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Long‐term exposure to ambient air pollution and risk of dementia: Results of the prospective Three‐City Study
Author(s) -
Mortamais Marion,
Gutierrez Laure Anne,
de Hoogh Kees,
Benmarhnia Tarik,
Helmer Catherine,
Tzourio Christophe,
Dartigues JeanFrançois,
Letellier Noemie,
Jacquemin Benedicte,
Berr Claudine
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.041059
Subject(s) - dementia , medicine , confounding , environmental health , hazard ratio , proportional hazards model , population , cohort study , cohort , epidemiology , demography , gerontology , confidence interval , disease , sociology
Background Chronic exposure to air pollution (AP) is associated with cardiovascular morbidity and mortality. Emerging epidemiological evidence suggests a relationship between exposure to various air pollutants (fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2)) and dementia. However, most of existing studies relied on population‐based health administrative databases to obtain a dementia diagnosis. In a large French population‐based cohort (the Three‐City Study) and using state‐of‐the‐art models for AP exposure, we aimed at assessing the effects of different air pollutants on dementia risk using reliable diagnosis tools. Methods Participants aged ≥65 years were recruited between 1999 and 2001 and followed for 12 years. At baseline and every 2 years, dementia diagnoses were preliminary made using DSM‐IV criteria and validated by an adjudication committee. Levels of NO2, O3, Black Carbon and PM2.5 were obtained at the residential addresses of participants using land‐use regression models developed for Europe in the ELAPSE project (de Hoogh et al., Env Int 120 (2018) 81‐92). For each year of follow‐up, we estimated for each subject a 10‐year moving window of mean past exposure to each pollutant. We used a Cox Proportional Hazard model where exposure to AP was included as a time‐varying variable. Analyses were adjusted for individual (age, sex, education, APOE4 genotype, vascular risk factors, depression, respiratory diseases) and contextual (neighborhood’s deprivation index) level confounders. Result At baseline, the mean (SD) age of the 7956 participants was 73.2 (5.4) years‐old. Sixty‐one percent of them were women. The mean time of follow‐up was 9.2 (3.6) years. Over the follow‐up period, the mean annual PM2.5 levels ranged from 15 to 33 µg/m 3 and 910 participants developed dementia. We observed a positive association between levels of PM2.5 and dementia risk [HR=1.16, 95%CI (1.02‐1.32) for a 5µg/m 3 increase in PM2.5]. We did not observe any relationship between exposure to the other air pollutants and dementia risk. Conclusion In this large cohort with reliable diagnosis of dementia and individual estimates of AP exposure, we observed that long‐term exposure to PM2.5 was associated with higher dementia incidence. These results suggest that PM2.5 exposure might be a modifiable risk factor of dementia.