title: Cigarette smoking, N-acetyltransferases 1 and 2, and breast cancer risk.
abstract: 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 the age of 50 and age 50 years or older. Among premenopausal women, there 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 was also no association with 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 years, 3.0 (1.3-6.7) for smoking 4-9 years ago, and 0.6 (0.3-1.4) for smoking 10-19 years ago. Neither N-acetyltransferase 1 (NAT1) nor N-acetyltransferase 2 (NAT2) genotype alone was associated with increased breast cancer risk. There was little evidence for modification of smoking effects according to genotype, except among postmenopausal women. Among postmenopausal women, ORs for smoking within the past 3 years were greater for women with the NAT1*10 genotype (OR, 9.0; 95% CI, 1.9-41.8) than NAT1-non*10 (OR, 2.5; 95% CI, 0.9-7.2) and greater for NAT2-rapid genotype (OR, 7.4; 95% CI, 1.6-32.6) than NAT2-slow (OR, 2.8; 95% CI, 0.4-8.0). Future studies of NAT genotypes and breast cancer should investigate the effects of environmental tobacco smoke, diet, and other exposures.
authors.affiliation: Department of Epidemiology, School of Public Health and Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill 27599-7400, USA.
authors.forename: R C
authors.initials: RC
authors.lastname: Millikan
authors.forename: G S
authors.initials: GS
authors.lastname: Pittman
authors.forename: B
authors.initials: B
authors.lastname: Newman
authors.forename: C K
authors.initials: CK
authors.lastname: Tse
authors.forename: O
authors.initials: O
authors.lastname: Selmin
authors.forename: B
authors.initials: B
authors.lastname: Rockhill
authors.forename: D
authors.initials: D
authors.lastname: Savitz
authors.forename: P G
authors.initials: PG
authors.lastname: Moorman
authors.forename: D A
authors.initials: DA
authors.lastname: Bell
mesh_terms: D000123:Acetyltransferases / Q000235:genetics*; D000328:Adult; D000368:Aged; D001191:Arylamine N-Acetyltransferase / Q000235:genetics*; D001943:Breast Neoplasms / Q000201:enzymology* / Q000453:epidemiology / Q000235:genetics*; D016022:Case-Control Studies; D005260:Female; D005838:Genotype; D006801:Humans; D007527:Isoenzymes; D008875:Middle Aged; D009657:North Carolina / Q000453:epidemiology; D017698:Postmenopause / Q000235:genetics; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects / Q000235:genetics
chemical_list: D007527:Isoenzymes; D000123:Acetyltransferases; D001191:Arylamine N-Acetyltransferase; C089384:N-acetyltransferase 1; C478900:NAT2 protein, human