Lauren A Paul1, Richard T Burnett2, Jeffrey C Kwong3, Perry Hystad4, Aaron van Donkelaar5, Li Bai6, Mark S Goldberg7, Eric Lavigne8, Ray Copes9, Randall V Martin10, Alexander Kopp11, Hong Chen12. 1. Department of Environmental and Occupational Health, Public Health Ontario, 480 University Ave. Suite 300, Toronto, ON M5G 1V2, Canada. Electronic address: lauren.paul@oahpp.ca. 2. Population Studies Division, Environmental Health Science and Research Bureau, Health Canada, Finance Bldg, 101 Tunney's Pasture Drwy, Ottawa, ON K1A 0K9, Canada. Electronic address: rick.burnett@canada.ca. 3. Public Health Ontario Laboratories, Public Health Ontario, 480 University Ave. Suite 300, Toronto, ON M5G 1V2, Canada; ICES, 2075 Bayview Ave. G1 06, Toronto, ON M4N 3M5, Canada; Dalla Lana School of Public Health, University of Toronto, 155 College St. Room 500, Toronto, ON M5T 3M7, Canada; Department of Family and Community Medicine, University of Toronto, 500 University Ave. 5(th) Floor, Toronto, ON M5G 1V7, Canada. Electronic address: jeff.kwong@utoronto.ca. 4. College of Public Health and Human Sciences, Oregon State University, Women's Bldg, 160 SW 26th St., Corvallis, OR 97331, USA. Electronic address: perry.hystad@oregonstate.edu. 5. Department of Physics and Atmospheric Science, Dalhousie University, Sir James Dunn Bldg, 6310 Coburg Rd., Halifax, NS B3H 4J5, Canada. Electronic address: aaron.van.donkelaar@dal.ca. 6. ICES, 2075 Bayview Ave. G1 06, Toronto, ON M4N 3M5, Canada. Electronic address: li.bai@ices.on.ca. 7. Department of Medicine, McGill University, 1001 Decarie Blvd Suite D05-2212, Montreal, QC H4A 3J1, Canada; Division of Clinical Epidemiology, McGill University Health Centre, 687 Pine Ave. W R4.29, Montreal, QC H3A 1A1, Canada. Electronic address: mark.goldberg@mcgill.ca. 8. Air Health Science Division, Health Canada, 269 Laurier Ave. W A.L. 4903B, Ottawa, ON K1A 0K9, Canada; School of Epidemiology and Public Health, University of Ottawa, Alta Vista Campus, 600 Peter Morand Cres. Room 101, Ottawa, ON K1G 5Z3, Canada. Electronic address: eric.lavigne@canada.ca. 9. Department of Environmental and Occupational Health, Public Health Ontario, 480 University Ave. Suite 300, Toronto, ON M5G 1V2, Canada; Dalla Lana School of Public Health, University of Toronto, 155 College St. Room 500, Toronto, ON M5T 3M7, Canada. Electronic address: ray.copes@oahpp.ca. 10. Department of Physics and Atmospheric Science, Dalhousie University, Sir James Dunn Bldg, 6310 Coburg Rd., Halifax, NS B3H 4J5, Canada. Electronic address: randall.martin@dal.ca. 11. ICES, 2075 Bayview Ave. G1 06, Toronto, ON M4N 3M5, Canada. Electronic address: alexander.kopp@ices.on.ca. 12. Department of Environmental and Occupational Health, Public Health Ontario, 480 University Ave. Suite 300, Toronto, ON M5G 1V2, Canada; Population Studies Division, Environmental Health Science and Research Bureau, Health Canada, Finance Bldg, 101 Tunney's Pasture Drwy, Ottawa, ON K1A 0K9, Canada; ICES, 2075 Bayview Ave. G1 06, Toronto, ON M4N 3M5, Canada; Dalla Lana School of Public Health, University of Toronto, 155 College St. Room 500, Toronto, ON M5T 3M7, Canada. Electronic address: hong.chen@canada.ca.
Abstract
PURPOSE: Growing evidence implicates ambient air pollutants in the development of major chronic diseases and premature mortality. However, epidemiologic evidence linking air pollution to diabetes remains inconclusive. This study sought to determine the relationships between selected air pollutants (nitrogen dioxide [NO2], fine particulate matter [PM2.5], ozone [O3], and oxidant capacity [Ox; the redox-weighted average of O3 and NO2]) and the incidence of diabetes, as well as the risk of cardiovascular or diabetes mortality among individuals with prevalent diabetes. RESEARCH DESIGN AND METHODS: We followed two cohorts, which included 4.8 million Ontario adults free of diabetes and 452,590 Ontario adults with prevalent diabetes, from 2001 to 2015. Area-level air pollution exposures were assigned to subjects' residential areas, and outcomes were ascertained using health administrative data with validated algorithms. We estimated hazard ratios for the association between each air pollutant and outcome using Cox proportional hazards models, and modelled the shape of the concentration-response relationships. RESULTS: Over the study period, 790,461 individuals were diagnosed with diabetes. Among those with prevalent diabetes, 26,653 died from diabetes and 64,773 died from cardiovascular diseases. For incident diabetes, each IQR increase in NO2 had a hazard ratio of 1.04 (95% CI: 1.03-1.05). This relationship was relatively robust to all sensitivity analyses considered, and exhibited a near-linear shape. There were also positive associations between incident diabetes and PM2.5, O3, and Ox, but these estimates were somewhat sensitive to different models considered. Among those with prevalent diabetes, almost all pollutants were associated with increased diabetes and cardiovascular mortality risk. The strongest association was observed between diabetes mortality and exposure to NO2 (HR = 1.08, 95% CI: 1.02-1.13). CONCLUSIONS: Selected air pollutants, especially NO2, were linked to an increased risk of incident diabetes, as well as risk of cardiovascular or diabetes mortality among persons with prevalent diabetes. As NO2 is frequently used as a proxy for road traffic exposures, this result may indicate that traffic-related air pollution has the strongest effect on diabetes etiology and survival after diabetes development. Crown
PURPOSE: Growing evidence implicates ambient air pollutants in the development of major chronic diseases and premature mortality. However, epidemiologic evidence linking air pollution to diabetes remains inconclusive. This study sought to determine the relationships between selected air pollutants (nitrogen dioxide [NO2], fine particulate matter [PM2.5], ozone[O3], and oxidant capacity [Ox; the redox-weighted average of O3 and NO2]) and the incidence of diabetes, as well as the risk of cardiovascular or diabetes mortality among individuals with prevalent diabetes. RESEARCH DESIGN AND METHODS: We followed two cohorts, which included 4.8 million Ontario adults free of diabetes and 452,590 Ontario adults with prevalent diabetes, from 2001 to 2015. Area-level air pollution exposures were assigned to subjects' residential areas, and outcomes were ascertained using health administrative data with validated algorithms. We estimated hazard ratios for the association between each air pollutant and outcome using Cox proportional hazards models, and modelled the shape of the concentration-response relationships. RESULTS: Over the study period, 790,461 individuals were diagnosed with diabetes. Among those with prevalent diabetes, 26,653 died from diabetes and 64,773 died from cardiovascular diseases. For incident diabetes, each IQR increase in NO2 had a hazard ratio of 1.04 (95% CI: 1.03-1.05). This relationship was relatively robust to all sensitivity analyses considered, and exhibited a near-linear shape. There were also positive associations between incident diabetes and PM2.5, O3, and Ox, but these estimates were somewhat sensitive to different models considered. Among those with prevalent diabetes, almost all pollutants were associated with increased diabetes and cardiovascular mortality risk. The strongest association was observed between diabetes mortality and exposure to NO2 (HR = 1.08, 95% CI: 1.02-1.13). CONCLUSIONS: Selected air pollutants, especially NO2, were linked to an increased risk of incident diabetes, as well as risk of cardiovascular or diabetes mortality among persons with prevalent diabetes. As NO2 is frequently used as a proxy for road traffic exposures, this result may indicate that traffic-related air pollution has the strongest effect on diabetes etiology and survival after diabetes development. Crown
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