers, light smokers, moderate smokers, and heavy smokers. Three asbestos exposure groups were also defined as being mild, moderate, or heavy, based on the duration of exposure (0-14 years, 15-19 years, and 30+ years, respectively). Three percent of the nonsmokers had interstitial disease, all of whom were concentrated in a heavy exposure group. By contrast, 8-12 percent of the smokers had significant interstitial disease, with the highest prevalence in the mild and moderate asbestos exposure groups. These differences between nonsmokers and smokers, however, were not statistically significant. The prevalence of pleural disease in heavy smokers was example. 15 percent of heavy smokers had certified asbestosis versus none in the nonsmoking and light smoking groups. By contrast, there were no apparent differences in the prevalence of asbestosis or other conditions among the five smoking groups from the earlier cohort, which incurred a higher mean cumulative exposure, was older, and had a longer period of followup than the more recent cohort. This study suggests that, although there may be differences in the prevalence of asbestosis among smokers and nonsmokers who have been exposed recently to asbestos, the prevalence of asbestosis among smokers and nonsmokers tends to be more similar as the latency period increases or at higher levels of exposure to asbestos. One additional study received since the November proposal is pertinent to this issue. Nicholson and his colleagues obtained chest x-rays and administered pulmonary function tests to 918 brake line repair and maintenance workers and approximately 205 nonexposed blue collar workers (Ex. 172-B). Chest x-ray abnormalities were defined to include parenchymal changes of 1/0 or greater, pleura! thickening, pleural plaques, and pleural calcification. Predicted values The pulmonary function lest data, when standardized for smoking, indicated virtually identical results for the unexposed controls, the brake repair workers, and individuals exposed or possibly exposed to asbestos (Ex. 172B). The investigators note that these findings are not surprising because "forced vital capacity is usually a less sensitive determination of asbestosrelated changes than the presence of xray abnormalities and forced expiratory volume in 1 second relates to exposures other than asbestos" (Ex. 172-B. p. 46). Although this study (Ex. 172-B) provides evidence that asbestos causes chest xray abnormalities over and above those that may be caused by smoking, the data were not sufficient to show that asbestos-exposed workers who smoke suffered more lung impairment than either asbestos-exposed nonsmokers or non-exposed smokers (Ex. 172-B). In summary, OSHA finds that there is limited though conflicting evidence that asbestos workers who smoke have a higher risk of dying from asbestosis. as . well as a higher prevalence of crepitations, lung function decrements, and small radiological opacities than their nonsmoking co-workers. 25 percent, compared with 9 percent in for spirometry were based on the F. Relationship of Fiber Size and Type nonsmokers. This difference was revised analysis by Miller et al. (1980) of of Risks from Asbestos-Related Disease statistically significant. The prevalence of pleural disease among the light and moderate smoking groups was similar to the 1971 data of Morris, Kuski and (ohnson (Ex. 172-B). The percentage of workers with any 1. Evidence for a Differential Risk by Fiber Type that in heavy smokers. The largest evidence of chest x-ray abnormality In the November proposal (48 FR difference in the prevalence of pleural among those with garage employment 51110), OSHA reviewed numerous disease between heavy smokers and was 24.2 percent compared with 18.8 epidemiological studies concerning the nonsmokers is. found in the group with percent among workers with ho stated toxicity and carcinogenicity of different mild asbestos exposure. These aJbest03 exposure or garage asbestos fiber types. OSHA concluded prevalence measures were not adjusted employment (Ex. 172-B). This overall that all fiber types, alone or in for age, however, and it cannot be difference between the two groups is combination, have been observed in concluded definitively that the accounted for by differences in the studies to Induce lung cancer, statistically significant difference in prevalence of parenchymal mesothelioma, and asbestosis in prevalence between heavy smokers and abnormalities (19.0 percent vs. 15.3 exposed workers, with the exception of nonsmokers is attributable to smoking percent) rather than pleural anthophyllite. which has been observed history alone. abnormalities (8.4 percent vs. 8.9 to induce lung cancer and asbestosis, Berry et al. (Ex. 84-020) studied 379 percent). However, significant but not mesothelioma (OSHA/NIOSH, men employed in an asbestos textile differences existed in the percentages of Ex. 84-200; for amosite: Seidman et al., . mill. Two cohorts were defined; those pleural abnormalities among those Exs. 84-87, 261-A; Anderson et al,, Ex. first employed before 1951 and those employed in work having direct 84-17; and Murphy et al., Ex. 84-311; for employed on or after 1951. The mean asbestos exposure (22-2 percent) or . chrysolite: McDonald et al., Ex. 84-65: cumulative exposure for the earlier shipyard employment (25.2 percent) and McDonald and Fry, Ex. 84-64; Liddell et cohort was approximately twice.that of those employed only in garage work (8.4 al., Ex. 84-59; Nicholson et al., Ex. 84-72; the more recent cohort. Smoking percenl) or having no asbestos exposure Rubino et al., Ex. 84-86; Dement et al.. histories were available for 376 men. (8.9 percent). Ex. 84-37; Acheson and Gardner, Ex. 84- Five smoking groups were defined; These results were interpreted by the 15; and Berry and Newhouse, Ex. 84-21; Nbver smoked, .1-4 cigarettes per day, 5- authors to mean that "pleural for crocidolite: Jones et al.. Ex. 84-138; 14i'cigarettes per day, 15+ cigarettes per abnormalities often appear from Hobbs et al.. Ex. 84-132; McDonald and day, and ex-smokers. In the most recent relatively low asbestos exposures and Newhouse, Ex. 163; Berry and GLEASON-000874