Michelle C Turner1,2,3,4, Michael Jerrett5, C Arden Pope6, Daniel Krewski1,7, Susan M Gapstur8, W Ryan Diver8, Bernardo S Beckerman5, Julian D Marshall9, Jason Su5, Daniel L Crouse10, Richard T Burnett11. 1. 1 McLaughlin Centre for Population Health Risk Assessment and. 2. 2 Centre for Research in Environmental Epidemiology, Barcelona, Spain. 3. 3 Universitat Pompeu Fabra, Barcelona, Spain. 4. 4 CIBER Epidemiología y Salud Pública, Madrid, Spain. 5. 5 Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, Berkeley, California. 6. 6 Department of Economics, Brigham Young University, Provo, Utah. 7. 7 School of Epidemiology, Public Health and Disease Prevention, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada. 8. 8 Epidemiology Research Program, American Cancer Society, Atlanta, Georgia. 9. 9 Department of Civil and Environmental Engineering, University of Washington, Seattle, Washington. 10. 10 Department of Sociology, University of New Brunswick, Fredericton, New Brunswick, Canada; and. 11. 11 Population Studies Division, Health Canada, Ottawa, Ontario, Canada.
Abstract
RATIONALE: Tropospheric ozone (O3) is potentially associated with cardiovascular disease risk and premature death. Results from long-term epidemiological studies on O3 are scarce and inconclusive. OBJECTIVES: In this study, we examined associations between chronic ambient O3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults. METHODS: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 μm [PM2.5]) and NO2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual- and ecological-level covariates. MEASUREMENTS AND MAIN RESULTS: In single-pollutant models, we observed significant positive associations between O3, PM2.5, and NO2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM2.5, significant positive associations remained between O3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO2. We also observed positive mortality associations with both PM2.5 (both near source and regional) and NO2 in multipollutant models. CONCLUSIONS: Findings derived from this large-scale prospective study suggest that long-term ambient O3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O3 concentrations.
RATIONALE: Tropospheric ozone (O3) is potentially associated with cardiovascular disease risk and premature death. Results from long-term epidemiological studies on O3 are scarce and inconclusive. OBJECTIVES: In this study, we examined associations between chronic ambient O3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults. METHODS: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 μm [PM2.5]) and NO2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual- and ecological-level covariates. MEASUREMENTS AND MAIN RESULTS: In single-pollutant models, we observed significant positive associations between O3, PM2.5, and NO2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM2.5, significant positive associations remained between O3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO2. We also observed positive mortality associations with both PM2.5 (both near source and regional) and NO2 in multipollutant models. CONCLUSIONS: Findings derived from this large-scale prospective study suggest that long-term ambient O3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O3 concentrations.
Entities:
Keywords:
air pollution; mortality; ozone; prospective study
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