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.
In 1974 changes in dyspnea, lung function, and pneumoconiotic radiographic abnormalities were recorded among the 1,015 Quebec chrysotile miners and millers surveyed in 1967-1968. The aim was to relate these changes to dust exposure--age, smoking, and earlier health status being taken into account. Dyspnea and lung function were assessed in 722 men, and for 277 recent radiographs were read separately by three experts for changes in the parenchyma and pleura. Each measure was analyzed independently for men without any abnormality when first seen (eligible for "attack") and for others (eligible for progression/regression). Age significantly influenced the rate of attack of pleural abnormality and the rates of attack and progression of dyspnea and lung function decline. Smoking had comparatively minor effects. The only associations with exposure were for progression of parenchymal change (one reader), and for progression of dyspnea. These essentially negative findings are similar to those obtained in a previous longitudinal survey of radiographs from the same workforce.
In 1967-68 an age-stratified random sample of 1069 current workers in Quebec asbestos mines and mills was surveyed. Questions concerning rheumatic complaints were included in a modified MRC questionnaire used at that time, and on this basis a rheumatic severity gradient was devised. No relationship could be detected between rheumatic complaints and pulmonary radiologic response to chrysotile dust exposure, despite implications in the literature that such a relationship might exist.
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Questionnaire, radiographic, and lung function information for 983 Quebec chrysotile workers at work in 1966 was used to develop five clinical response scales (i.e., parenchymal and pleural fibrosis, airflow limitation, chronic bronchitis, and airway reactivity). The relationship of the scales to variables describing temporal patterns of exposure was studied, taking into account cumulative exposure, age, and smoking. All response scales related to variables containing only time information, and in all cases temporal patterns of exposure influenced exposure response relationships. For pulmonary fibrosis, the strongest relationships were to cumulative exposure; for pleural fibrosis to exposure peaks and residence time of dust in the lung; for airway reactivity to early and recent exposure; and for airflow limitation and chronic bronchitis to smoking and to dust level and load over time. These results add to the gathering evidence that exposures to environments containing airborne asbestos may result in airway abnormalities.