The risk of lung cancer in cigarette smokers is directly related to the number of cigarettes smoked. At low-to-average levels of smoking, this relationship is approximately linear and with no apparent threshold, although there are good theoretical reasons to believe that the true dose-response curve should be curvilinear and probably quadratic (Doll and Peto, 1978; Gart and Schneiderman, 1979). Among smokers, an increase in exposure leads to an increase in risk, as long as the additional tobacco smoke, whether through active or passive smoking, reaches the bronchial epithelium. Passive smoking would, therefore, be expected to cause some increase in risk of lung cancer in active smokers, as well as in any other persons in whom the appropriate tissues are exposed.
The studies reviewed in this chapter have attempted to address the questions of whether an increase in risk of lung cancer does occur in nonsmokers exposed to ETS and whether the dose-response relationship is similar to that in smokers. In part, this depends on whether there is a threshold dose of cigarette smoke exposure below which there is no increase in risk. Biological theory and current evidence on low-dose exposure to carcinogens do not provide evidence for such a threshold, and it is generally thought that one is unlikely (Office of Science and Technology Policy, 1985). If there is no threshold, it follows that exposure to tobacco smoke at low concentrations, such as that experienced by nonsmokers exposed to ETS, will cause an increased risk of lung cancer. The risk, of course, will be expected to be very much smaller than that associated with active smoking because of the much lower exposure of the bronchial epithelium to tobacco smoke.