An experimental and theoretical investigation is made into the range and nature of the exposure of the nonsmoking public to respirable suspended particulates from cigarette smoke. A model incorporating both physical and sociological parameters is shown to be useful in understanding particulate levels from cigarette smoke in indoor environments. Observed levels of particulates correlate with the predictions of the model. It is shown that nonsmokers are exposed to significant air pollution burdens from indoor smoking. An assessment of the public health policy implications of these burdens is presented.

A molecular structure investigation of the enol and keto tautomers of acetylacetone has been carried out by electron diffraction. It was found that the concentration of the enol form in the sample of the vapor at 105°w as 66 ± 5%. The enol tautomer contains a short internal hydrogen bond, • • O = 2.381 ± 0.020 Á, which appears to be linear and symmetric. The hydrogen bond is part of a planar ring in which the bonded distances,

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Environmental tobacco smoke (ETS) has recently been determined by U.S. environmental and occupational health authorities to be a human carcinogen. We develop a model which permits using atmospheric nicotine measurements to estimate nonsmokers' ETS lung cancer risks in individual workplaces for the first time. We estimate that during the 1980s, the U.S. nonsmoking adult population's median nicotine lung exposure (homes and workplaces combined) was 143 micrograms (micrograms) of nicotine daily, and that most-exposed adult nonsmokers inhaled 1430 micrograms/day. These exposure estimates are validated by pharmacokinetic modeling which yields the corresponding steady-state dose of the nicotine metabolite, cotinine. For U.S. adult nonsmokers of working age, we estimate median cotinine values of about 1.0 nanogram per milliliter (ng/ml) in plasma, and 6.2 ng/ml in urine; for most-exposed nonsmokers, we estimate cotinine concentrations of about 10 ng/ml in plasma and 62 ng/ml in urine. These values are consistent to within 15% of the cotinine values observed in contemporaneous clinical epidemiological studies. Corresponding median risk from ETS exposure in U.S. nonsmokers during the 1980s is estimated at about two lung cancer deaths (LCDs) per 1000 at risk, and for most-exposed nonsmokers, about two LCDs per 100. Risks abroad appear similar. Modeling of the lung cancer mortality risk from passive smoking suggests that de minimis [i.e., "acceptable" (10(-6))], risk occurs at an 8-hr time-weighted-average exposure concentration of 7.5 nanograms of ETS nicotine per cubic meter of workplace air for a working lifetime of 40 years. This model is based upon a linear exposure-response relationship validated by physical, clinical, and epidemiological data. From available data, it appears that workplaces without effective smoking policies considerably exceed this de minimis risk standard. For a substantial fraction of the 59 million nonsmoking workers in the U.S., current workplace exposure to ETS also appears to pose risks exceeding the de manifestis risk level above which carcinogens are strictly regulated by the federal government.

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