|
Workplace Exposure to Asbestos:
|
---|
Groups
|
Exposure to asbestos
|
History of cigarette smoking |
Death* rate
|
Mortality ratio
|
---|---|---|---|---|
Control
|
No
|
No
|
11.3
|
1.00 |
Asbestos workers
|
Yes
|
No
|
58.4
|
5.17
|
Control
|
No
|
Yes
|
122.6
|
10.85
|
Asbestos workers
|
Yes
|
Yes
|
601.6
|
53.24
|
*Rates per 100,000 man-years standardized for age on the distribution of the man-years of all the asbestos workers. Number of lung cancer deaths based on death certificate information.
Asbestos workers who did not smoke showed about a 5 times greater risk of dying of lung cancer when compared to the nonsmoking control population. Asbestos workers who did smoke also had a 5 times greater risk of dying of lung cancer as compared to the controls who smoked. This means the relative risk associated with asbestos is about 5-fold for smokers and nonsmokers alike. Therefore, the probability that their lung cancer was due to asbestos exposure is about 80% in both smokers and nonsmokers
The combined effect of smoking and asbestos exposure appears to be more than simple addition. If the combined effect were additive, one would expect death rates of 169.7 per 100,000 man-years among asbestos workers who smoked. This rate was derived from the sum of the baseline rate (11.3) plus the excess over that baseline due to asbestos (58.4-11.3=47.1) plus the excess due to smoking (122.6-11.3=111.3). The data seem rather to satisfy a multiplicative model. It was shown that smoking alone increased the death rate about 11 times, and asbestos alone increased it 5 times. Therefore, for a multiplicative model, the mortality ratio for those exposed to both asbestos and smoking would be 55 (5 times 11) times greater than those who were exposed neither to asbestos nor to smoking. The mortality ratio for those exposed to asbestos and to cigarettes was actually 53.24.
Liddell et al. (1977) further analyzed the mortality experience of a cohort of chrysotile asbestos miners and millers previously studied by McDonald et al. (1973,1974) and McDonald and McDonald (1976). This cohort of 10,951 men born between 1891 and 1920, and who had at least 1 month of employment, was followed through December 31, 1973. Cause of death was ascertained for 97% of the 4,037 known deaths, whereas 1,117 (10%) were lost to followup. Smoking habits were ascertained through a questionnaire administered to those living or to relatives of deceased workers who died after 1951. Unlike previous reports on this cohort, person-years were accumulated by 5-year age groups and 5-year periods of calendar time, with expected deaths by cause calculated using mortality rates for males in the Province of Quebec.
For this cohort, the SMR for all causes was 107, and a SMR of 125 was observed for cancer of the lung and pleura. There also were 40 pneumoconiosis deaths. Using the whole cohort as the referent population, an excess of respiratory cancer was observed only after cumulative exposures of 300 mppcf-years (relative risk = 1.39). However, only 15 of the 40 pneumoconiosis deaths occurred with exposures greater than 300 mppcf-years. When available smoking data were taken into account, lung cancer SMRs of 48 and 46 were calculated for nonsmokers and ex-smokers, increasing to 206 for heavy smokers. There were seven mesothelioma deaths among the cohort.
The Liddell et al. study suffers in that an "unexposed" group is not used for dose-response analyses of lung cancer; thus, risk at low doses could not be estimated. Secondly, smoking-specific death rates were not used for calculation of expected lung cancer deaths, thus underestimating risks among nonsmokers
There is little or no evidence that cigarette smoking is related to increased risk of pleural or peritoneal mesothelioma (Hammond et al., 1972, 1979).
Data from two studies suggest that cigarette smoking may contribute to the risk of asbestosis. Hammond et al. (1979) reported that the asbestosis death rate of asbestos workers who smoked was 2.8 times as high as that of nonsmoking asbestos workers. Weiss (1971) reported a prevalence of pulmonary fibrosis of 40% (30/75) among asbestos workers who smoked in contrast to a prevalence of 24% (6/25) among non smoking asbestos workers.
A small experimental study indicated that the particle clearance in the smokers was considerably slower than in the nonsmokers Cohen et al. (1979) reported that after a year 50 percent of magnetic dust (Fe 3 O4) originally deposited remained in the lungs of the smokers while only 10 percent remained in the lungs of the nonsmokers The authors suggested that smoking may impair the clearance of other dusts, including those that are toxic. This may help to explain the higher incidence of lung disease in smokers.
In summary, both asbestos and smoking are independently capable of increasing the risk of lung cancer mortality. When exposure to both occurs, the combined effect with respect to lung cancer appears to be multiplicative rather than additive. From the evidence presented, we may conclude that asbestos is a carcinogen capable of causing, independent of smoking, lung cancer and mesothelioma.
Memorandum on Asbestos Update and Recommended
Occupational Standard
I. Asbestos Nomenclature/Definitions
II. Asbestos Sampling and Analysis
III. Biologic Effects of Exposure to
Asbestos in Animals
IV. Biologic Effects of Exposure to
Asbestos in Humans
V. Smoking and Asbestos
VI. Exposure to Asbestiform Minerals
other than Commerically Mined Asbestos
VII. Non-Occupational Exposure to Commerical
Sources of Asbestos
VIII. Dose-Response Relationships
References
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