BackgroundThe widespread availability of powerful tools in commercial geographic information system (GIS) software has made address geocoding a widely employed technique in spatial epidemiologic studies.ObjectiveThe objective of this study was to determine the effect of the positional error in geocoding on the analysis of exposure to traffic-related air pollution of children at school locations.MethodsFor a case study of Orange County, Florida, we determined the positional error of geocoding of school locations through comparisons with a parcel database and digital orthophotography. We used four different geocoding techniques for comparison to establish the repeatability of geocoding, and an analysis of proximity to major roads to determine bias and error in environmental exposure assessment.ResultsResults indicate that the positional error in geocoding of schools is very substantial: We found that the 95% root mean square error was 196 m using street centerlines, 306 m using TIGER roads, and 210 and 235 m for two commercial geocoding firms. We found bias and error in proximity analysis to major roads to be unacceptably large at distances of < 500 m. Bias and error are introduced by lack of positional accuracy and lack of repeatability of geocoding of school locations.ConclusionsThese results suggest that typical geocoding is insufficient for fine-scale analysis of school locations and more accurate alternatives need to be considered.
Exposure to polychlorinated biphenyls (PCBs) and other persistent organic pollutants (e.g., toxaphene) has been linked to an increased risk for melanoma in occupational settings. Great Lakes fish bioaccumulate PCBs and organochlorine pesticides, thus consumption is thought to be an important non-occupational exposure route. We investigated the consumption of sport-caught fish from Lake Ontario and the incidence of melanoma in the New York State Angler Cohort Study (NYSACS), a prospective cohort of 17,097 anglers and their spouses aged 18 to 40 years old at enrollment. Participants completed a mailed self-administered questionnaire upon enrollment in 1991. The questionnaire queried for the number of years that fish from L. Ontario were consumed, frequency of species specific fish consumption as well as demographic factors, smoking history and other selected potential confounders. As of December 31, 2008, fifty-one histologically confirmed, first primary, incident melanoma cases were identified via the New York State Cancer Registry. Vital status was determined by linkage with the Social Security Administration Death file. Prevalent cancer cases (n = 196) were excluded. Of the remaining 16,901cohort members, 10% (n=1,672) were lost to follow-up and censored in the year they left New York State. Analyses were restricted to Caucasians (n= 16,326). Fish consumption was dichotomized into never vs. ever. Duration of consumption was categorized into tertiles based on the distribution among the cases reporting eating Lake Ontario sport-caught fish. Poisson regression was used to calculate rate ratios (RR) and 95% confidence intervals, adjusting for age, income, years of education and number of years fishing in New York State. Lake Ontario sport-caught fish consumption was weakly associated with melanoma risk RR=1.33(0.6-2.99) as compared with non-consumers. Duration of Lake Ontario fish consumption was not convincingly associated with melanoma incidence (non-eaters RR = 1.0 (ref); 1st tertile RR = 1.07 (95% CI = 0.38-3.06); 2nd tertile RR = 1.41 (95% CI = 0.49-4.03); 3rd tertile RR = 2.16 (95% CI = 0.79-5.89); p-for trend =0.10. Although interpretation of our preliminary results is complicated by a small number of cases (n=52) and inability to control for potential confounding from sun exposure, they suggest that consumption of Great Lakes fish contaminated with PCBs and other organochlorine compounds was not associated with incidence of melanoma. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5480. doi:1538-7445.AM2012-5480
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 association between Lake Ontario fish consumption and prostate cancer risk. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1914. doi:10.1158/1538-7445.AM2011-1914
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