Matthew Shane Loop1, Leslie A McClure2, Emily B Levitan3, Mohammad Z Al-Hamdan4, William L Crosson4, Monika M Safford5. 1. Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address: matthew_loop@unc.edu. 2. Department of Epidemiology and Biostatistics, Drexel University, Philadelphia, PA, USA. 3. Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA. 4. Universities Space Research Association, NASA Marshall Space Flight Center, Huntsville, AL, USA. 5. Division of General Internal Medicine, Weill Cornell Medical College, New York City, NY, USA.
Abstract
Chronic exposure to fine particulate matter (PM2.5) is accepted as a causal risk factor for coronary heart disease (CHD). However, most of the evidence for this hypothesis is based upon cohort studies in whites, comprised of either only males or females who live in urban areas. It is possible that many estimates of the effect of chronic exposure to PM2.5 on risk for CHD do not generalize to more diverse samples. METHODS: Therefore, we estimated the relationship between chronic exposure to PM2.5 and risk for CHD in among participants in the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort who were free from CHD at baseline (n=17,126). REGARDS is a sample of whites and blacks of both genders living across the continental United States. We fit Cox proportional hazards models for time to CHD to estimate the hazard ratio for baseline 1-year mean PM2.5 exposure, adjusting for environmental variables, demographics, and other risk factors for CHD including the Framingham Risk Score. RESULTS: The hazard ratio (95% CI) for a 2.7-μg/m3 increase (interquartile range) 1-year mean concentration of PM2.5 was 0.94 (0.83-1.06) for combined CHD death and nonfatal MI, 1.13 (0.92-1.40) for CHD death, and 0.85 (0.73-0.99) for nonfatal MI. We also did not find evidence that these associations depended upon overall CHD risk factor burden. CONCLUSIONS: Our results do not provide strong evidence for an association between PM2.5 and incident CHD in a heterogeneous cohort, and we conclude that the effects of chronic exposure to fine particulate matter on CHD require further evaluation.
Chronic exposure to fine particulate matter (PM2.5) is accepted as a causal risk factor for coronary heart disease (CHD). However, most of the evidence for this hypothesis is based upon cohort studies in whites, comprised of either only males or females who live in urban areas. It is possible that many estimates of the effect of chronic exposure to PM2.5 on risk for CHD do not generalize to more diverse samples. METHODS: Therefore, we estimated the relationship between chronic exposure to PM2.5 and risk for CHD in among participants in the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort who were free from CHD at baseline (n=17,126). REGARDS is a sample of whites and blacks of both genders living across the continental United States. We fit Cox proportional hazards models for time to CHD to estimate the hazard ratio for baseline 1-year mean PM2.5 exposure, adjusting for environmental variables, demographics, and other risk factors for CHD including the Framingham Risk Score. RESULTS: The hazard ratio (95% CI) for a 2.7-μg/m3 increase (interquartile range) 1-year mean concentration of PM2.5 was 0.94 (0.83-1.06) for combined CHD death and nonfatal MI, 1.13 (0.92-1.40) for CHD death, and 0.85 (0.73-0.99) for nonfatal MI. We also did not find evidence that these associations depended upon overall CHD risk factor burden. CONCLUSIONS: Our results do not provide strong evidence for an association between PM2.5 and incident CHD in a heterogeneous cohort, and we conclude that the effects of chronic exposure to fine particulate matter on CHD require further evaluation.
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