Nitrate and nitrite ingestion and risk of ovarian cancer among postmenopausal women in Iowa |
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Authors: | Maki Inoue‐Choi Rena R. Jones Kristin E. Anderson Kenneth P. Cantor James R. Cerhan Stuart Krasner Kim Robien Peter J. Weyer Mary H. Ward |
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Affiliation: | 1. Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD;2. National Institute on Minority Health and Health Disparities, National Institutes of Health, Bethesda, MD;3. Division of Epidemiology & Community Health, School of Public Health, University of Minnesota, Minneapolis, MN;4. Masonic Cancer Center, University of Minnesota, Minneapolis, MN;5. Division of Epidemiology, Mayo Clinic, Rochester, MN;6. Metropolitan Water District of Southern California, Los Angeles, CA;7. Department of Exercise and Nutrition Sciences, Milken Institute School of Public Health, George Washington University, Washington, DC;8. Center for Health Effects of Environmental Contamination, University of Iowa, Iowa City, IA |
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Abstract: | Nitrate and nitrite are precursors in the endogenous formation of N‐nitroso compounds (NOC), potential human carcinogens. We evaluated the association of nitrate and nitrite ingestion with postmenopausal ovarian cancer risk in the Iowa Women's Health Study. Among 28,555 postmenopausal women, we identified 315 incident epithelial ovarian cancers from 1986 to 2010. Dietary nitrate and nitrite intakes were assessed at baseline using food frequency questionnaire data. Drinking water source at home was obtained in a 1989 follow‐up survey. Nitrate‐nitrogen (NO3‐N) and total trihalomethane (TTHM) levels for Iowa public water utilities were linked to residences and average levels were computed based on each woman's duration at the residence. We computed multivariable‐adjusted hazard ratios (HR) and 95% confidence intervals (CI) using Cox proportional hazards regression. We tested interactions of nitrate with TTHMs and dietary factors known to influence NOC formation. Ovarian cancer risk was 2.03 times higher (CI = 1.22–3.38, ptrend = 0.003) in the highest quartile (≥2.98 mg/L) compared with the lowest quartile (≤0.47 mg/L; reference) of NO3‐N in public water, regardless of TTHM levels. Risk among private well users was also elevated (HR = 1.53, CI = 0.93–2.54) compared with the same reference group. Associations were stronger when vitamin C intake was pinteraction = 0.01 and 0.33 for private well and public supplies, respectively). Dietary nitrate was inversely associated with ovarian cancer risk (ptrend = 0.02); whereas, dietary nitrite from processed meats was positively associated with the risk (ptrend = 0.04). Our findings indicate that high nitrate levels in public drinking water and private well use may increase ovarian cancer risk among postmenopausal women. |
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Keywords: | nitrate nitrite ovarian cancer diet drinking water disinfection byproducts |
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