After Helsinki: a multidisciplinary review of the relationship between asbestos exposure and lung cancer, with emphasis on studies published during 1997-2004

Our plain-English summary of After Helsinki: a multidisciplinary review of the relationship between asbestos exposure and lung cancer, with emphasis on studies published during 1997-2004, by D.W. Henderson, K. Rödelsperger, H.J. Woitowitz, et al (Pathology, 2004).

The study

• Authors: D.W. Henderson, K. Rödelsperger, H.J. Woitowitz, J. Leigh
• Journal: Pathology
• Published: 2004;36(6):517-50
• Type of article: Review
• Cited by: 75 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Despite an extensive literature, the relationship between asbestos exposure and lung cancer remains the subject of controversy, related to the fact that most asbestos-associated lung cancers occur in those who are also cigarette smokers: because smoking represents the strongest identifiable lung cancer risk factor among many others, and lung cancer is not uncommon across industrialised societies, analysis of the combined (synergistic) effects of smoking and asbestos on lung cancer risk is a more complex exercise than the relationship between asbestos inhalation and mesothelioma. As a follow-on from previous reviews of prevailing evidence, this review critically evaluates more recent studies on this relationship--concentrating on those published between 1997 and 2004--including lung cancer to mesothelioma ratios, the interactive effects of cigarette smoke and asbestos in combination, and the cumulative exposure model for lung cancer induction as set forth in The Helsinki Criteria and The AWARD Criteria (as opposed to the asbestosis-->cancer model), together with discussion of differential genetic susceptibility/resistance factors for lung carcinogenesis by both cigarette smoke and asbestos. The authors conclude that: (i) the prevailing evidence strongly supports the cumulative exposure model; (ii) the criteria for probabilistic attribution of lung cancer to mixed asbestos exposures as a consequence of the production and end-use of asbestos-containing products such as insulation and asbestos-cement building materials--as embodied in The Helsinki and AWARD Criteria--conform to, and are further consolidated by, the new evidence discussed in this review; (iii) different attribution criteria (e.g., greater cumulative exposures) are appropriate for chrysotile mining/milling and perhaps for other chrysotile-only exposures, such as friction products manufacture, than for amphibole-only exposures or mixed asbestos exposures; and (iv) emerging evidence on genetic susceptibility/resistance factors for lung cancer risk as a consequence of cigarette smoking, and potentially also asbestos exposure, suggests that genotypic variation may represent an additional confounding factor potentially affecting the strength of association and hence the probability of causal contribution in the individual subject, but at present there is insufficient evidence to draw any meaningful conclusions concerning variation in asbestos-mediated lung cancer risk relative to such resistance/susceptibility factors.

In plain English

This article was a narrative review, not a new study. The authors re-examined published research on asbestos and lung cancer, concentrating on studies published between 1997 and 2004. Topics included lung cancer to mesothelioma ratios, how smoking and asbestos combine, and whether lung cancer should be attributed to asbestos only when asbestosis (asbestos-related lung scarring) is present, or according to cumulative exposure as in The Helsinki Criteria. The authors argued against requiring asbestosis. They cited a study of South Carolina textile workers in which lung cancer rates rose at exposures too low to cause asbestosis visible under the microscope. The Helsinki Criteria treat 25 fibre-years of exposure as roughly doubling lung cancer risk. After Germany adopted this standard, compensated lung (plus laryngeal) cancers outnumbered mesotheliomas, at 1.24 to 1 for 1995 to 2000. The authors concluded that the evidence strongly supports the cumulative exposure model. They also concluded that higher exposure thresholds are appropriate for chrysotile mining and milling, and perhaps for other chrysotile-only work. Finally, they concluded that genetic data are not yet adequate to adjust attribution for individuals.

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: Multidisciplinary narrative review of published studies (epidemiological, lung fibre-burden, pathological, genetic and laboratory)
• Who was studied: No new study population. The review covered published studies on asbestos and lung cancer, with emphasis on those published 1997 to 2004
• Exposure: Occupational and environmental asbestos exposure (chrysotile, amphiboles including amosite, crocidolite and tremolite, and mixed exposures), alone and combined with cigarette smoke
• Main results:
  • The authors argued against the view that asbestosis must be present before lung cancer can be attributed to asbestos. They cited a published study of South Carolina chrysotile textile workers: among white males, the SMR was 2.59 and the standardised risk ratio was 2.63 (95% CI 1.20 to 5.75) at 2.7 to 6.8 fibres/mL-years. That exposure was below the level at which a separate autopsy study of the same cohort found histological asbestosis.
  • The review described The Helsinki Criteria, which state that relative risk of lung cancer is roughly doubled at a cumulative exposure of 25 fibre-years or an equivalent occupational history, with or without asbestosis.
  • In Germany, after a 25 fibre-year compensation standard was introduced in 1992, the ratio of compensated asbestos-related lung cancers (plus laryngeal cancers since 1997) to mesotheliomas rose to 1.24:1 for 1995 to 2000. The UK figure for the same period was 0.07:1.
  • From a cited pooled analysis of German case-referent data, 25 fibre-years corresponded to a lung cancer odds ratio of 1.99 (95% CI 1.20 to 3.30).
  • From a cited Stockholm case-referent study (Gustavsson et al.) of mainly low-dose chrysotile exposure, the calculated lung cancer risk at 4.0 fibres/mL-years was 1.90 (95% CI 1.32 to 2.74).
  • The review reported the Hodgson and Darnton estimates of the increase in lung cancer risk per fibre/mL-year: 4.2% for crocidolite and 5.2% for amosite, a summary estimate of 0.062% for chrysotile cohorts dominated by Quebec miners, and 0.47% for mixed exposures. The authors argued that the mixed-exposure figure does not necessarily apply to broader end-use exposures.
• The authors' conclusion: The authors concluded that the evidence strongly supports the cumulative exposure model. They concluded that The Helsinki and AWARD Criteria fit the newer evidence for mixed exposures such as insulation and asbestos-cement products. They held that different criteria (e.g. greater cumulative exposures) are appropriate for chrysotile mining/milling and perhaps for other chrysotile-only exposures such as friction products manufacture. They found the evidence on genetic susceptibility insufficient to draw meaningful conclusions.
• Limitations the authors state:
  • The authors stated that existing genetic susceptibility/resistance data cannot yet be applied to attribution in individual patients, because the data are contradictory and inadequate.
  • The authors noted that retrospective assessment of asbestos exposure is a major problem in the case-referent studies reviewed, especially at low exposures.
  • The authors noted that meta-analyses of heterogeneous published studies are of limited use for estimating dose-response.

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, Mesothelioma, Cumulative Exposure, Helsinki Criteria, Carcinogenesis, Attribution, Asbestos-Cement.

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