Interaction between tobacco smoking and occupational exposures in the causation of lung cancer

Our plain-English summary of Interaction between tobacco smoking and occupational exposures in the causation of lung cancer, by K. Steenland, M. Thun (Journal of Occupational Medicine., 1986).

The study

• Authors: K. Steenland, M. Thun
• Journal: Journal of Occupational Medicine.
• Published: 1986;28(2):110-8
• Type of article: Review
• Cited by: 49 articles, as counted by NIH iCite
• Read it: PubMed
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 000439).

Abstract

The nature of the interaction between smoking and occupational exposure is controversial, in part because of lack of agreement on the definition of interaction and in part because of the scarcity of adequate epidemiologic data. Occupational investigators have assessed interaction primarily as a departure from an additive rather than from a multiplicative model of relative risks (or rate ratios). To determine whether smoking modifies the effect of occupational lung carcinogens, the literature was reviewed for the only four established occupational lung carcinogens for which there are data on smoking: radon daughters, asbestos, arsenic, and chloromethyl ethers. Where possible, departure was assessed from both an additive (synergism) and a multiplicative model (effect modification). Only nine studies were considered to have sufficient sample size and to provide sufficient information on tobacco use and occupational exposure to evaluate interaction. The existing data were contradictory for three of the agents studied: asbestos, radon daughters, and arsenic. Inconclusive or contradictory findings may result from small sample size or lack of comparability of the level of occupational or tobacco exposure. It is noteworthy that, for these four agents, whenever smoking did modify the effect of occupational exposure, the lung cancer rate ratio was greater for nonsmokers (compared to nonexposed nonsmokers) than smokers (compared to nonexposed smokers). However, with the exception of chloromethyl ethers, absolute lung cancer rates were higher for smokers than nonsmokers, regardless of occupational exposure.

In plain English

This article was a review. It reviewed research on whether smoking changes the lung cancer risk from asbestos, radon daughters, arsenic and chloromethyl ethers. Nine studies were judged adequate; where possible, the authors assessed whether results departed from additive and multiplicative models. For asbestos, a study of male insulators suggested no effect modification by smoking, but had only four deaths among nonsmoking asbestos workers. A study of Quebec chrysotile miners and millers pointed to a combined effect between additive and multiplicative. Two factory studies found higher asbestos rate ratios in nonsmokers than in smokers. In one, a factory using only amosite, the rate ratio was 17.50 (95% confidence interval 7.1 to 36.1) for nonsmokers and 4.69 (3.42 to 6.37) for smokers. Radon daughter and arsenic results were also contradictory. For all four agents, whenever smoking modified the effect, the exposure's rate ratio was higher in nonsmokers (versus nonexposed nonsmokers) than in smokers (versus nonexposed smokers). The authors stressed this did not mean smoking "protects" workers, since smokers' absolute lung cancer risk generally stayed higher. They concluded the data could not support definitive conclusions.

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: Literature review of studies on the interaction between smoking and occupational lung carcinogens
• Who was studied: Published studies of workers exposed to four occupational lung carcinogens with smoking data. Nine studies were judged adequate: four on asbestos, two on radon daughters, two on arsenic and one on chloromethyl ethers.
• Exposure: Tobacco smoking combined with radon daughters, asbestos, arsenic, or chloromethyl ethers. The asbestos studies covered insulation workers, Quebec chrysotile miners and millers, a factory using exclusively amosite, and English asbestos factory workers (type of asbestos not reported).
• Main results:
  • In the Hammond et al study of male insulators, the rate ratio for asbestos changed little between smokers and nonsmokers, so there was no effect modification. However, there were only four deaths among nonsmoking asbestos workers, so firm conclusions were impossible.
  • In the Liddell et al nested case-control study of Quebec chrysotile miners and millers, nonsmokers exposed to more than 100 fibers per milliliter-years had an odds ratio of 2.98 (95% CI 1.17 to 7.60). Cigarette smokers exposed to more than 100 fibers per milliliter-years had an odds ratio of 1.66 (95% CI 1.19 to 2.33). Each was compared with the less-exposed group of the same smoking status, and the confidence intervals overlapped. The original authors concluded the combined effect was between additive and multiplicative.
  • In the Selikoff et al 1980 study of 582 men at a factory using exclusively amosite, the lung cancer rate ratio for asbestos was 17.50 (7.1 to 36.1) in nonsmokers and 4.69 (3.42 to 6.37) in smokers. Each was compared with smoking-specific rates of nonasbestos blue-collar workers, and nonsmokers here included pipe and cigar smokers. The reviewers judged these rate ratios significantly different.
  • In the Berry et al study of 1,250 male and 420 female asbestos factory workers (men and women combined), nonsmokers had the highest rate ratio for lung cancer death, 10.0 (2.7 to 25.6). Ex-smokers followed at 4.46 (2.38 to 7.64), then smokers at 2.21 (1.68 to 2.81). Differences between groups were not always significant due to sample size.
  • For radon daughters, Swedish iron ore miners showed a rate ratio of 2.9 (90% CI 2.1 to 3.9) for smoking miners and 10.0 (90% CI 6.5 to 14.8) for nonsmoking miners. The most thorough US uranium miner analysis showed no departure from a multiplicative model.
  • For arsenic, the Pinto et al data suggested effect modification, though this was not statistically significant. The Pershagen et al data did not suggest it.
  • For chloromethyl ethers, a study of 51 men showed effect modification so extreme that the combined rate ratios were less than both multiplicative and additive. The reviewers noted this study was based on an extremely small number of person-years.
  • For all four agents, whenever effect modification was observed, the occupational-exposure rate ratio was higher among nonsmokers (compared to nonexposed nonsmokers) than among smokers (compared to nonexposed smokers).
  • Absolute lung cancer risk remained generally higher in smokers than in nonsmokers.
• The authors' conclusion: The authors concluded that the available data, though nearly all that exists, are clearly insufficient to support definitive conclusions about the interaction between smoking and occupation for lung cancer. They also concluded that higher rate ratios in nonsmokers should not be taken to mean smoking protects workers from occupational exposure.
• Limitations the authors state:
  • Many results rest on such small numbers that the estimates of rate ratios have large variance, so the contradictory findings may not truly be contradictory.
  • Estimates of smoking habits and exposure may be substantially inaccurate. Amount smoked is often not quantified, former smokers and pipe or cigar smokers are classified differently between studies, and dose data are poor.
  • Studies using an internal nonexposed or low-exposed referent group may fail to detect effect modification, because those referents may themselves be at increased risk.
  • The summary table uses point estimates that may vary widely, and it ignores ex-smokers.

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: Occupational Exposure, Causation, Lung Cancer, Relative Risk, rate ratio.

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