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Unit of Cancer Epidemiology (INSERM U351), Institut Gustave-Roussy, 94805 Villejuif, France [S. B.]; Department of Industrial Hygiene and Toxicology, Finnish Institute of Occupational Health, Helsinki 00250, Finland [M. R., A. H.]; Geneva Cancer Registry, Geneva 1205, Switzerland [C. B.]; and Division of Clinical Pharmacology, University Hospital, Geneva 1211, Switzerland [P. D.]
Microsomal epoxide hydrolase (mEH) is involved in the metabolism of tobacco-derived carcinogens. Polymorphisms in exons 3 and 4 of the EPHX gene have been reported to be associated with variations in mEH activity. We examined whether the predicted mEH activity modified the lung cancer risk among 150 cases and 172 controls, all French Caucasian smokers. A significant association was found between predicted mEH activity and lung cancer (P < 0.02), with a dose-effect relationship (P < 0.005). The risks associated with intermediate and high activities, compared to low activity, were 1.65 (95% CI, 0.95–2.86) and 2.66 (95% CI, 1.33–5.33), respectively. The effect of mEH activity on lung cancer risk was not significantly modified by smoking exposure, CYP1A1 genotype, or GSTM1 genotype. mEH may thus be an important genetic determinant of smoking-induced lung cancer.
1 Supported by the Swiss Cancer League, Switzerland (FOR063); League against Cancer of Fribourg, Switzerland (FOR381.88); Cancer Research, Switzerland (AKT 617); and Fund for Clinical Research against Cancer, Gustave-Roussy Institute, Villejuif, France (88D28).
2 To whom requests for reprints should be addressed, at INSERM U351, Institut Gustave-Roussy, 94805 Villejuif, France. Phone: 33-1-42-11-41-39; Fax: 33-1-42-11-53-15; E-mail: simone.benhamou@igr.fr.
Received 8/ 7/98. Accepted 10/12/98.
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