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A Case-Control Study of Microsomal Epoxide Hydrolase, Smoking, Meat Consumption, Glutathione S-Transferase M3, and Risk of Colorectal Adenomas¹

Departments of Preventive Medicine [V. C., K. S., Q. C., N. Z., A. D., R. H.] and Biochemistry and Molecular Biology [Q-s. Z., D. L.], University of Southern California, Keck School of Medicine, Los Angeles, California 90089, and Division of Gastroenterology, Kaiser Permanente Medical Center [H. F., E. L.], Los Angeles, CA 90027 and Bellflower, CA 90706

We estimated associations between polymorphisms in the gene encoding microsomal epoxide hydrolase (mEH) among 464 cases diagnosed with first occurrence of colorectal adenoma and 510 matched controls. In an analysis controlling only for the matching variables, we found little or no association between adenoma and mEH genotypes defined by polymorphisms at either codon 113 and 139 or mEH activity predicted by both polymorphisms. However, in subsequent analyses, high predicted mEH activity was significantly associated with adenoma among certain subgroups defined by smoking history [odds ratio (OR), 4.27; 95% confidence interval (CI), 1.68–10.81 among current smokers; interaction, P = 0.11], meat consumption (OR, 2.47; CI, 0.99–6.19 among individuals who regularly eat well-done meat; interaction, P = 0.03), and genotypes for the *A/*B polymorphism in the gene encoding glutatione S-transferase M3 (OR, 2.60; CI, 1.28–5.28 among individuals with *A*A genotype; interaction, P = 0.03). These findings are consistent with causal roles for environmental polycyclic aromatic hydrocarbons and genetically encoded variants in enzymes whose actions lead to the production of activated polycyclic aromatic hydrocarbon metabolites.

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