Asbestos exposure, asbestosis, and lung cancer

Our plain-English summary of Asbestos exposure, asbestosis, and lung cancer, by D.E. Banks, M.L. Wang, J.E. Parker (Chest, 1999).

The study

• Authors: D.E. Banks, M.L. Wang, J.E. Parker
• Journal: Chest
• Published: 1999;115(2):320-2
• Type of article: Comment, Editorial
• Cited by: 13 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

This editorial commented on a review by Weiss, published in the same issue of Chest, of 39 English-language reports of cohorts exposed to asbestos. The review addressed whether excess lung cancer in asbestos-exposed workers is caused by asbestosis (the "Browne hypothesis") or by asbestos exposure itself. The authors summarized early evidence. A 1949 report found lung cancer in 35 of 235 (13.2%) autopsied deaths where asbestosis was identified. A 1955 cohort study found lung cancer in 18 of 105 deaths, 15 of them in association with asbestosis. The authors argued that the seven cohorts Weiss used as a comparison group, which showed neither asbestosis nor excess lung cancer (mean relative risk 1.00), had weaknesses: small numbers of deaths, low exposures, high worker turnover, or selection of subcohorts with shorter exposure. They cited studies linking pleural plaques and chest radiograph abnormalities other than small opacities to raised lung cancer risk. Among people with pleural plaques independent of asbestosis, the lung cancer SMR was 1.4. They stated that one of Weiss's relative risk calculations appeared to be in error. They also cited expert estimates that lung cancer risk roughly doubles at a cumulative exposure of 25 fiber-years, a level at which asbestosis may or may not be present. The authors concluded that asbestosis indicates high exposure and adds risk. However, they judged the hypothesis that excess lung cancer occurs only among those with asbestosis insufficient to explain the heightened risk.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This was an editorial, not an original study. The authors commented on a review by Weiss in the same issue of CHEST. That review examined 39 English-language reports of asbestos-exposed cohorts to address the "Browne hypothesis": the idea that excess lung cancer in asbestos workers is due to asbestosis (scarring of the lung caused by asbestos) rather than to asbestos exposure itself. The authors argued that the seven cohorts Weiss used for comparison, which showed neither more asbestosis nor more lung cancer, had weaknesses. Some had too few deaths, and some had rapid worker turnover. They cited an earlier study (Hillerdal) that reported a lung cancer SMR of 1.4 among people with pleural plaques independent of asbestosis. They also cited an expert estimate that lung cancer risk is roughly doubled at a cumulative exposure of 25 fiber-years, a level at which asbestosis may or may not be present. The authors agreed that people with asbestosis have a high risk of dying from lung cancer. They concluded, in their opinion, that the hypothesis that excess risk occurs only among workers with asbestosis is insufficient to explain the heightened risk.

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: Editorial commentary on a review by Weiss of asbestos cohort studies (no new data collected)
• Who was studied: No study population of its own; the editorial discusses the 39 cohort reports reviewed by Weiss, focusing on the seven comparison cohorts
• Exposure: Occupational asbestos exposure and asbestosis, with pleural plaques also discussed, in relation to lung cancer
• Main results:
  • The authors argued that the seven comparison cohorts Weiss used had their own weaknesses, and that in some instances their inclusion appeared forced
  • The authors noted that two of the seven comparison cohorts had populations with rapid worker turnover, making a workplace-related effect hard to identify
  • Citing an earlier study (Hillerdal), the authors reported that people with pleural plaques independent of asbestosis had an SMR for lung cancer of 1.4
  • The authors stated that Weiss's calculated relative risk for workers aged 40 to 69 appeared to be in error, because age had been mistaken for years from first exposure
  • Citing an expert consensus report, the authors stated that the relative risk for lung cancer is roughly doubled for cohorts at a cumulative exposure of 25 fiber-years, a level at which asbestosis may or may not be present
  • The authors agreed that patients with clinical and radiographic evidence of asbestosis have a high risk of dying from lung cancer
• The authors' conclusion: The authors concluded, in their opinion, that the hypothesis that excess lung cancer in asbestos-exposed workers occurs only among those with asbestosis is insufficient to explain the heightened risk. They stated that asbestosis is an indicator of high exposure and adds risk beyond that of sufficient asbestos exposure alone.
• Limitations the authors state:
  • The authors noted that none of the papers they discussed in detail were designed to define the interaction between asbestos exposure, asbestosis, and lung cancer

Topics

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

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Lung Cancer, Cohort Study, Relative Risk, Pleural Plaques, Chest X-Ray, Cumulative Exposure, Fiber Year.

Related studies

• Asbestosis: a marker for the increased risk of lung cancer among workers exposed to asbestos — W. Weiss (1999)
• Does asbestos exposure cause airway obstruction, in the absence of confirmed asbestosis? — J. Ameille, M. Letourneux, et al. (2010)
• Pleural plaques and asbestosis: dose- and time-response relationships based on HRCT data — C. Paris, S. Thierry, et al. (2009)
• Chrysotile-induced asbestosis: changes in the free cell population, pulmonary surfactant and whole lung tissue of rats — T.D. Tetley, P.M. Hext, et al. (1976)
• Is asbestos or asbestosis the cause of the increased risk of lung cancer in asbestos workers? — K. Browne (1986)
• The natural history of asbestosis in former crocidolite workers of Wittenoom Gorge — W. Cookson, N. De Klerk, et al. (1986)

Browse more research in Chest, or return to medical research.