Abstract
The linear, no-threshold model is commonly used for estimating lifetime lung cancer risk from asbestos exposures. Studies of chrysotile workers have observed shallow slopes for the exposure-response relationship for miners/millers, friction products manufacturing workers and asbestos-cement (primarily chrysotile) workers but a steeper slope (approximately 16 times higher) for textile workers. For chrysotile exposures in buildings, where short fibres constitute the great majority of the fibres, the shallow slope is judged more appropriate. Using this slope the data regarding exposure levels to building occupants and maintenance workers, the annualized risks of lung cancer would be approximately 0.01 and 0.6 per million for these groups, respectively. Using the higher slope would result in risks 16 times higher, still considerably lower than those commonly accepted. Contrary to the model's assumption of increased risk for any amount of exposure, a number of studies have demonstrated evidence that lung cancer risk is not associated with years exposed to low exposure levels. Moreover, the accumulating evidence that asbestos-induced lung cancer may require lung fibrosis suggests a practical threshold since detectable lung fibrosis will not result from environmental exposure levels. Evidence suggests that the relative risk to non-smokers bay be slightly higher than to smokers (by a factor of 1.8). However, if this is true, this has little effect on risk assessment due to the low absolute risk in non-smokers. Tremolite has been associated with an increased risk of lung cancer in a study of vermiculite miners; the slope of the exposure-response relationship was similar to that for crocidolite miners and much higher than that of chrysotile miners. In spite of a recent report indicating that asbestos-associated lung cancer risk may be limited only to adenocarcinomas, the bulk of the evidence fails to confirm this.
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