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Primary Prevention Insights

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Exposure to Persistent Organic Pollutants Increases Hospitalization Rates for Myocardial Infarction with Comorbid Hypertension

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Publication Date: 23 Mar 2010

Type: Original Research

Journal: Primary Prevention Insights

Citation: Primary Prevention Insights 2010:2 1-9

doi: 10.4137/PPRI.S4332

Abstract

Studies suggest that environmental exposure to persistent organic pollutants (POPs) may be an emerging risk factor for ischemic heart disease, including acute myocardial infarction (AMI). However, some studies indicate that exposure to POPs may also be a risk factor for hypertension, a well-established risk factor for AMI. To investigate effect of POPs on the environmental burden of cardiovascular disease, a study of AMI with comorbid hypertension in populations environmentally exposed to persistent organic pollutants, based on the zip code of residence, was conducted. Data on hospital discharges for AMI with comorbid hypertension were obtained from the New York Statewide Planning and Research Cooperative System for 1993–2004. Patients residing in zip codes containing or abutting POPs contaminated sites were considered environmentally exposed. Relative risks (RR) — with corresponding 95% confidence intervals (95% CI) — of hospitalization for AMI with comorbid hypertension were estimated by Poisson regression, adjusting for known confounders. Adjusted hospitalization rates for AMI with comorbid hypertension were 12.4% higher in populations residing in proximity to a POPs site (adjusted RR = 1.124, 95% CI 1.025–1.233, p < 0.05), compared to not in proximity to a POPs site. Also, hos- pitalization rates for AMI with comorbid hypertension were higher in males than in females (adjusted RR = 2.157, 95% CI 2.100–2.215, p < 0.05), in African Americans than in Caucasians (adjusted RR = 1.631, 95% CI 1.483–1.794, p < 0.05), and in older age groups (p for trend < 0.05). These findings are consistent with the established effects of non-modifiable risk factors and serve as indirect quality indicators for our model. In conclusion, our results support the hypothesis that environmental exposure to POPs increases the burden of cardiovascular disease in exposed populations.


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