Sindana D Ilango1,2, Hong Chen3,4,5,6, Perry Hystad7, Aaron van Donkelaar8, Jeffrey C Kwong4,5,6,9,10, Karen Tu9,10, Randall V Martin8,11, Tarik Benmarhnia2,12. 1. Graduate School of Public Health, San Diego State University, San Diego, CA, USA. 2. Department of Family Medicine and Public Health, University of California San Diego, La Jolla, CA, USA. 3. Population Studies Division, Environmental Health Science and Research Bureau, Health Canada, Ottawa, ON, Canada. 4. Public Health Ontario, Toronto, ON, Canada. 5. ICES, Toronto, ON, Canada. 6. Dalla Lana School of Public Health, University of Toronto, Toronto, ON, Canada. 7. College of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA. 8. Department of Physics and Atmospheric Science, Dalhousie University, Halifax, NS, Canada. 9. Department of Family and Community Medicine, University of Toronto, Toronto, ON, Canada. 10. Toronto Western Family Health Team, University Health Network, Toronto, ON, Canada. 11. Harvard-Smithsonian Centre for Astrophysics, Cambridge, MA, USA. 12. Scripps Institution of Oceanography, University of California, San Diego, La Jolla, CA, USA.
Abstract
BACKGROUND: Evidence suggests a link between air pollution and dementia. Cardiovascular disease (CVD) may be a potential determinant of dementia. This motivated us to quantify the contribution of CVD to the association between air pollution and dementia. METHODS: A cohort of Canadian-born residents of Ontario, who participated in the 1996-2003 Canadian Community Health Surveys, was followed through 2013 or until dementia diagnosis. Exposure to nitrogen dioxide (NO2) and fine particulate matter (PM2.5) was estimated with a 3-year average and 5-year lag before dementia diagnosis. Incident CVD was evaluated as a mediator. We used multi-level Cox proportional and Aalen additive hazard regression models, adjusting for individual- and neighbourhood-level risk factors to estimate associations with NO2 and PM2.5. We estimated the total, direct and indirect effects of air pollution on dementia through cardiovascular disease. RESULTS: This study included 34 391 older adults. At baseline, the mean age of this cohort was 59 years. The risk of dementia was moderately higher among those more exposed to NO2 (hazard ratio (HR) 1.10, 95% confidence interval (CI) 0.99-1.19; and 100 additional cases per 100 000 [standard error (SE) <100x10-5]) and PM2.5 [(HR 1.29, 95% CI 0.99-1.64; 200 additional cases per 100 000] [SE 100x10-5]) after adjusting for covariates; however, these estimates are imprecise. A greater proportion of the relationship between PM2.5 and dementia was mediated through CVD than NO2 for both scales. CONCLUSIONS: These results suggest some of the association between air pollution and dementia is mediated through CVD, indicating that improving cardiovascular health may prevent dementia in areas with higher exposure to air pollution.
BACKGROUND: Evidence suggests a link between air pollution and dementia. Cardiovascular disease (CVD) may be a potential determinant of dementia. This motivated us to quantify the contribution of CVD to the association between air pollution and dementia. METHODS: A cohort of Canadian-born residents of Ontario, who participated in the 1996-2003 Canadian Community Health Surveys, was followed through 2013 or until dementia diagnosis. Exposure to nitrogen dioxide (NO2) and fine particulate matter (PM2.5) was estimated with a 3-year average and 5-year lag before dementia diagnosis. Incident CVD was evaluated as a mediator. We used multi-level Cox proportional and Aalen additive hazard regression models, adjusting for individual- and neighbourhood-level risk factors to estimate associations with NO2 and PM2.5. We estimated the total, direct and indirect effects of air pollution on dementia through cardiovascular disease. RESULTS: This study included 34 391 older adults. At baseline, the mean age of this cohort was 59 years. The risk of dementia was moderately higher among those more exposed to NO2 (hazard ratio (HR) 1.10, 95% confidence interval (CI) 0.99-1.19; and 100 additional cases per 100 000 [standard error (SE) <100x10-5]) and PM2.5 [(HR 1.29, 95% CI 0.99-1.64; 200 additional cases per 100 000] [SE 100x10-5]) after adjusting for covariates; however, these estimates are imprecise. A greater proportion of the relationship between PM2.5 and dementia was mediated through CVD than NO2 for both scales. CONCLUSIONS: These results suggest some of the association between air pollution and dementia is mediated through CVD, indicating that improving cardiovascular health may prevent dementia in areas with higher exposure to air pollution.
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