Urine cotinine underestimates exposure to the tobacco-derived lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in passive compared with active smokers.
Urine cotinine underestimates exposure to the tobacco-derived lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in passive compared with active smokers.
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DOI:
10.1158/1055-9965.epi-10-0497
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发表时间:
2010-11
期刊:
影响因子:
--
通讯作者:
Jacob P 3rd
中科院分区:
文献类型:
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作者:
Benowitz N;Goniewicz ML;Eisner MD;Lazcano-Ponce E;Zielinska-Danch W;Koszowski B;Sobczak A;Havel C;Jacob P 3rd
Cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) are widely used biomarkers for tobacco-derived nicotine and the lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), respectively. The discrepancy between cotinine levels in relation to disease risk comparing active vs. passive smoking suggests a non-linear tobacco smoke dose-response and/or that cotinine is not providing an accurate measure of exposure to tobacco smoke toxic constituents from secondhand smoke. Cotinine and NNAL were measured in urine of 373 active smokers and 228 passive smokers. Average cotinine levels were 1,155 (IQR 703-2,715) for active smokers and 1.82 (0.45-7.33) ng/mg creatinine for passive smokers. Average NNAL levels were 183 (103-393) and 5.19 (2.04-11.6) pg/mg creatinine, respectively. NNAL/cotinine ratio in urine was significantly higher for passive smokers when compared to active smokers (2.85×103 vs. 0.16×103, p<0.0001). Passive smoking is associated with a much higher ratio of NNAL/cotinine in the urine compared to active smoking. Cotinine measurement leads to an underestimation of exposure to the carcinogen NNK from second-hand smoke when compared with active smoking.