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Cancer Epidemiology Biomarkers & Prevention 16, 1547-1553, August 1, 2007. doi: 10.1158/1055-9965.EPI-07-0210
© 2007 American Association for Cancer Research

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Concentrations of the Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone in Sidestream Cigarette Smoke Increase after Release into Indoor Air: Results from Unpublished Tobacco Industry Research

Suzaynn F. Schick and Stanton Glantz

Center for Tobacco Control Research and Education and the Lung Biology Center, Department of Medicine, University of California, San Francisco, California

Requests for reprints: Suzaynn Schick, University of California San Francisco, Box 0854, San Francisco, CA 94143-1390. Phone: 415-206-5904; Fax: 415-206-4123. E-mail: sschick{at}medsfgh.ucsf.edu

Research has shown that the toxicity of sidestream cigarette smoke, the primary constituent of secondhand smoke, increases over time. To find potential mechanisms that would explain the increase in sidestream smoke toxicity over time, we analyzed unpublished research reports from Philip Morris Co. using the internal tobacco industry documents now available at the University of California San Francisco Legacy Tobacco Documents Library and other Web sites. Unpublished research from Philip Morris Tobacco Company shows that 4-(methylnitrosamino)-I-(3-pyridyl)-1-butanone (NNK), a highly carcinogenic tobacco-specific nitrosamine, can form in sidestream cigarette smoke after it has been released into ambient air. In experiments done between 1983 and 1997, Philip Morris scientists measured the concentration of NNK in sidestream smoke in a sealed stainless steel test chamber at initial particle concentrations of 24 mg/m3 over the course of 6 to 18 h. They repeatedly showed that airborne NNK concentrations in sidestream cigarette smoke can increase by 50% to 200% per hour during the first 6 h after cigarettes are extinguished. Two experiments done in a real office showed that NNK concentrations increase for the first 2 h after cigarettes are extinguished. If NNK formation also occurs in the lower smoke concentrations observed in real smoking environments, these results suggest that nitrosation of nicotine and/or nicotine breakdown products in aging secondhand smoke is a significant contributor to nitrosamine exposure in humans. (Cancer Epidemiol Biomarkers Prev 2007;16(8):1547–53)




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I. Stepanov, P. Upadhyaya, S. G. Carmella, R. Feuer, J. Jensen, D. K. Hatsukami, and S. S. Hecht
Extensive Metabolic Activation of the Tobacco-Specific Carcinogen 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone in Smokers
Cancer Epidemiol. Biomarkers Prev., July 1, 2008; 17(7): 1764 - 1773.
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Copyright © 2007 by the American Association for Cancer Research.