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.
It has been demonstrated that the total content of food fibers in the daily diet of the Donbas population diets amounts to 24.0-26.3 g (cellulose 5.9-6.7 g, pectin 2.0-2.7 g, hemicellulose 16.1-16.9 g). Baked goods account for the major part of hemicellulose (about 85%) and 1/3 of cellulose. Potato and vegetables (fruit) account for half of pectin and 1/3 of cellulose. The daily requirement of cellulose and pectin was satisfied by about 1/3, which is accounted for by a high relative significance of refined products (about 60% of the diet caloric value).
We report a further follow-up of a birth cohort of 11 379 workers exposed to chrysotile. The cohort consisted of 10 939 men and 440 women, born 1891-1920, who had worked for at least a month in the mines and mills of Asbestos and Thetford Mines in Quebec. For all subjects, length of service and estimates of accumulated dust exposure were obtained, with a smoking history for the vast majority. Three methods of analysis, two based on the "man-years" methods, the other a "case-and-multiple-controls" approach, gave results consistent with one another and with previous analyses. By the end of 1975, 4463 men and 84 women had died. Among men, the overall excess mortality, 1926-75 was 2% at Asbestos and 10% at Thetford Mines, much the dustier region. The women, mostly employed at Asbestos, had a standardised mortality ratio (SMR) all causes, 1936-75) of 0.90. Analysis of deaths 20 years or more after first employment showed that in men with short service (less than five years) there was no discernible correlation with dust exposure. Among men employed at least 20 years, there were clear excesses in those exposed to the heaviest dust concentrations. Reanalysis in terms of exposure to age 45 showed definite and consistent trends for SMRs for total mortality, for lung cancer, and for pneumoconiosis to be higher the heavier the exposure. The response to increasing dose was effectively linear for lung cancer and for pneumoconiosis. Lung cancer deaths occurred in non-smokers, and showed a greater increase of incidence with increasing exposure than did lung cancer in smokers, but there was insufficient evidence to distinguish between multiplicative and additive risk models. There were no excess deaths from laryngeal cancer, but a clear association with smoking. Ten men and one woman died from pleural mesothelioma. If the only subjects studied had been the 1904 men with at least 20 years' employment in the lower dust concentrations, averaging 6.6 million particles per cubic foot (or about 20 fibres/cc), excess mortality would not have been considered statistically significant, except for pneumoconiosis. The inability of such a large epidemiological survey to detect increased risk at what, today, are considered unacceptable dust concentrations, and the consequent importance of exposure-response models are therefore emphasised.
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