This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hecht, S. S. Articles by Carmella, S. G. Search for Related Content PubMed PubMed Citation Articles by Hecht, S. S. Articles by Carmella, S. G.

Longitudinal Study of Urinary Phenanthrene Metabolite Ratios: Effect of Smoking on the Diol Epoxide Pathway

The Cancer Center and Transdisciplinary Tobacco Use Research Center, University of Minnesota, Minneapolis, Minnesota

Requests for reprints: Stephen S. Hecht, The Cancer Center, University of Minnesota, Mayo Mail Code 806, 420 Delaware Street Southeast, Minneapolis, MN 55455. Phone: 612-624-7604; Fax: 612-626-5135. E-mail: hecht002{at}umn.edu

We have proposed that urinary phenanthrene metabolites could be used in a carcinogen metabolite phenotyping approach to identify individuals who may be susceptible to cancer induction by polycyclic aromatic hydrocarbons (PAH). In support of this proposal, we have developed methods for quantitation of r-1,t-2,3,c-4-tetrahydroxy-1,2,3,4-tetrahydrophenanthrene (PheT) and phenanthrols (HOPhe) in human urine. PheT is the end product of the diol epoxide metabolic activation pathway of PAH, whereas HOPhe are considered as detoxification products. In this study, we investigated the longitudinal consistency of these metabolites over time in smokers and nonsmokers and compared their levels. Twelve smokers and 10 nonsmokers provided urine samples daily for 7 days, then weekly for 6 weeks. Levels of PheT, HOPhe, and PheT/HOPhe ratios were relatively constant in most individuals, with mean coefficients of variation ranging from 29.3% to 45.7%. There were no significant changes over time in levels of the metabolites or in ratios. These results indicate that a single urine sample should be sufficient when comparing phenanthrene metabolites in different groups. PheT/HOPhe ratios were significantly higher in smokers than in nonsmokers, showing that smoking induces the diol epoxide metabolic activation pathway of phenanthrene. This finding is consistent with previous studies indicating that inducibility of PAH metabolism contributes to cancer risk in smokers. (Cancer Epidemiol Biomarkers Prev 2005;14(12):2969–74)

This article has been cited by other articles:

				S. S. Hecht, P. W. Villalta, and J.B. Hochalter Analysis of phenanthrene diol epoxide mercapturic acid detoxification products in human urine: relevance to molecular epidemiology studies of glutathione S-transferase polymorphisms Carcinogenesis, May 1, 2008; 29(5): 937 - 943. [Abstract] [Full Text] [PDF]

				B. Pesch, M. Kappler, K. Straif, B. Marczynski, R. Preuss, B. Rossbach, H.-P. Rihs, T. Weiss, S. Rabstein, C. Pierl, et al. Dose-Response Modeling of Occupational Exposure to Polycyclic Aromatic Hydrocarbons with Biomarkers of Exposure and Effect Cancer Epidemiol. Biomarkers Prev., September 1, 2007; 16(9): 1863 - 1873. [Abstract] [Full Text] [PDF]

				S. S. Hecht, S. G. Carmella, A. Yoder, M. Chen, Z.-z. Li, C. Le, R. Dayton, J. Jensen, and D. K. Hatsukami Comparison of polymorphisms in genes involved in polycyclic aromatic hydrocarbon metabolism with urinary phenanthrene metabolite ratios in smokers. Cancer Epidemiol. Biomarkers Prev., October 1, 2006; 15(10): 1805 - 1811. [Abstract] [Full Text] [PDF]

				S. G. Carmella, A. Yoder, and S. S. Hecht Combined Analysis of r-1,t-2,3,c-4-Tetrahydroxy-1,2,3,4-Tetrahydrophenanthrene and 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanol in Smokers' Plasma. Cancer Epidemiol. Biomarkers Prev., August 1, 2006; 15(8): 1490 - 1494. [Abstract] [Full Text] [PDF]