Dust exposure and mortality in chrysotile mining, 1910-75. 1980

Our plain-English summary of Dust exposure and mortality in chrysotile mining, 1910-75. 1980, by J.C. McDonald, F.D. Liddell, G.W. Gibbs, et al (British Journal of Industrial Medicine, 1993).

The study

• Authors: J.C. McDonald, F.D. Liddell, G.W. Gibbs, G.E. Eyssen, A.D. McDonald
• Journal: British Journal of Industrial Medicine
• Published: 1993;50(12):1058-72
• Type of article: Historical article
• Cited by: 4 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

We report a further follow-up of a birth cohort of 11 379 workers exposed to chrysotile. The cohort consisted of all 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" method, 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.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

In plain English

This further follow-up studied 10,939 men and 440 women, born 1891-1920, who had worked at least a month in the chrysotile mines and mills of Asbestos and Thetford Mines, Quebec. Each worker's accumulated dust exposure was estimated; by the end of 1975, 4463 men and 84 women had died. Compared with Quebec death rates, men's 1926-75 deaths were 2% above expected at Asbestos and 10% above at Thetford Mines, the dustier area. One analysis looked only at deaths in 1951-75 that occurred at least 20 years after first employment. It found no discernible link with dust exposure among men with under five years' service, but clear excesses among the most heavily exposed men employed at least 20 years. Deaths from lung cancer and pneumoconiosis rose with exposure, in a pattern the authors described as effectively linear. Lung cancer also occurred in non-smokers. Laryngeal cancer showed no excess but was linked with smoking. Ten men and one woman died of pleural mesothelioma. The authors concluded the exposure-response relations were essentially linear, while noting their findings did not prove this.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Follow-up of a historical birth cohort of chrysotile miners and millers. Two analyses used the man-years method, comparing observed deaths with deaths expected from Quebec death rates (standardised mortality ratios, SMRs). A third used a case-and-multiple-controls method with controls drawn from within the cohort.
• Who was studied: 10,939 men and 440 women, born 1891-1920, employed at least one month in the chrysotile mines and mills of Asbestos and Thetford Mines, Quebec, followed from first employment (the earliest in 1904) to the end of 1975.
• Exposure: Chrysotile dust in mining and milling. A dust concentration in millions of particles per cubic foot (mpcf) was estimated for each job and year. The estimates rested on more than 4000 midget impinger dust counts taken between 1949 and 1966, and on interviews with long-service employees for earlier years. Exposure was summed as accumulated exposure in mpcf multiplied by years (mpcf-y).
• Main results:
  • By the end of 1975, 4463 men and 84 women had died. Among men, overall excess mortality for 1926-75 was 2% at Asbestos and 10% at Thetford Mines, the dustier region.
  • All men, 1926-75: 4350 deaths observed against 4107 expected from Quebec death rates. The article prints the SMR as 106, meaning about 6% more deaths than expected.
  • The women, mostly employed at Asbestos, had an all-cause SMR for 1936-75 of 0.90.
  • The analysis by length of service covered 3291 men's deaths that occurred from 1951 to 1975 and 20 or more years after first employment.
  • In that analysis of deaths 20 years or more after first employment, men with less than five years' service showed no discernible correlation with dust exposure. Among men employed at least 20 years, those with the heaviest dust concentrations had clear excesses.
  • Lung cancer in men, by dust exposure accumulated to age 45: 91 deaths, SMR 0.93 (under 30 mpcf-y); 81 deaths, SMR 1.18 (30 to under 300 mpcf-y); 70 deaths, SMR 2.25 (300 mpcf-y or more).
  • Pneumoconiosis in men, by dust exposure accumulated to age 45: 5 deaths, SMR 2.98 (under 30 mpcf-y); 12 deaths, SMR 10.81 (30 to under 300 mpcf-y); 27 deaths, SMR 54.00 (300 mpcf-y or more).
  • A linear dose-response line was fitted for lung cancer, so far without regard for smoking: relative risk = 1 + 0.0014 multiplied by mpcf-y.
  • Lung cancer deaths occurred in non-smokers. In non-smokers, lung cancer increased more with rising exposure than in smokers. The evidence was insufficient to distinguish between multiplicative and additive risk models.
  • There were no excess deaths from laryngeal cancer, but there was a clear association between laryngeal cancer and smoking.
  • Ten men and one woman died from pleural mesothelioma.
  • The men most heavily exposed had a substantial excess of deaths from cancer of the upper gastrointestinal tract, confined to Thetford Mines.
  • Consider only the 1904 men with at least 20 years' employment at the lower dust concentrations, which averaged 6.6 mpcf (about 20 fibres/cc). In this group alone, excess mortality would not have been statistically significant, except for pneumoconiosis. Their total mortality was 620 deaths, SMR 0.94.
• The authors' conclusion: The authors concluded that essentially linear relations had been shown between exposure (dust concentration multiplied by length of service) and lung cancer, pneumoconiosis and total deaths. They emphasised that even a survey this large could not detect increased risk at dust concentrations now considered unacceptable, and therefore stressed the importance of exposure-response models.
• Limitations the authors state:
  • There were few dust measurements before 1949, so exposures for the earlier years are estimates.
  • Death certificates may have over-diagnosed dust-related disease in heavily exposed men.
  • Selective entry into and exit from jobs (the 'healthy worker effect') cannot be corrected for in observational studies.
  • The results fit a linear exposure-response model but do not prove it.
  • Smoking histories were missing for most men lost to view and for about 800 men who died before 1950, and there were some coding errors.
  • Some employment gaps were missing from work histories at Asbestos, so exposures there may be slightly overstated.

Mines named here

Asbestos mines this study is about. Each mine's page says who ran it, when it worked, and what it produced.

• Jeffrey mine, Asbestos, Quebec

All asbestos mines

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Chrysotile.

Medical terms in this study, explained in our Lexicon: Chrysotile, Thetford Mines, Lung Cancer, Pneumoconiosis, Laryngeal Cancer, Pleural Mesothelioma, Million Particles per Cubic Foot (mppcf).

Related studies

• Dust exposure and mortality in chrysotile mining, 1910-75 — J.C. McDonald, F.D. Liddell, et al. (1980)
• Exposure to chrysotile mining dust and digestive cancer mortality in a Chinese miner/miller cohort — S. Lin, X. Wang, et al. (2014)
• The 1891-1920 birth cohort of Quebec chrysotile miners and millers: development from 1904 and mortality to 1992 — F.D. Liddell, A.D. McDonald, et al. (1997)
• The 1891-1920 birth cohort of Quebec chrysotile miners and millers: mortality 1976-88 — J.C. McDonald, F.D. Liddell, et al. (1993)
• Dust exposure and mortality in chrysotile mining, 1910-76 — M. Greenberg (1994)
• Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis — P. Sebastien, J.C. McDonald, et al. (1989)

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