Employing incidence data from the Quebec Tumor Registry, we examined the relative risks of cancer of all sites for the years 1969-73 in the asbestos-mining, rural, and metropolitan counties of Quebec Province, Canada. Generally, rates for males exceeded those for females, and the relative risks in the asbestos-mining counties for 7-10 different sites of cancer, all of low incidence, were from 1.50 to 8.08 times those of other rural counties of the Province for both sexes. Metropolitan counties exhibited equally high risk for many of these sites. We discovered higher risks among males in asbestos-mining counties for cancer of the pleura, peritoneum, lip, tongue, salivary gland, mouth, and small intestine and higher risks among females for cancer of the pleura, lip, kidney, salivary gland, and for melanoma. Because of the likelihood of a long latent period for asbestos-related cancers, the risks we observed were possibly the product of since-altered occupational and environmental conditions existing 20-30 years ago in the asbestos-mining areas. The similarities in risks for most cancers in asbestos-mining and urban areas were noteworthy.
There is a relationship between dust exposure, on the one hand, and serious disease and death, on the other, in chrysotile asbestos mine and mill workers of Quebec. Studies in current working populations indicate that prevalence of abnormality increases with increasing exposure. However, the relationship is weak and offers only a partial explanation of between-subject variability. In addition, there is no certain way to detect or predict change. Because of the relative nonspecificity of the health measurements examined and their poor relationship to exposure, control should be based on environmental monitoring, with biologic monitoring considered in a complementary role. This leaves the clinician with the dilemma of how best to advise the worker in whom questionable changes have been detected. At present, there appears little doubt that the decision must remain essentially clinical, based, on one hand, on all available information about the man, his job, and the plant or mine in which he works, from which an estimate of likely outcome must be made, and, on the other hand, on the social and human factors concerned, including the fact that removal from exposure does not necessarily prevent the appearance of abnormality.
Although it is well known that both cigarette smoke and microscopic airborne asbestos fibres can cause lung cancer, evidence as to how these two agents combine is nebulous. Many workers have believed in the multiplicative theory, whereby asbestos increases the risk in proportion to the risk from other causes. However, evidence against this theory is mounting: a recent review concluded that the multiplicative hypothesis was untenable, and that the relative risk of lung cancer from asbestos exposure was about twice as high in non-smokers as in smokers, a finding largely independent of type of asbestos fibre. The criteria for entry to the current study were met by 7279 men in the 1891-1920 birth cohort of Quebec chrysotile miners and millers. The data consisted of date of birth, place of employment, smoking habit, asbestos exposure accumulated to age 55 and, for those 5527 who died between 1950 and June 1992, date and cause of death; 533 of the deaths were from lung cancer. For the principal analyses, ex-smokers were excluded from the study cohort, which comprised 5888 men, of whom 473 died of lung cancer. The conventional form of analysis is simply of the double dichotomy: non-smokers of cigarettes, 'unexposed' and exposed; all others, 'unexposed' and exposed. The respective standardized lung cancer mortality ratios (SMRs) were 0.29 and 0.62; and 1.37 and 1.72. Thus, the differences in relative risk, due to exposure, were closely similar, 0.33 and 0.35. On the other hand, the effects of asbestos measured by the corresponding ratios, 2.12 and 1.25, did differ, being 1.7 times as high in non-smokers as in others. The principal analysis was much more penetrating: the method was to fit models to a 'disaggregated' 6 x 10 array, by smoking habit (excluding ex-smokers) and asbestos exposure, of lung cancer SMRs. Both linear and log-linear models were fitted: the former included the additive and linear-multiplicative; the latter embraced the more conventional multiplicative form. The additive model fitted much the best. The fit of each multiplicative model was improved by the introduction of an interaction term that implied a less than multiplicative relationship. Thus smoking and exposure to chrysotile appear to have acted independently in causing lung cancer, with 10 cigarettes a day having an effect roughly equivalent to exposure amounting to 700 million particles per cubic foot x years. The refutation of the multiplicative hypothesis in these data reinforces its inapplicability in general; but the additive hypothesis is not generally applicable either. Indeed, there seems to be no good reason to believe that interactions conform to any simple theory. The implications are important.