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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This study was carried out to assess Future Workshop (FW) regarding its usefulness as a participatory ergonomics method, using a descriptive evaluation design analysed by phenomenographical approach. The study was conducted among professional cleaners, health care personnel and miners, with a sample of 105 participating subjects in 8 different FWs. Multiple methods, giving a combination of both qualitative and quantitative data, were used for data collection. Good involvement of participants was observed during workshops. Evaluations immediately after FWs and 3 months later showed a strong relationship with high correlation, indicating that the perception of FW participants was very positive. Interviews revealed conformity between developed problem identification and proposed changes. Participants' own perceptions of FW's influence on creativity depict their belief of developed ideas and solutions in order to identify and solve workplace problems. FW is considered to be a useful ergonomics tool, and its qualities are related to structure and practical performance.
BACKGROUND: The association between occupational quartz exposure and ventilatory function was investigated in men in a general population after adjusting for other potential determinants of outcome. METHODS: All eligible men aged 30-46 years living in western Norway (n = 45,380) were invited to a cross sectional community survey. This included a self administered questionnaire (with respiratory symptoms, smoking habits and occupational exposures), spirometric recordings (using dry wedge below spirometers), and a chest radiograph (65% attendance). Measurements of forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were obtained in 91% (n = 26,803) of those who participated, 26,106 of whom performed successful spirometric tests and had normal chest radiographs and remained for further analysis. Age, body mass index, and technician standardised residuals ((observed minus predicted value)/residual standard error) of maximum FEV1/height2 and FVC/height2 were used as outcome variables for adjusted lung function levels, respectively. RESULTS: Occupational quartz exposure was reported by 13% (n = 3445) of those who participated in the survey, with a mean duration of seven years. Among those exposed to quartz, significant inverse linear relationships were observed between years of exposure and FEV1 level and the ratio of FEV1/FVC, independent of host characteristics. Multiple linear regression analyses showed that the difference in FEV1 associated with each year of quartz exposure was -4.3 ml (95% CI -1.1 to -7.5 ml; p = 0.01) compared with -6.9 ml (95% CI -4.7 to -9.1 ml; p
One of objective methods of early and differential diagnosis of occupational pulmonary diseases in miners (pneumoconiosis, silicotuberculosis, dust bronchitis) is bronchoscopy with a cytologic examination of bronchoalveolar lavage fluid (BAF). BAF-examination was carried out in a total of 88 patients with incipient and advanced forms of dust bronchitis, pneumoconiosis and silicotuberculosis. A direct relationship has been revealed between a decline in local cell-bound immunity caused by a dust-inducted affection mononuclear phagocytes and advancing of stages of dust-related diseases.
New material was presented from pending publications arising from the follow-up to 1988 of the Quebec cohort of over 10,000 chrysotile miners and millers born 1891-1920. In reviewing these and previous findings, the following conclusions were drawn; they are supported, insofar as this is possible, by the only other relevant information, that from Balangero, in Northern Italy. There is strong evidence that the risk of lung cancer as a result of exposure to chrysotile at concentrations of less than 15 million particles per cubic foot is vanishingly small. At higher concentrations, the relative risk of lung cancer is elevated, but less so in smokers of 20 or more cigarettes a day than in others. The magnitude of this risk cannot be evaluated with any certainty, but this is unimportant as these higher concentrations (above about 50 f ml-1) are well outside the range of experience nowadays. There is no evidence that the risk of laryngeal cancer or of stomach cancer are adversely affected by exposure to chrysotile. Nor is there evidence of increased risks of other abdominal malignancies or of kidney cancer among chrysotile miners and millers. The risk of mesothelioma in chrysotile miners and millers is very low compared with the risks in populations exposed to amphiboles or to mixtures of fibres including even small proportions of amphiboles.
A cohort of 54,128 men who worked in Ontario mines was observed for mortality between 1955 and 1986. Most of these men worked in nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was found among the 13,603 Ontario gold miners in the study (standardised mortality ratio (SMR) 129, 95% confidence interval (95% CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141, 95% CI 105-184). The excess mortality from lung cancer in the gold miners was confined to men who began gold mining before 1946. No increase in the mortality from carcinoma of the lung was evident in men who began mining gold after the end of 1945, in men who began mining nickel after 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6-11.4%); each year of employment before the end of 1945 in mines in which the host rock contained 0.1% arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CI 1.1-5.1%); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02-2.4%). A comparison of two models shows that the excess of lung cancer mortality in Ontario gold miners is associated with exposure to high dust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcinoma of the lung in Ontario gold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung in Ontario gold miners is probably due to exposure to arsenic and radon decay products.
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