Metabolites of a tobacco-specific lung carcinogen in nonsmoking casino patrons

Abstract

Epidemiologic data have shown increased risks of lung cancer in nonsmokers exposed to environmental tobacco smoke (ETS). We measured biomarkers in urine samples from nonsmokers before and after a 4-h visit to a casino where smoking is allowed. The tobacco-specific lung carcinogen, NNK [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone] is a constituent of ETS. Urinary metabolites of NNK, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) and its glucuronides (NNAL-Gluc), are excellent biomarkers of human uptake of NNK and NNAL. NNAL, as with NNK, is a potent pulmonary carcinogen. Subjects collected a spot urine sample before the casino visit and all urine samples for the 24-h period starting after the visit. We analyzed samples for creatinine, total cotinine (cotinine and cotinine-glucuronide), and total NNAL (NNAL plus NNAL-Gluc). Paired samples showed statistically significant mean increases in total cotinine (0.044 nmol/mg creatinine, P < 0.0001) and total NNAL (0.018 pmol/mg creatinine, P < 0.001). These findings demonstrate that exposure of nonsmokers to ETS in a commercial setting results in uptake of a tobacco-specific lung carcinogen.