A cohort of some 11,000 men born 1891-1920 and employed for at least one month in the chrysotile mines and mills of Quebec, was established in 1966 and has been followed ever since. Of the 5351 men surviving into 1976, only 16 could not be traced; 2508 were still alive in 1989, and 2827 had died; by the end of 1992 a further 698 were known to have died, giving an overall mortality of almost 80%. This paper presents the results of analysis of mortality for the period 1976 to 1988 inclusive, obtained by the subject-years method, with Quebec mortality for reference. In many respects the standardised mortality ratios (SMRs) 20 years or more after first employment were similar to those for the period 1951-75--namely, all causes 1.07 (1951-75, 1.09); heart disease 1.02 (1.04); cerebrovascular disease 1.06 (1.07); external causes 1.17 (1.17). The SMR for lung cancer, however, rose from 1.25 to 1.39 and deaths from mesothelioma increased from eight (10 before review) to 25; deaths from respiratory tuberculosis fell from 57 to five. Among men whose exposure by age 55 was at least 300 million particles per cubic foot x years (mpcf.y), the SMR (all causes) was elevated in the two main mining regions, Asbestos and Thetford Mines, and for the small factory in Asbestos; so were the SMRs for lung cancer, ischaemic heart disease, cerebrovascular disease, and respiratory disease other than pneumoconiosis. Except for lung cancer, however, there was little convincing evidence of gradients over four classes of exposure, divided at 30, 100, and 300 mpcf.y. Over seven narrower categories of exposure up to 300 mpcf.y the SMR for lung cancer fluctuated around 1.27 with no indication of trend, but increased steeply above that level. Mortality form pneumoconiosis was strongly related to exposure, and the trend for mesothelioma was not dissimilar. Mortality generally was related systematically to cigarette smoking habit, recorded in life from 99% of survivors into 1976; smokers of 20 or more cigarettes a day had the highest SMRs not only for lung cancer but also for all causes, cancer of the stomach, pancreas, and larynx, and ischaemic heart disease. For lung cancer SMRs increased fivefold with smoking, but the increase with dust exposure was comparatively slight for non-smokers, lower again for ex-smokers, and negligible for smokers of at least 20 cigarettes a day; thus the asbestos-smoking interaction was less than multiplicative. Of the 33 deaths from mesothelioma in the cohort to date, 28 were in miners and millers and five were in employees of a small asbestos products factory where commercial amphiboles had also been used. Preliminary analysis also suggest that the risk of mesothelioma was higher in the mines and mills at Thetford Mines than in those at Asbestos. More detailed studies of these differences and of exposure-response relations for lung cancer are under way.
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It has been a matter of controversy whether there is an increased risk of lung cancer among asbestos-exposed workers without radiographic asbestosis. A previous study of lung cancer risk among asbestos-cement workers has been updated with an additional 12 years of follow-up.
Subjects had received radiographic examination at 20 and 25 years from first exposure to asbestos. Radiographs were interpreted by a single National Institute of Safety and Health (NIOSH)-certified B-reader using the 1971 International Labor Office (ILO) Classification of the pneumoconioses as reference standard. Asbestosis was defined as an ILO coding of 1/0 or higher. Standardized Mortality Ratios (SMRs) were calculated using the general population of Ontario as reference.
Among asbestos-cement workers without radiographic asbestosis at 20 years latency the lung cancer SMR was 3.84 (2.24-6.14). Among workers without asbestosis when examined at 25 years latency the SMR was 3.69 (1.59-7.26).
Workers from an Ontario asbestos-cement factory who did not have radiographic asbestosis at 20 or 25 years from first exposure to asbestos continued to have an increased risk of death from lung cancer during an additional 12 years of follow-up.
Comment In: Am J Ind Med. 2011 Jun;54(6):495-6; author reply 497-821328422
The aim of the study was to determine the pulmonary concentrations of mineral fibers in the Finnish male urban population and to evaluate the analysis of pulmonary fiber burden by scanning electron microscopy (SEM) as an indicator of past fiber exposure.
The pulmonary concentration of mineral fibers was determined by SEM and compared with occupational history for a series of 300 autopsies of urban men aged 33 to 69 years.
The concentration of fibers (f) longer than 1 micron ranged from
Cohorts of Finnish asbestos sprayers and of asbestosis and silicosis patients were followed for cancer with the aid of the Finnish Cancer Registry in the period 1967-1994. Compared with the cancer incidence of the total Finnish population, asbestos sprayers had an increased risk for total cancer (standardized incidence ratio [SIR] 6.7, 95% confidence interval [95% CI] 4.2-10); lung cancer (SIR 17.95% CI 8.2-31); and mesothelioma (SIR 263, 95% CI 85-614). The SIR of the asbestosis patients was 3.7 (95% CI 2.8-5.0) for all sites, 10 (95% CI 6.9-14) for lung cancer, and 65 (95% CI 13-188) for mesothelioma. The silicosis patients also had significantly high SIR values for all sites (1.5, 95% CI 1.0-2.1) and lung cancer (2.7, 95% CI 1.5-4.5). The values for the SIR and the standardized mortality ratio for all sites and lung cancer were very similar, and therefore it seems that both are reliable indicators of the occurrence of occupational cancer. It was concluded that pneumoconioses patients and asbestos-exposed workers have a markedly elevated risk for cancer. Asbestos-induced occupational cancers are not only diseases of the elderly, since the relative risk is high also for middle-aged people.
To study associations between chest HRCT signs and subsequent deaths in long-term follow-up.
Lung and pleural signs of 633 asbestos exposed workers (age 45-86, mean 65) screened with HRCT were recorded by using the International Classification of Occupational and Environmental Respiratory Diseases (ICOERD) system, which contains detailed instructions for use and reference images. Subsequent mortality was checked from the national register. Cox regression adjusted for covariates (age, sex, BMI, asbestos exposure, pack-years) was used to explore the relations between HRCT signs and all-cause deaths, cardiovascular and benign respiratory deaths, and deaths from neoplasms - all according to the ICD-10 diagnostic system.
The follow-up totalled 5271.9 person-years (mean 8.3 y/person, range .04-10.3). 119 deaths were reported. Irregular/linear opacities, honeycombing, emphysema, large opacities, visceral pleural abnormalities and bronchial wall thickening were all significantly related to all-cause deaths. Most of these signs were associated also with deaths from neoplasms and benign respiratory disease. Deaths from cardiovascular disease were predicted by emphysema and visceral pleural abnormalities.
Several HRCT signs predicted deaths. Careful attention should be paid on subjects with radiological signs predictive of deaths and new secondary preventive strategies developed. This calls for further focused studies among different populations.
We compared death certificates for asbestos-associated diseases (mesothelioma, lung cancer, asbestosis) in two asbestos workers' cohorts. One (insulation workers) had current or recent employment and a strong, continuing union support system which gave them much information about the effects of asbestos exposure. The second cohort, asbestos factory workers, had no such advantage. The factory had closed almost 30 years before, and its workers had dispersed into many areas of the state and nation. Accuracy of medical diagnosis was comparable in the two groups, but occupational listings were not. Three-quarters of the insulators' death certificates told of asbestos work, while virtually none of the factory workers' certificates provided such information, even for deaths of mesothelioma and asbestosis. The data indicate that disease categories, based on medical and pathological diagnoses, at least for asbestos-associated disease, tend to be accurate. Attempts to identify groups at risk by sorting occupational categories can give variable results, good for those with current exposures, much less satisfactory for those with long-past occupational exposures.
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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To define the relationships between chrysotile exposure in fibre terms and death from specific cancers, and pneumoconiosis, all 11,379 persons born 1891-1920 who had worked in the asbestos mines and mills of Quebec for a month or more before 1967 were followed to the end of 1975. Among the 10,939 men, there had been 4,463 deaths, 634 from these causes. For each death, referents were randomly selected from among men in the cohort born in the same year as the case and known to have survived to a greater age. For each case and his referents, exposures accumulated up to nine years before the death of the case had been obtained as (million particles per cubic foot) x years. Fibre counts were estimated for each work-place so that all exposures could be expressed in (fibres/ml) x years. The ratio of the means for all 2,586 accumulated exposures was 3.46 (f/ml)/mpcf. Relative Risks (RR) were related to exposure by matched analysis. For pneumoconiosis and lung cancer, RR = 1 + b.(f/ml).y fitted well, with b estimated as 0.00647 and 0.00038, respectively. For cancers of upper and of lower G.I. tract, severe exposure was associated with elevated RRs, but rather unclearly. For other abdominal cancers, and laryngeal cancer, risks and exposure were not positively associated. The asbestos-smoking interaction in lung cancer was closer to multiplicative than to additive.