A TOBACCO-SPECIFIC LUNG CARCINOGEN IN THE URINE OF MEN EXPOSED TO CIGARETTE-SMOKE

Background. Environmental tobacco smoke has been classified by the Env ironmental Protection Agency as a carcinogen causally associated with lung cancer in adults, but there have been no reports of lung carcinog ens or their metabolites in the body fluids or tissues of nonsmokers e xposed to environmental tobacco smoke. Methods. Five male nonsmokers w ere exposed to sidestream cigarette smoke generated by machine smoking of reference cigarettes tor 180 minutes on each of two days, six mont hs apart. Sidestream smoke is the smoke that originates from the smold ering end of a cigarette between puffs. Twenty-four-hour urine samples were collected before and after exposure. The urine samples were anal yzed for 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronide, which are metabolites of 4-(methylnitrosamino)-1-(3-pyrid yl)-1-butanone (NNK), a powerful lung carcinogen in rodents. NNAL is a lso a lung carcinogen in rodents.Results. The urinary excretion of the metabolites increased after exposure to sidestream smoke in all the m en. The mean (+/-SD) amount of NNAL and NNAL glucuronide was significa ntly higher after exposure than at base line (33.9+/-20.0 vs. 8.4+/-11 .2 ng per 24 hours [127+/-74 vs. 31+/-41 pmol per day], P<0.001) and w as correlated with urinary cotinine excretion (r = 0.89, P<0.001). The nicotine concentrations in the air to which the men were exposed were comparable to those in a heavily smoke-polluted bar. Conclusions. Non smokers exposed to sidestream cigarette smoke take up and metabolize a lung carcinogen, which provides experimental support for the proposal that environmental tobacco smoke can cause lung cancer.