several orders of magnitude higher. A possible, although unlikely, explanation is that the measurements of BaP levels in ETS (summarized in Table 2–10) inappropriately reflect total environmental BaP, which includes contributions from cooking, coal burning, and other sources, and that the contribution of BaP from ETS to total BaP is of the order of 2% or less.
The large uncertainty in d0 seen in Table D-4 restricts the utility of these dosimetric calculations, especially given the lack of knowledge concerning the identity of the active carcinogens in ETS and mainstream smoke. In fact, the limitations of our dosimetric data may be even more serious than Table D-4 would lead one to believe. Specifically:
the range of values entered in Table D-4 for NDMA could actually be orders of magnitude too high (see step 4 of Remark 11),
the range of values for RSP and BaP do not reflect differences between the particulate phase of ETS and that of mainstream smoke with regard to deposition sites, clearance rates, and particle size,
the range of values given for BaP in Table D-4 could be orders of magnitude too high if, as discussed above, the BaP entries in Table 2–10 represent the total environmental BaP inhaled by a nonsmoker, and
the ratio of urinary nicotine (or cotinine) in nonsmokers to that in active smokers may not reflect, even qualitatively, the ratio of the biologically effective dose of active lung carcinogen absorbed by nonsmokers to the dose absorbed by active smokers (see Remark 12).
An estimate of the total number of lung cancer deaths among lifelong nonsmoking women in 1985 is ∑t I0(t)N(t), where N(t) is the number of nonsmoking women at risk at age t in 1985 and I0(t) is the age-specific lung cancer death rate among nonsmoking women in 1985. Data on I0(t) are given in Garfinkel (1981) for 1972; thus, this may be somewhat inaccurate for 1985. National Health Interview Survey data on N(t) were made available from