Asbestos, Smoking and Lung Cancer: An Update

Our plain-English summary of Asbestos, Smoking and Lung Cancer: An Update, by S. Klebe, J. Leigh, D.W. Henderson, et al (International Journal of Environmental Research and Public Health, 2019).

The study

• Authors: S. Klebe, J. Leigh, D.W. Henderson, M. Nurminen
• Journal: International Journal of Environmental Research and Public Health
• Published: 2019;17(1)
• Type of article: Review
• Cited by: 102 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

This review updates the scientific literature concerning asbestos and lung cancer, emphasizing cumulative exposure and synergism between asbestos exposure and tobacco smoke, and proposes an evidence-based and equitable approach to compensation for asbestos-related lung cancer cases. This update is based on several earlier reviews written by the second and third authors on asbestos and lung cancer since 1995. We reevaluated the peer-reviewed epidemiologic studies. In addition, selected in vivo and in vitro animal studies and molecular and cellular studies in humans were included. We conclude that the mechanism of lung cancer causation induced by the interdependent coaction of asbestos fibers and tobacco smoke at a biological level is a multistage stochastic process with both agents acting conjointly at all times. The new knowledge gained through this review provides the evidence for synergism between asbestos exposure and tobacco smoke in lung cancer causation at a biological level. The evaluated statistical data conform best to a multiplicative model for the interaction effects of asbestos and smoking on the lung cancer risk, with no requirement for asbestosis. Any asbestos exposure, even in a heavy smoker, contributes to causation. Based on this information, we propose criteria for the attribution of lung cancer to asbestos in smokers and non-smokers.

In plain English

This article was a review, not a new study. The authors reread key epidemiological, pathological and basic biology papers published since an earlier review by two of them. They also included selected animal, cell and human molecular studies. They did not carry out a formal meta-analysis. In the authors' assessment, lung cancer risk was related to cumulative asbestos exposure itself, with no requirement for asbestosis. They also judged that the statistical data conformed to a multiplicative model for the combined effect of asbestos and tobacco smoke. They argued that the two act together at a biological level, so that any asbestos exposure, even in a heavy smoker, could be considered to contribute to causation. They proposed attribution criteria. All cases required a latency of at least 10 years. For current smokers, one qualifying route was 25 fiber-years of mixed-fiber end-use exposure. For chrysotile-only exposure the figures were 200 fiber-years (Canadian chrysotile miners and millers, friction products) or 100 fiber-years (other chrysotile-only exposure). For never-smokers or people who quit 30 or more years before diagnosis, the figure was 5 fiber-years. The authors noted that the exact mechanisms are not fully understood and that apportionment models cannot perfectly reflect biological reality.

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: Narrative review of published literature (no formal meta-analysis), with proposed criteria for attributing lung cancer to asbestos
• Who was studied: Published peer-reviewed epidemiologic studies, plus selected animal (in vivo and in vitro) studies and molecular and cellular studies in humans, published since the authors' earlier review
• Exposure: Asbestos (the review discusses chrysotile, amosite, crocidolite and other types), measured as cumulative exposure in fiber-years, and tobacco smoke, including their combined effect
• Main results:
  • In the authors' assessment, the weight of evidence indicated that lung cancer risk is related to cumulative asbestos exposure itself, with no requirement for asbestosis
  • The authors judged that the statistical data they evaluated conformed to a multiplicative model for the combined effect of asbestos and smoking on lung cancer risk
  • The authors argued that, because asbestos and tobacco smoke interact biologically, any asbestos exposure, even in a heavy smoker, could be considered to contribute to causation
  • Proposed criteria required asbestos exposure with a minimum latency of 10 years
  • For current smokers, one proposed route was a cumulative exposure of 25 fiber-years or more for mixed-fiber, end-use exposure
  • For chrysotile-only exposure, the proposed figure was 200 fiber-years for Canadian chrysotile miners and millers and friction products, and 100 fiber-years for other chrysotile-only exposure
  • For never-smokers or those who stopped smoking 30 years or more before diagnosis, the proposed figure was 5 fiber-years, or one-third of the work durations set out for smokers
  • The authors proposed replacing the fixed Helsinki lung fiber-count thresholds with an amphibole fiber count above the fifth percentile for asbestosis cases measured by the same laboratory
  • The authors stated that the proposed criteria are meant mainly for statutory compensation, where smoking is not considered
  • The authors held that asbestos makes some joint contribution to causation even below 25 fiber/mL-years, which they said should be proportionally compensated
• The authors' conclusion: The authors concluded that their review gives evidence for synergism between asbestos and tobacco smoke in lung cancer causation at a biological level. They also concluded that the data conform to a multiplicative model with no requirement for asbestosis, and that any asbestos exposure, even in a heavy smoker, contributes to causation.
• Limitations the authors state:
  • No formal meta-analysis was performed
  • The exact mechanisms of the synergism between tobacco smoke and asbestos are not fully understood
  • Apportionment schemes for taking smoking into account are contrived mathematical models that cannot perfectly reflect biological reality

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Mesothelioma.

Medical terms in this study, explained in our Lexicon: Lung Cancer, Cumulative Exposure, Asbestos Exposure, Causation, Attribution.

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