Hong Chen1, Jeffrey C Kwong2, Ray Copes3, Perry Hystad4, Aaron van Donkelaar5, Karen Tu6, Jeffrey R Brook7, Mark S Goldberg8, Randall V Martin9, Brian J Murray10, Andrew S Wilton11, Alexander Kopp11, Richard T Burnett12. 1. Public Health Ontario, Toronto, ON, Canada; Institute for Clinical Evaluative Sciences, Toronto, ON, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada. Electronic address: hong.chen@oahpp.ca. 2. Public Health Ontario, Toronto, ON, Canada; Institute for Clinical Evaluative Sciences, Toronto, ON, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada; Department of Family and Community Medicine, University of Toronto, Toronto, ON, Canada. 3. Public Health Ontario, Toronto, ON, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada. 4. College of Public Health and Human Sciences, Oregon State University, Corvallis, USA. 5. Department of Physics and Atmospheric Science, Dalhousie University, Halifax, NS, Canada. 6. Institute for Clinical Evaluative Sciences, Toronto, ON, Canada; Department of Family and Community Medicine, University of Toronto, Toronto, ON, Canada; Toronto Western Hospital Family Health Team, University Health Network, Canada. 7. Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada; Air Quality Research Division, Environment and Climate Change Canada, Toronto, ON, Canada. 8. Department of Medicine, McGill University, Montreal, QC, Canada. 9. Department of Physics and Atmospheric Science, Dalhousie University, Halifax, NS, Canada; Harvard-Smithsonian Centre for Astrophysics, Cambridge, MA, USA. 10. Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Canada. 11. Institute for Clinical Evaluative Sciences, Toronto, ON, Canada. 12. Population Studies Division, Health Canada, Ottawa, ON, Canada.
Abstract
INTRODUCTION: Emerging studies have implicated air pollution in the neurodegenerative processes. Less is known about the influence of air pollution, especially at the relatively low levels, on developing dementia. We conducted a population-based cohort study in Ontario, Canada, where the concentrations of pollutants are among the lowest in the world, to assess whether air pollution exposure is associated with incident dementia. METHODS: The study population comprised all Ontario residents who, on 1 April 2001, were 55-85years old, Canadian-born, and free of physician-diagnosed dementia (~2.1 million individuals). Follow-up extended until 2013. We used population-based health administrative databases with a validated algorithm to ascertain incident diagnosis of dementia as well as prevalent cases. Using satellite observations, land-use regression model, and an optimal interpolation method, we derived long-term average exposure to fine particulate matter (≤2.5μm in diameter) (PM2.5), nitrogen dioxide (NO2), and ozone (O3), respectively at the subjects' historical residences based on a population-based registry. We used multilevel spatial random-effects Cox proportional hazards models, adjusting for individual and contextual factors, such as diabetes, brain injury, and neighborhood income. We conducted various sensitivity analyses, such as lagging exposure up to 10years and considering a negative control outcome for which no (or weaker) association with air pollution is expected. RESULTS: We identified 257,816 incident cases of dementia in 2001-2013. We found a positive association between PM2.5 and dementia incidence, with a hazard ratio (HR) of 1.04 (95% confidence interval (CI): 1.03-1.05) for every interquartile-range increase in exposure to PM2.5. Similarly, NO2 was associated with increased incidence of dementia (HR=1.10; 95% CI: 1.08-1.12). No association was found for O3. These associations were robust to all sensitivity analyses examined. These estimates translate to 6.1% of dementia cases (or 15,813 cases) attributable to PM2.5 and NO2, based on the observed distribution of exposure relative to the lowest quartile in concentrations in this cohort. DISCUSSION: In this large cohort, exposure to air pollution, even at the relative low levels, was associated with higher dementia incidence. Crown
INTRODUCTION: Emerging studies have implicated air pollution in the neurodegenerative processes. Less is known about the influence of air pollution, especially at the relatively low levels, on developing dementia. We conducted a population-based cohort study in Ontario, Canada, where the concentrations of pollutants are among the lowest in the world, to assess whether air pollution exposure is associated with incident dementia. METHODS: The study population comprised all Ontario residents who, on 1 April 2001, were 55-85years old, Canadian-born, and free of physician-diagnosed dementia (~2.1 million individuals). Follow-up extended until 2013. We used population-based health administrative databases with a validated algorithm to ascertain incident diagnosis of dementia as well as prevalent cases. Using satellite observations, land-use regression model, and an optimal interpolation method, we derived long-term average exposure to fine particulate matter (≤2.5μm in diameter) (PM2.5), nitrogen dioxide (NO2), and ozone (O3), respectively at the subjects' historical residences based on a population-based registry. We used multilevel spatial random-effects Cox proportional hazards models, adjusting for individual and contextual factors, such as diabetes, brain injury, and neighborhood income. We conducted various sensitivity analyses, such as lagging exposure up to 10years and considering a negative control outcome for which no (or weaker) association with air pollution is expected. RESULTS: We identified 257,816 incident cases of dementia in 2001-2013. We found a positive association between PM2.5 and dementia incidence, with a hazard ratio (HR) of 1.04 (95% confidence interval (CI): 1.03-1.05) for every interquartile-range increase in exposure to PM2.5. Similarly, NO2 was associated with increased incidence of dementia (HR=1.10; 95% CI: 1.08-1.12). No association was found for O3. These associations were robust to all sensitivity analyses examined. These estimates translate to 6.1% of dementia cases (or 15,813 cases) attributable to PM2.5 and NO2, based on the observed distribution of exposure relative to the lowest quartile in concentrations in this cohort. DISCUSSION: In this large cohort, exposure to air pollution, even at the relative low levels, was associated with higher dementia incidence. Crown
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