Wald and Ritchie (1984) have shown that “unexposed” individuals have, on average, 8.5 ng/ml of cotinine in their urine. Since virtually the only source of cotinine or nicotine in body fluids is tobacco products, primarily through tobacco smoke exposures, it follows that “unexposed” individuals are exposed to ETS. For this reason, whenever we refer to such “unexposed” subjects, we place the word “unexposed” in quotation marks. If the “unexposed” subjects have, in fact, been exposed to ETS, the observed relative risk of 1.3 would be an underestimate of the true adverse effect of ETS on “exposed” individuals. The correct measure of the adverse effect of ETS on “exposed” individuals would be the ratio of the lung cancer mortality rate in “exposed” individuals to the rate in truly unexposed individuals (which we shall call the true relative risk in the “exposed”).

In Section D-1, we use the data collected by Wald and Ritchie (1984) on levels of urinary cotinine in “exposed” and “unexposed” individuals to estimate this true relative risk by two different methods.

In Section D-2, we combine the existing epidemiologic data on active smokers with data on nonsmokers exposed to ETS to estimate the ETS exposure of an average nonsmoker in cigarette-equivalents per day. Additionally, we compare this estimate to independent estimates of ETS exposure based on (1) levels of respirable suspended particulates (RSP), benzo[a]pyrene (BaP), and N-nitrosodimethylamine (NDMA) in ETS and in mainstream smoke and (2) levels of urinary cotinine and nicotine in active smokers and nonsmokers.

In Section D-3, we compute how many of the lung cancer deaths estimated to occur among (lifelong) nonsmoking persons in 1985 might be attributable to ETS. The estimate is made separately for women and for men.

Many environmental exposures are regulated to a level where the anticipated lifetime risk of death attributable to exposure is less than 1 in 100,000 or 1 in 1,000,000. In Section D-4, we consider whether the lifetime risk of death (from lung cancer) attributable to ETS among nonsmokers with moderate ETS exposure is in excess of 1 in 100,000. (Although we do not estimate the lifetime risk of death attributable to ETS from causes other than lung cancer, this does not imply that we believe that lung cancer is the only cause of mortality influenced by ETS exposure. The decision to restrict the analysis to lung cancer mortality reflects the fact

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