Environmental and Dietary Cadmium Exposure and the Risk of Endometrial CancerAbstract Number:2564 Rudolph Rull, Alison Canchola, Debbie Goldberg, Robert Gunier, Christine Duffy, Peggy Reynolds*, Pamela Horn-Ross Rudolph Rull School of Community Health Sciences, University of Nevada-Reno, United States, E-mail Address: [email protected] Search for more papers by this author , Alison Canchola Cancer Prevention Institute of California, United States, E-mail Address: [email protected] Search for more papers by this author , Debbie Goldberg Cancer Prevention Institute of California, United States, E-mail Address: [email protected] Search for more papers by this author , Robert Gunier School of Public Health, University of California, Berkeley, United States, E-mail Address: [email protected] Search for more papers by this author , Christine Duffy Cancer Prevention Institute of California, United States, E-mail Address: [email protected] Search for more papers by this author , Peggy Reynolds* Cancer Prevention Institute of California, United States, E-mail Address: [email protected] Search for more papers by this author , and Pamela Horn-Ross Cancer Prevention Institute of California, United States, E-mail Address: [email protected] Search for more papers by this author AbstractBACKGROUND Most endometrial cancer is caused by stimulation of the endometrium via circulating estrogens unopposed by the modulating inhibitory influence of progestins. Cadmium (Cd) is a carcinogenic metal that exhibits potent estrogen-like activity. Non-occupational exposure to Cd occurs from smoking, diet and inhalation of polluted air. OBJECTIVE Our objective was to evaluate whether exposures to Cd from environmental and dietary sources increased the risk of Type I endometrial cancer among 85,000 women, without a prior hysterectomy, enrolled in the California Teachers Study (CTS) cohort.METHODS For each CTS participant’s geocoded residential addresses, we estimated and assigned: a) Cd emissions from industrial sources within 5 kilometers, b) vehicular traffic density within 300 meters, and c) modeled ambient air concentrations of Cd at the census-tract level. Average daily calorie-adjusted dietary Cd intake was estimated by linking food- frequency questionnaire data, including portion size, collected at baseline with the Total Diet Study, a database of contaminant residues in foods. A total of 887 cases of endometrial cancer diagnosed between 1996 and 2010 were identified via linkage with the California Cancer Registry. Hazard ratios were estimated using Cox proportional- hazards regression.RESULTS We observed no associations between Type I endometrial cancer risk and environmental Cd exposure sources, including industrial emissions, traffic, and ambient air. Dietary Cd also was not associated with endometrial cancer risk (adjusted hazard ratio for highest quintile of intake = 0.99; 95% confidence interval = 0.79-1.26; p-trend = 0.90). We did not observe any effect modification for any of these measures by cigarette smoking, body size, menopausal status, or other factors.CONCLUSIONS These results indicate that Cd from environmental or dietary sources is not associated with endometrial cancer risk at levels of exposure experienced by the general California population.