possible effect, the results from studies of urinary cotinine are used here to adjust for the proportion of self-reported “unexposed” nonsmokers who, in fact, may have been exposed to ETS.
The only source of cotinine or nicotine in body fluids is tobacco smoke exposure. Therefore, urinary cotinine provides an objective measure of (recent) exposure. It has been reported (Jarvis et al., 1984; Wald et al., 1984) that urinary nicotine and cotinine are 3 times as high in “exposed” nonsmoking spouses of current smokers than in “unexposed” nonsmoking spouses of current nonsmokers. For example, Wald and Ritchie (1984) report urinary cotinine in the ratio 1:3:215 for “unexposed” nonsmokers, ETS-exposed nonsmokers, and regular smokers, respectively.
Several assumptions need to be made to permit the use of these data before any quantitative risk computation can be made:
Current smoking patterns reflect past patterns.
Cotinine or nicotine concentrations in the urine are linearly related to recent exposures to ETS and to the carcinogens in ETS among nonsmokers.
All subjects in the various studies began to be exposed to ETS at the same age and have continued to be exposed at the same rate throughout the follow-up period.
The excess relative risk for lung cancer in nonsmokers is proportional to the dose (in cigarette equivalents) of ETS absorbed.
An assumption of a linear dose-response relationship implies that if the risk (i.e., mortality rate) at a given age (t) for a specific calendar period(s), given some absorbed dose (d), then γ(t,s|d)
This equation expresses the risk as equal to the base mortality risk, γ0(t,8), for a truly unexposed person for the same age and calendar period, multiplied by an excess relative risk that increases linearly with dose, i.e. (1+βd), where β is the amount of increase