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Heme iron from meat and risk of adenocarcinoma of the esophagus and stomach

Ward, Mary H.a; Cross, Amanda J.b; Abnet, Christian C.b; Sinha, Rashmib; Markin, Rodney S.c; Weisenburger, Dennis D.c

European Journal of Cancer Prevention: March 2012 - Volume 21 - Issue 2 - p 134–138
doi: 10.1097/CEJ.0b013e32834c9b6c
Short Paper: Colorectal cancer

Iron can cause oxidative stress and DNA damage, and heme iron can catalyze endogenous formation of N-nitroso compounds, which are potent carcinogens. Dietary iron promotes esophageal cancer incidence in animal studies and has been identified as a growth factor for Helicobacter pylori, an established risk factor for stomach cancer. We conducted a population-based case–control study of adenocarcinoma of the esophagus (n=124) and stomach (n=154) and 449 controls in Nebraska. Heme iron and total iron intake were estimated from a food frequency questionnaire and databases of heme and total iron. We used logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs) adjusted for known risk factors. Esophageal cancer was positively associated with higher intakes of heme iron (ORQ4 vs. Q1=3.04, 95% CI: 1.20–7.72; P trend=0.009) and total iron from meat sources (ORQ4 vs. Q1=2.67, 95% CI: 0.99–7.16; P trend=0.050). Risk of stomach cancer was elevated among those with higher intakes of heme iron (ORQ4 vs.Q1=1.99, 95% CI: 1.00–3.95; P trend=0.17) and total iron from meat (OR=2.26, 95% CI: 1.14–4.46; P trend=0.11). Iron intake from all dietary sources was not significantly associated with risk of either cancer. Our results suggest that high intakes of heme and iron from meat may be important dietary risk factors for esophageal and stomach cancer and may partly explain associations with red meat.

aDepartment of Health and Human Services, Occupational and Environmental Epidemiology Branch

bNutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland

cDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA

Correspondence to Dr Mary H. Ward, PhD, Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, 6120 Executive Blvd EPS-8006, Bethesda, MD 20892-7240, USA Tel: +1 301 435 4713; fax: +1 301 402 1819; e-mail: wardm@mail.nih.gov

Received May 11, 2011

Accepted July 16, 2011

© 2012 Lippincott Williams & Wilkins, Inc.