Asbestos and lung cancer: an analysis of the epidemiological evidence on the asbestos-smoking interaction

Our plain-English summary of Asbestos and lung cancer: an analysis of the epidemiological evidence on the asbestos-smoking interaction, by R. Saracci (International Journal of Cancer, 1977).

The study

• Author: R. Saracci
• Journal: International Journal of Cancer
• Published: 1977;20(3):323-31
• Cited by: 167 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M nos. 001049, 002251).

Abstract

Three simple models for the asbestos-smoking interaction on human lung cancer production are considered. In the first model the excess incidence of lung cancer independently due to asbestos and to smoking adds together when both agents are present (additive model). In the second the addition of each one of the two agents produces an effect (increase in lung cancer incidence) which is proportional to the effect of the other (multiplicative model). In the third, asbestos can only increase lung cancer incidence in the presence of smoking. As previously found by other investigators, the additive model appears the least plausible in the light of the data from two published epidemiological studies. A discrimination between the other two models is attempted through a detailed analysis of the five published epidemiological studies today available which provide information on occupational asbestos exposure, smoking habits and lung cancer risk. Although the data do not allow a definitive discrimination, the multiplicative model appears to be more plausible, being also consistent with a multi-stage carcinogenic mechanism and with evidence from animal (rat) experiments. It is relevant both for biology and for public health that in this model asbestos and smoking are regarded as independently capable of producing lung cancer in humans and that they act synergistically when exposure to both occurs.

In plain English

This 1977 article from the International Agency for Research on Cancer was a review and re-analysis of published studies of asbestos-exposed workers. It asked how asbestos and smoking combine to cause lung cancer. The author compared three models: the two effects add together, they multiply, or asbestos raises lung cancer only in smokers. Earlier analyses of insulation and factory workers gave some evidence that the adding model fit poorly. The author re-analyzed studies of Quebec chrysotile miners, three groups of insulation workers, asbestos factory workers and a hospital case-control study. No data set examined refuted the multiplicative model at p = 0.05. Among never-smoking women with severe factory exposure, the standardized mortality ratio was 8.5 (95% confidence limits 1.2 to 36.1). The author read this as contradicting the model in which asbestos acts only in smokers. The author concluded that the multiplicative model was the more plausible: asbestos and smoking can each cause lung cancer on their own and act synergistically together. The author noted that the data were too limited for a clear-cut choice, mainly because smoking information was incomplete and non-smoker groups were small.

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: Review and statistical re-analysis of published epidemiological studies (mortality studies and one case-control study), testing three models of how asbestos and smoking interact in causing lung cancer
• Who was studied: Workers in previously published studies, all occupational. They were 5,958 Quebec chrysotile miners followed 1950 to 1955 (from 6,091 male workers), 370 New York-New Jersey insulation workers, 17,800 US-Canada insulation workers, 170 Belfast insulation and pipe-covering workers, 1,834 male and 658 female asbestos factory workers, and a case-control study of 201 men with bronchial carcinoma and 201 matched controls. Canadian chrysotile and Finnish anthophyllite mine studies were mentioned but could not be analyzed.
• Exposure: Occupational asbestos exposure together with smoking habits. Fibers were chrysotile for the Quebec miners, chrysotile and amosite for the US insulation workers, and chrysotile, amosite and crocidolite for the Belfast insulators and the factory. The case-control study involved some exposure among men who had never worked in asbestos manufacturing.
• Main results:
  • Earlier fits of the additive model to insulation and factory worker data showed fewer observed than expected lung cancer deaths in non-smokers. This suggested a joint effect greater than additive.
  • Quebec chrysotile miners: 9 'proved' lung cancer deaths were observed against 3.1 expected from Quebec Province rates, an SMR of 2.9 with 95% confidence limits 1.3 and 5.9.
  • Quebec miners, after correcting expected values for smoking: the SMR for 'proved' cases was 3.1 (1.4-5.9) in smokers and 0 (0-18.4) in non-smokers. There was no indication that the asbestos-related relative risk differed between the two groups.
  • 370 insulation workers, first report: the SMR was 8.1 (5.2-12.0) in smokers (24 observed) and 0 (0-73.8) in non-smokers (0 observed), giving a common SMR of 7.9 (5.1-11.8).
  • 370 insulation workers at 11 years: smokers had 45 observed against 7.47 expected, an SMR of 6.0 (4.4-8.1). Non-smokers had 0 observed, an SMR of 0 (0-24.6). The common SMR was 5.90 (4.3-7.9).
  • 17,800 US-Canada insulation workers: smoking habits were unknown for one person in three. 94 lung cancer deaths occurred in that group, against one among non-smokers. The joint effect could therefore not be assessed reliably.
  • Belfast insulation workers: 28 respiratory cancer deaths were observed against 1.64 expected, none among the five non-smokers. The author judged no inference about smoking possible.
  • Factory workers, low-moderate exposure: the SMRs were not significantly different from 1 in any smoking category.
  • Factory workers, severe exposure: never-smoking women had 2 observed lung cancer deaths (1.7 adjusted) against 0.2 expected, an SMR of 8.5 (1.2-36.1). The author took this as refuting the idea that non-smokers' risk is not increased.
  • Case-control study: some asbestos exposure was reported by 58/201 (28.9%) cases and 29/201 (14.4%) controls. The relative risk across all smoking classes was 2.35 (1.39-3.97). The apparent rise in relative risk with heavier smoking was not statistically significant.
• The authors' conclusion: The author concluded that, on the evidence then available, the multiplicative model was the more plausible explanation. In it, asbestos and smoking are each independently capable of producing lung cancer and act synergistically when both are present. The author also cited consistency with multi-stage carcinogenesis and with rat inhalation experiments.
• Limitations the authors state:
  • The data were not adequate to discriminate clearly even between the three simple models.
  • The studies differed in asbestos exposure (intensity, duration, fiber type), in design, and in how smoking and exposure were defined and ascertained.
  • Partial ascertainment of smoking habits and small numbers of non-smokers limited the analysis.
  • The studies used external populations, rather than non-smoking workers not exposed to asbestos, as the reference.
  • Comparing indirectly standardized SMRs between smokers and non-smokers in this review may introduce a bias from differences in age structure.
  • Looking at non-smokers alone in the miner and insulator studies, an asbestos relative risk of 1 (no increase) could not be ruled out.

Topics

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

Medical terms in this study, explained in our Lexicon: Lung Cancer, Asbestos Exposure, Habit, Carcinogenic.

Related studies

• Absence of synergism between exposure to asbestos and cigarette smoking in asbestosis — J.M. Samet, G.R. Epler, et al. (1979)
• Interaction of asbestos, age, and cigarette smoking in producing radiographic evidence of diffuse pulmonary fibrosis — K.H. Kilburn, R. Lilis, et al. (1986)
• The interactions of tobacco smoking and other agents in cancer etiology — R. Saracci (1987)
• Epidemiological evidence indicates asbestos causes laryngeal cancer — A.H. Smith, M.A. Handley, et al. (1990)
• The interaction of asbestos and smoking in lung cancer: a modified measure of effect — G. Berry, F.D. Liddell (2004)
• Low-dose exposure to asbestos and lung cancer: dose-response relations and interaction with smoking in a population-based case-referent study in Stockholm, Sweden — P. Gustavsson, F. Nyberg, et al. (2002)

Browse more research in International Journal of Cancer, or return to medical research.