Revisiting The Association Between Environmental Tobacco Smoke Exposure And Lung Cancer Risk
We examine in detail arguments put forward to support the claim that exposure to environmental tobacco smoke (ETS) increases the risk of lung cancer in non-smokers. Hackshaw et al. [Br Med J 1997;315:980-988] have esti mated that the risk increases by 23% (95% Cl 14-32%) per 10 cigarettes/day smoked by the husband. The esti mated increase essentially disappears if proper adjust ment is made for smoking misclassification bias, if cor rection is made for the joint effects of confounding by fruit, vegetables, dietary fat and education, if errors in published data in one study are corrected, and if results from all pertinent studies are included (and not just those which report risk by level of smoking by the husband). Taking account of all these factors and using un- weighted estimates of the association between ETS ex posure and the confounding variables (as one very large study reported results discrepant from those for numer ous smaller studies), the risk increase per 10 cigarettes/ day was found to be 2% (95% Cl -3 to +7.5%), based on data from 47 ETS/lung cancer studies. Using weighted estimates, the risk increase was 5.5% (95% Cl 0 to +11 %). Restricting attention to the 36 studies that had adjusted for age, the increase was reduced further to -2% (95% Cl -6 to+3%) using un-weighted estimates, or to + 1 % (95% Cl -4 to +6%) using weighted estimates. These estimates are not materially affected by bias due to the reference group (non-smokers married to non-smokers) having some ETS exposure from other sources. Other sources of potential upward and downward bias, not formally taken account of in the analysis, are discussed. Based on extrapolation from the known lung cancer risk in smok ers, Hackshaw et al. [Br Med J 1997;315:980-988] esti mate that environmental tobacco smoke exposure would be expected to increase the risk of lung cancer in non-smokers by 19%. Using more appropriate assump tions (for the relative exposure to smoke constituents of passive and active smokers, for the lung cancer risk in those who have ever smoked and for the dose-response model) leads to a much lower estimate of about 0.5%. Even this estimate is open to question as a threshold might exist for the effects of tobacco smoke constituents on lung cancer risk. Whether or not a true risk exists, it is clear that this is not demonstrated by the overall evi dence. The true increase in risk per 10 cigarettes/day smoked by the husband is very unlikely to be as large as 23%. It might be as much as 5%, but it could well be 1 % or less, or even zero.