摘要：Background Polycyclic aromatic hydrocarbons (PAHs) may increase breast cancer risk, and the association may be modified by inherited differences in deactivation of PAH intermediates by glutathione S -transferases (GSTs). Few breast cancer studies have investigated the joint effects of multiple GSTs and a PAH biomarker. Objective We estimated the breast cancer risk associated with multiple polymorphisms in the GST gene ( GSTA1 , GSTM1 , GSTP1 , and GSTT1 ) and the interaction with PAH–DNA adducts and cigarette smoking. Methods We conducted unconditional logistic regression using data from a population-based sample of women (cases/controls, respectively): GST polymorphisms were genotyped using polymerase chain reaction and matrix-assisted laser desorption/ionization time-of-flight assays ( n = 926 of 916), PAH–DNA adduct blood levels were measured by competitive enzyme-linked immunosorbent assay ( n = 873 of 941), and smoking status was assessed by in-person questionnaires ( n = 943 of 973). Results Odds ratios for joint effects on breast cancer risk among women with at least three variant alleles were 1.56 [95% confidence interval (CI), 1.13–2.16] for detectable PAH–DNA adducts and 0.93 (95% CI, 0.56–1.56) for no detectable adducts; corresponding odds ratios for three or more variants were 1.18 (95% CI, 0.82–1.69) for ever smokers and 1.44 (95% CI, 0.97–2.14) for never smokers. Neither interaction was statistically significant ( p = 0.43 and 0.62, respectively). Conclusion We found little statistical evidence that PAHs interacted with GSTT1 , GSTM1 , GSTP1 , and GSTA1 polymorphisms to further increase breast cancer risk.
关键词：breast cancer; GST; Long Island; PAH-DNA adducts; smoking
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