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- Pebbles Fagan, Pallav Pokhrel, Thaddeus A Herzog, Ian S Pagano, Adrian A Franke, Mark S Clanton, Linda A Alexander, Dennis R Trinidad, Kari-Lyn K Sakuma, Carl A Johnson, and Eric T Moolchan.
- Cancer Prevention and Control Program, University of Hawaii Cancer Center, University of Hawaii at Manoa, Honolulu, HI; pfagan@cc.hawaii.edu.
- Nicotine Tob. Res. 2016 Apr 1; 18 (4): 437-46.
IntroductionMenthol cigarette smoking may increase the risk for tobacco smoke exposure and inhibit nicotine metabolism in the liver. Nicotine metabolism is primarily mediated by the enzyme CYP2A6 and the nicotine metabolite ratio (NMR = trans 3' hydroxycotinine/cotinine) is a phenotypic proxy for CYP2A6 activity. No studies have examined differences in this biomarker among young adult daily menthol and nonmenthol smokers. This study compares biomarkers of tobacco smoke exposure among young adult daily menthol and nonmenthol smokers.MethodsSaliva cotinine and carbon monoxide were measured in a multiethnic sample of daily smokers aged 18-35 (n = 186). Nicotine, cotinine, the cotinine/cigarette per day ratio, trans 3' hydroxycotinine, the NMR, and expired carbon monoxide were compared.ResultsThe geometric means for nicotine, cotinine, and the cotinine/cigarette per day ratio did not significantly differ between menthol and nonmenthol smokers. The NMR was significantly lower among menthol compared with nonmenthol smokers after adjusting for race/ethnicity, gender, body mass index, and cigarette smoked per day (0.19 vs. 0.24, P = .03). White menthol smokers had significantly higher cotinine/cigarettes per day ratio than white nonmenthol smokers in the adjusted model. White menthol smokers had a lower NMR in the unadjusted model (0.24 vs. 0.31, P = .05) and the differences remained marginally significant in the adjusted model (0.28 vs. 0.34, P = .06). We did not observe these differences in Native Hawaiians and Filipinos.ConclusionsYoung adult daily menthol smokers have slower rates of nicotine metabolism than nonmenthol smokers. Studies are needed to determine the utility of this biomarker for smoking cessation treatment assignments.© The Author 2015. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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