Hong Chen1, Richard T Burnett, Jeffrey C Kwong, Paul J Villeneuve, Mark S Goldberg, Robert D Brook, Aaron van Donkelaar, Michael Jerrett, Randall V Martin, Alexander Kopp, Jeffrey R Brook, Ray Copes. 1. From Public Health Ontario, Toronto, Ontario, Canada (H.C., J.C.K., R.C.); Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada (H.C., J.C.K., P.J.V., R.C.); Institute for Clinical Evaluative Sciences, Toronto, Ontario, Canada (H.C., J.C.K., A.K.); Population Studies Division, Health Canada, Ottawa, Ontario, Canada (R.T.B.); Department of Family and Community Medicine, University of Toronto, Toronto, Ontario, Canada (J.C.K.); Department of Health Sciences, Carleton University, Ottawa, Ontario, Canada (P.J.V.); Department of Medicine, McGill University, Montreal, Quebec, Canada (M.S.G.); Division of Clinical Epidemiology, McGill University Health Centre, Montreal, Quebec, Canada (M.S.G.); Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor (R.D.B.); Department of Physics and Atmospheric Science, Dalhousie University, Halifax, Nova Scotia, Canada (A.v.D., R.V.M.); Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley (M.J.); Harvard-Smithsonian Center for Astrophysics, Cambridge, MA (R.V.M.); and Air Quality Research Division, Environment Canada, Toronto, Ontario, Canada (J.R.B.).
Abstract
BACKGROUND: Laboratory studies suggest that exposure to fine particulate matter (≤2.5 μm in diameter) (PM2.5) can trigger a combination of pathophysiological responses that may induce the development of hypertension. However, epidemiological evidence relating PM2.5 and hypertension is sparse. We thus conducted a population-based cohort study to determine whether exposure to ambient PM2.5 is associated with incident hypertension. METHODS AND RESULTS: We assembled a cohort of 35 303 nonhypertensive adults from Ontario, Canada, who responded to 1 of 4 population-based health surveys between 1996 and 2005 and were followed up until December 31, 2010. Incident diagnoses of hypertension were ascertained from the Ontario Hypertension Database, a validated registry of persons diagnosed with hypertension in Ontario (sensitivity=72%, specificity=95%). Estimates of long-term exposure to PM2.5 at participants' postal-code residences were derived from satellite observations. We used Cox proportional hazards models, adjusting for various individual and contextual risk factors including body mass index, smoking, physical activity, and neighbourhood-level unemployment rates. We conducted various sensitivity analyses to assess the robustness of the effect estimate, such as investigating several time windows of exposure and controlling for potential changes in the risk of hypertension over time. Between 1996 and 2010, we identified 8649 incident cases of hypertension and 2296 deaths. For every 10-µg/m(3) increase of PM2.5, the adjusted hazard ratio of incident hypertension was 1.13 (95% confidence interval, 1.05-1.22). Estimated associations were comparable among all sensitivity analyses. CONCLUSIONS: This study supports an association between PM2.5 and incident hypertension.
BACKGROUND: Laboratory studies suggest that exposure to fine particulate matter (≤2.5 μm in diameter) (PM2.5) can trigger a combination of pathophysiological responses that may induce the development of hypertension. However, epidemiological evidence relating PM2.5 and hypertension is sparse. We thus conducted a population-based cohort study to determine whether exposure to ambient PM2.5 is associated with incident hypertension. METHODS AND RESULTS: We assembled a cohort of 35 303 nonhypertensive adults from Ontario, Canada, who responded to 1 of 4 population-based health surveys between 1996 and 2005 and were followed up until December 31, 2010. Incident diagnoses of hypertension were ascertained from the Ontario Hypertension Database, a validated registry of persons diagnosed with hypertension in Ontario (sensitivity=72%, specificity=95%). Estimates of long-term exposure to PM2.5 at participants' postal-code residences were derived from satellite observations. We used Cox proportional hazards models, adjusting for various individual and contextual risk factors including body mass index, smoking, physical activity, and neighbourhood-level unemployment rates. We conducted various sensitivity analyses to assess the robustness of the effect estimate, such as investigating several time windows of exposure and controlling for potential changes in the risk of hypertension over time. Between 1996 and 2010, we identified 8649 incident cases of hypertension and 2296 deaths. For every 10-µg/m(3) increase of PM2.5, the adjusted hazard ratio of incident hypertension was 1.13 (95% confidence interval, 1.05-1.22). Estimated associations were comparable among all sensitivity analyses. CONCLUSIONS: This study supports an association between PM2.5 and incident hypertension.
Entities:
Keywords:
air pollution; cohort studies; epidemiology; hypertension
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