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Exposure to air pollution and risk of incident dementia in the UK Biobank.
Parra, Kimberly L; Alexander, Gene E; Raichlen, David A; Klimentidis, Yann C; Furlong, Melissa A.
Afiliação
  • Parra KL; Department of Epidemiology & Biostatistics, University of Arizona Mel and Enid Zuckerman College of Public Health, Tucson, AZ, USA. Electronic address: klparra@email.arizona.edu.
  • Alexander GE; Departments of Psychology and Psychiatry, Neuroscience and Physiological Sciences Graduate Interdisciplinary Programs, BIO5 Institute, and Evelyn F. McKnight Brain Institute, University of Arizona, Tucson, AZ, USA; Arizona Alzheimer's Consortium, Phoenix, AZ, USA.
  • Raichlen DA; Department of Biological Sciences, Human and Evolutionary Biology Section, University of Southern California, Los Angeles, CA, USA.
  • Klimentidis YC; Department of Epidemiology & Biostatistics, University of Arizona Mel and Enid Zuckerman College of Public Health, Tucson, AZ, USA.
  • Furlong MA; Department of Community, Environment, and Policy, Division of Environmental Health Sciences, University of Arizona Mel and Enid Zuckerman College of Public Health, Tucson, AZ, USA.
Environ Res ; 209: 112895, 2022 06.
Article em En | MEDLINE | ID: mdl-35149105
ABSTRACT

BACKGROUND:

Air pollution may cause inflammatory and oxidative stress damage to the brain, leading to neurodegenerative disease. The association between air pollution and dementia, and modification by apolipoprotein E genotype 4 (APOE-ε4) has yet to be fully investigated.

OBJECTIVES:

To examine associations of air pollution with three types of incident dementias (Alzheimer's disease (AD), frontotemporal dementia (FTD), and vascular dementia (VAD)), and their potential modification by APOE-ε4 genotype.

METHODS:

The UK Biobank enrolled >500,000 participants (2006-2010) with ongoing follow-up. We used annual averages of air pollution (PM2.5, PM10, PM2.5-10, PM2.5absorbance, NO2, NOX) for 2010 scaled to interquartile ranges (IQR). We included individuals aged ≥60 years, with no dementia diagnosis prior to January 1, 2010. Time to incident dementia and follow-up time were reported from baseline (January 01, 2010) to last censor event (death, last hospitalization, or loss to follow-up). Cox proportional hazard ratios (HR) and 95% confidence intervals (95% CI) were calculated to estimate the association of air pollutants and incident dementia, and modification of these associations by APOE-ε4.

RESULTS:

Our sample included 187,194 individuals (including N = 680 AD, N = 377 VAD, N = 63 FTD) with a mean follow-up of 7.04 years. We observed consistent associations of PM2.5 with greater risk of all-cause dementia (HR = 1.17, 95% CI 1.10, 1.24) and AD (HR = 1.17, 95% CI 1.06, 1.29). NO2 was also associated with greater risk of any incident dementia (HR = 1.18, 95% CI 1.10, 1.25), AD (HR = 1.15, 95% CI 1.04, 1.28) and VAD (HR = 1.18, 95% CI 1.03, 1.35). APOE-ε4 did not modify the association between any air pollutants and dementia.

DISCUSSION:

PM2.5 and NO2 levels were associated with several types of dementia, and these associations were not modified by APOE-ε4. Findings from the UK Biobank support and extend to other epidemiological evidence for the potential association of air pollutants with detrimental brain health during aging.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Neurodegenerativas / Poluentes Atmosféricos / Poluição do Ar / Doença de Alzheimer País/Região como assunto: Europa Idioma: En Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Doenças Neurodegenerativas / Poluentes Atmosféricos / Poluição do Ar / Doença de Alzheimer País/Região como assunto: Europa Idioma: En Ano de publicação: 2022 Tipo de documento: Article