Abstract
Epidemiological studies of active smokers have shown that the duration of smoking has a much greater effect on lung cancer risk than the amount smoked. This observation suggests that passive smoking might be much more harmful than would be predicted from measures of the level of exposure alone, as it is often of very long duration frequently beginning in early childhood. In this paper we have investigated this using a multistage model with five stages. The model is shown to provide an excellent fit to data on the incidence of lung cancer among smokers, ex-smokers and non-smokers in a cohort of male British doctors. Contrary to our expectation the model predicted only a slight increase in relative risk with increasing duration of passive exposure. Allowing for exposures early in life does not therefore explain the discrepancy between the relative risk of about 1.5 calculated from epidemiological studies of lung cancer and the low levels of exposure indicated by cotinine measurements in those passively exposed.
Highlights
For example heavy smokers (30 cigarettes per day) of 15 years duration have been shown to have only about one tenth the excess lung cancer risk of moderate smokers (15 cigarettes per day) who have smoked for 30 years, the total number of cigarettes smoked is the same (Peto & Doll, 1984). This observation suggests that exposure to tobacco smoke at the low levels incurred during passive smoking might be much more harmful than would be predicted from measures of the level of the exposure alone, as passive exposure is often of very long duration frequently beginning in early childhood
In this paper we have investigated the possible effects of such long duration exposure to passive smoking starting in childhood by modelling the effect of cigarette smoke on lung cancer incidence using a multistage model, and compared the estimates so obtained to those observed in epidemiological studies
The general effect of making the allowance for passive smoking is a small increase in the predicted relative risks which is of the order of 10 to 20% for passive smoking exposures of half to one cigarette per day equivalent
Summary
The idea that a cancer is generated only after a cell has undergone a series of distinct, ordered, transformations or 'stages' was introduced to explain the observation that the mortality rates for many sites of cancer that are epithelial in origin increase as the fourth, fifth, or sixth power of age. The model as proposed originally by Armitage & Doll (1961) is the best known formulation and a brief description of it is given in the Appendix In this formulation, if there are k stages involved for the cancer in question ., stage k=cancer cell), we denote the probability that a cell which is at stage i-I transforms into stage i in unit time as a ai, i=l,...,k According to this model, if these ai remain constant throughout life, and if the time for a fully transformed malignant cell to grow into a clinically detectable tumour is ignored, the incidence rate at age t will be proportional to tk-'. When attention is restricted to smokers of cigarettes only, who have a record of unchanging smoking habits, the relation between lung cancer incidence and number of cigarettes smoked per day is greater than linear, see Figure 2, and this provides additional evidence that more than one stage in the process is affected (Doll & Peto, 1978)
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