Biomonitoring of environmental tobacco smoke (ETS)-related exposure to 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)

The exposure of non-smokers to the tobacco-specific N-nitrosamine 4-(N-meth ylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a rodent lung carcinogen, wa s determined in the air of various indoor em environments as well as by bio monitoring of nonsmokers exposed to environmental tobacco smoke (ETS) under real-life conditions using the urinary NNK metabolites 4-(N-methylnitrosam ino)-1-(3-pyridyl)-1-(NNAL) and [4-(N-methylnitrosamino)-1-(3-pyridyl)but-1 -yl]-beta-O-D-glucosiduronic acid (NNAL-Gluc). NNK was not delectable (< 0. 5 ng m(-3)) in 11 rooms in which smoking did not occur. The mean NNK concen tration in 19 rooms in which smoking took place was 17.5 (2.4-50.0) ng m(-3 ). The NNK levels significantly correlated with the nicotine levels (r = 0. 856; p < 0.0001). Of the 29 non-smokers investigated, 12 exhibited no detec table NNAL and NNAL-Gluc excretion (< 3 pmol day) in their urine. The mean urinary excretion of NNAL and NNAL-Gluc of the 17 remaining non-smokers was 20.3 (< 3-63.2) and 22.9 (< 3-90.0) pmol day(-1), respectively. Total NNAL excretion (NNAL + NNAL-Gluc) in all non-smokers investigated significantly correlated with the amount of nicotine on personal samplers worn during th e week prior to urine collection (r = 0.88; < 0.0001) and with the urinary cotinine levels (r = 0.40; p = 0.038). No correlation was found between NNA L excretion and the reported extent of ETS exposure. Average total NNAL exc retion in the non-smokers with detectable NNAL levels was 74 times less tha n in 20 smokers who were also investigated. The cotinine/total NNAL ratios in urine of smokers (9900) and non-smokers (9300) were similar. This appear s to beat variance with the ratios of the corresponding precursors (nicotin e/NNK) in mainstream smoke (16400) and ETS (1000). Possible reasons for thi s discrepancy are discussed. The possible role of NNK as a lung carcinogen in non-smokers is unclear, especially since NNK exposure in non-smokers is several orders of magnitude lower than the ordinary exposure to exogenous a nd endogenous N-nitrosamines and the role of NNK as a human lung carcinogen is not fully understood.