Abstract 1914: Consumption of Lake Ontario sport fish and prostate cancer incidence in the New York State Angler Cohort Study (NYSACS)

Fish from the Great Lakes are an important source of exposure to persistent organic pollutants, including polychlorinated biphenyls (PCBs) and organochlorine pesticides (e.g., Mirex and DDT). Some of these pollutants are hypothesized to be hormonally active and therefore may increase the risk of prostate cancer. Conversely, fish are also a source of micro- and macro-nutrients hypothesized to have chemopreventive properties. We investigated the consumption of sport-caught fish from Lake Ontario and the incidence of prostate cancer in the NYSACS, a prospective cohort of 17,110 anglers and their spouses aged 18 to 40 years old at enrollment. Participants completed a mailed self-administered questionnaire upon enrollment in 1991. Demographic factors, smoking history and selected potential confounders were ascertained. The questionnaire also queried for the number of years that fish from Lakes Ontario and Erie were consumed as well as the preparation and cooking practices for sport caught fish. As of December 31, 2008 fifty-eight first primary incident prostate cancers were identified via the New York State Cancer Registry. Vital status was determined by linkage with the Social Security Administration Death file. Of the 10,436 males enrolled at baseline, 10% (n=1,075) were lost to follow-up. Fish consumption was dichotomized into never vs. ever. Duration of consumption was categorized into tertiles based on the distribution among the cases who reported eating L Ontario sport caught fish. Poisson regression was used to calculate rate ratios (RR) and 95% confidence intervals, adjusting for age, education and pack-years of smoking. Ever eating Lake Ontario fish was inversely associated with prostate cancer incidence (RRadjusted=0.5 (95% CI=0.3-0.9)) compared with never consumers. In addition, we found a suggestion of an inverse association with increasing duration of L. Ontario fish consumption (non-eaters RR = 1.0 (ref); 1st tertile RR = 0.6 (95% CI = 0.3-1.3); 2nd tertile RR = 0.4 (95% CI = 0.2-1.0); 3rd tertile RR = 0.5 (95% CI = 0.2-1.0); although the exposure-response gradient was neither monotonic nor significant (ptrend = 0.157). The exposure-response gradients were similar when consumption was lagged 5- and 10-years (5-year lag ptrend = 0.289; 10-year ptrend = 0.269). While interpretation is complicated by a lack of information on family history of prostate cancer, and a small number of cases, these preliminary results are suggestive of an inverse associat