CIGARETTE-SMOKING, N-ACETYLTRANSFERASES 1 AND 2, AND BREAST-CANCER RISK

To examine the effects of smoking and N-acetylation genetics on breast cancer risk, we analyzed data from an ongoing, population-based, case -control study of invasive breast cancer in North Carolina. The study population consisted of 498 cases and 473 controls, with approximately equal numbers of African-American and white women, and women under th e age of 50 and age 50 years or older. Among premenopausal women, ther e was no association between current smoking [odds ratio (OR), 0.9; 95 % confidence interval (CI), 0.5-1.5] or past smoking (OR, 1.0; 95% CI, 0.6-1.6) and breast cancer risk. Among postmenopausal women, there wa s also no association,vith current smoking (OR, 1.2; 95% CI, 0.7-2.0); however, a small increase in risk was observed for past smoking (OR, 1.5; 95% CI, 1.0-2.4). For postmenopausal women who smoked in the past , ORs and 95% CIs were 3.4 (1.4-8.1) for smoking within the past 3 yea rs, 3.0 (1.3-6.7) for smoking 4-9 years ago, and 0.6 (0.3-1.4) for smo king 10-19 years ago. Neither N-acetyltransferase 1 (NAT1) nor N-acety ltransferase 2 (NAT2) genotype alone was associated with increased bre ast cancer risk. There was little evidence for modification of smoking effects according to genotype, except among postmenopausal women. Amo ng postmenopausal women, ORs for smoking within the past 3 years were greater for women with the NAT110 genotype (OR, 9.0; 95% CI, 1.9-41.8 ) than NAT1-non10 (OR, 2.5; 95% CI, 0.9-7.2) and greater for NAT2-rap id genotype (OR, 7.4; 95% CI, 1.6-32.6) than NAT2-slow (OR, 2.8; 95% C I, 0.4-8.0). Future studies of NAT genotypes and breast cancer should investigate the effects of environmental tobacco smoke, diet, and othe r exposures.