Asbestos, asbestosis, and lung cancer: observations in Quebec chrysotile workers

Our plain-English summary of Asbestos, asbestosis, and lung cancer: observations in Quebec chrysotile workers, by B.W. Case, A. Dufresne (Environmental Health Perspectives, 1997).

The study

• Authors: B.W. Case, A. Dufresne
• Journal: Environmental Health Perspectives
• Published: 1997;105 Suppl 5(Suppl 5):1113-9
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

One prospective epidemiologic study of asbestos cement workers with radiological small opacities has been cited as a rationale for attributing excess lung cancer to asbestosis. This approach could have considerable practical value for disease attribution in an era of decreasing exposure. However, a recent International Agency for Research on Cancer review concludes that the mechanism of production of asbestos-related lung cancer are unknown. Asbestosis, therefore, cannot be a biologically effective dose marker of lung cancer susceptibility. Asbestosis nonetheless would be useful in identifying asbestos-attributable lung cancer cases if it could be proven an infallible exposure indicator. In this study, we tested this hypothesis in the chrysotile miners and millers of Quebec, Canada. We examined exposure histories, autopsy records, and lung fiber content for 111 Quebec chrysotile miners and millers. If the hypothesis of an asbestosis requirement for lung cancer attribution were accurate, we would expect as asbestosis diagnosis to separate those with lung cancer and high levels of exposure from those with lower levels of exposure in a specific and sensitive manner. This is the first such study in which historical job-based individual estimates based on environmental measurements, lung fiber content, exposure timing, and complete pathology records including autopsies were available for review. We found significant excesses of lung tremolite and chrysotile and estimated cumulative exposure in those with lung cancer and asbestosis compared to those with lung cancer without asbestosis. However, when the latter were directly compared on a case-by-case basis, there was a marked overlap between lung cancer cases with and without asbestosis regardless of the measure of exposure. Smoking habits did not differ between lung cancer cases with and without asbestosis. In regression models, smoking pack-years discriminated between those with the without lung cancer, regardless of asbestosis status. Most seriously, the pathologic diagnosis of asbestosis itself seemed arbitrary in many cases. We conclude that although the presence of pathologically diagnosed asbestosis is a useful marker of exposure, the absence of this disease must be regarded as one of many factors in determining individual exposure status and disease causation.

In plain English

This study examined 111 deceased Quebec chrysotile miners and millers from a birth cohort, autopsied at two hospitals. The authors compared autopsy-recorded asbestosis with estimated cumulative exposure, lung fiber content and, where available, smoking. Of the 111, 19 had lung cancer with asbestosis, 7 lung cancer without asbestosis, 45 asbestosis alone and 40 neither. As groups, men with asbestosis had higher exposure estimates and lung fiber levels. Counting only asbestos fibers longer than 5 micrometres and more than three times as long as wide, men with both diseases had a median of 55 per microgram of dry lung, against 11 for men with lung cancer alone. Individually, however, exposure overlapped widely: the lung cancer case with the highest estimated exposure had no asbestosis. In a statistical model of Thetford Mines men with smoking data, only smoking was significantly related to lung cancer. The authors judged asbestosis diagnoses arbitrary in many cases. They concluded that, unless lung fibrosis is shown to cause lung cancer, asbestosis cannot be the only factor in attributing lung cancer to asbestos. They acknowledged autopsy selection bias.

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: Autopsy-based study of deceased members of an occupational birth cohort. It re-analyzed cases from two earlier lung-fiber studies and compared autopsy-recorded asbestosis with job-based exposure estimates, lung fiber content and smoking.
• Who was studied: 111 male chrysotile miners and millers from the Quebec birth cohort (born 1891 to 1920). Twenty-two came from the Jeffrey Pit in Asbestos, Quebec, with consecutive autopsies from 1979 through 1983 at Sherbrooke University Hospital. Eighty-nine came from the Thetford Mines/Black Lake area, autopsied between 1963 and 1984 and selected ad hoc.
• Exposure: Chrysotile mining and milling. Exposure was measured in two ways. The first was cumulative exposure in million particles per cubic foot times years worked (MPCFY), estimated from historical midget impinger dust counts applied to job histories. The second was retained lung fiber content (tremolite, chrysotile, crocidolite and amosite fibers longer than 5 micrometres, aspect ratio greater than 3:1), measured by electron microscopy. The best estimate was that 100 MPCFY corresponds to 300 to 400 fiber-years.
• Main results:
  • Of the 111 men, 19 had lung cancer with asbestosis, 7 had lung cancer without asbestosis, 45 had asbestosis alone, and 40 had neither disease.
  • Counting only fibers longer than 5 micrometres with aspect ratio greater than 3:1, men with both asbestosis and lung cancer had the highest median total lung asbestos fiber content: 55 fibers per microgram of dry lung (p less than 0.01 versus all other groups). Men with asbestosis alone had 41 (p less than 0.01 versus both groups without asbestosis). Men with lung cancer alone had 11 and men with neither disease had 7.5; the difference between these two was not significant.
  • Median cumulative exposure was 385 MPCFY for men with asbestosis and lung cancer and 363 MPCFY for men with asbestosis alone.
  • Median cumulative exposure was 161 MPCFY for men with neither disease (p less than 0.05 versus both asbestosis groups).
  • Median cumulative exposure was 81 MPCFY for the seven lung cancers without asbestosis.
  • For the seven lung cancers without asbestosis, the article's jumbled lines appear to report p less than 0.01 versus asbestosis cases without cancer, but p = 0.09 versus lung cancer cases with asbestosis.
  • Among the 22 Thetford Mines lung cancer cases, the 17 with asbestosis had a median cumulative exposure of 284 MPCFY, against 81 for the 5 without. Median lung tremolite was 62.5 versus 13.1, and chrysotile 20 versus 2.9, fibers per microgram of dry lung. The authors reported lung chrysotile and tremolite as significantly higher in those with asbestosis.
  • On a case-by-case basis there was substantial overlap in exposure between lung cancer cases with and without asbestosis. The lung cancer case with the highest MPCFY (2531 MPCFY, 47 years employed) had no asbestosis. Three lung cancer cases with asbestosis had MPCFY below 100, while three cases without asbestosis had higher values.
  • Smoking differences were not obvious between Thetford Mines lung cancer cases with and without asbestosis (mean years smoked was 46 in both groups).
  • Among Thetford Mines men with smoking data, the 18 with lung cancer smoked more than the 47 without: a median of 58 versus 34 pack-years and 1.3 versus 0.8 packs per day, both p less than 0.05.
  • In logistic regression for these 65 men, smoking was the only exposure variable significantly related to lung cancer. The other variables entered were asbestosis, cumulative exposure, duration of exposure and lung fiber concentrations.
  • Four of the seven lung cancer cases not diagnosed with asbestosis had lung fibrosis recorded at autopsy. One of these cases, with diffuse interstitial fibrosis and asbestos bodies, was called 'idiopathic'.
• The authors' conclusion: The authors concluded that asbestosis is a good surrogate for asbestos exposure. However, unless and until it is established that lung fibrosis causes lung cancer, asbestosis cannot be used as the only factor in attributing lung cancer to asbestos exposure. They added that all exposure measures should be examined in individual cases.
• Limitations the authors state:
  • Autopsy selection bias: the autopsies were markedly selected toward possible asbestos-related cancers.
  • The Thetford Mines cases were selected ad hoc, and data were available for fewer than one-third of the 302 cohort members autopsied there.
  • Because asbestosis itself is compensable, families may have self-selected cases with more ambiguous asbestosis diagnoses for autopsy.
  • The lung cancer cases analyzed were a small fraction of those in the cohort.
  • Asbestosis severity could not be graded, because the pathologists' criteria for severity modifiers were unspecified. Only presence or absence was used.
  • MPCFY measures total particles rather than fibers, and conversion to fibers has wide confidence limits. In two cases the authors judged the MPCFY estimates probably wrong.
  • Smoking data were unavailable for the four lung cancer cases from the Asbestos area.

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, Lung cancer.

Medical terms in this study, explained in our Lexicon: Lung Cancer, Quebec Chrysotile, Asbestos-Cement, Attribution, Chrysotile, Autopsy, Pathology, Tremolite.

Related studies

• The biopersistence of brazilian chrysotile asbestos following inhalation — D.M. Bernstein, R. Rogers, et al. (2004)
• The 1891-1920 birth cohort of Quebec chrysotile miners and millers: mortality 1976-88 — J.C. McDonald, F.D. Liddell, et al. (1993)
• A 37-year observation of mortality in Chinese chrysotile asbestos workers — X. Wang, E. Yano, et al. (2012)
• The combination of effects on lung cancer of cigarette smoking and exposure in quebec chrysotile miners and millers — F.D. Liddell, B.G. Armstrong (2002)
• The health of chrysotile asbestos mine and mill workers of Quebec — J.C. McDonald, M.R. Becklake, et al. (1974)
• Temporal patterns of exposure and nonmalignant pulmonary abnormality in Quebec chrysotile workers — R. Copes, D. Thomas, et al. (1985)

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