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Similar Exposure to a Tobacco-Specific Carcinogen in Smokeless Tobacco Users and Cigarette Smokers

¹ Cancer Center and Transdisciplinary Tobacco Use Research Center, University of Minnesota, Minneapolis, Minnesota and ² PICS, Inc., Reston, Virginia

Requests for reprints: Stephen S. Hecht, University of Minnesota Cancer Center, 420 Delaware Street Southeast, MMC 806, Minneapolis, MN 55455. Phone: 612-626-7604; Fax: 612-626-5135. E-mail: hecht002{at}umn.edu

Smokeless tobacco has been proposed as a reduced risk substitute for smoking, but no large studies have investigated exposure to the powerful carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in smokeless tobacco users versus smokers. The purpose of this study was to carry out such a comparison. Levels of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronides (total NNAL), a biomarker of NNK exposure, and cotinine, a biomarker of nicotine exposure, were quantified in the urine of 420 smokers and 182 smokeless tobacco users who were participants in studies designed to reduce their use of these products. The measurements were taken at baseline, before intervention. Levels of total NNAL per milliliter of urine were significantly higher in smokeless tobacco users than in smokers (P < 0.0001). When adjusted for age and gender, levels of total NNAL per milligram of creatinine were also significantly higher in smokeless tobacco users than in smokers (P < 0.001). Levels of cotinine per milliliter of urine and per milligram of creatinine were significantly higher in smokeless tobacco users than in smokers (P < 0.001). These results show similar exposures to the potent tobacco-specific carcinogen NNK in smokeless tobacco users and smokers. These findings do not support the use of smokeless tobacco as a safe substitute for smoking. (Cancer Epidemiol Biomarkers Prev 2007;16(8):1567–72)

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