Exposure to air pollution and risk of incident dementia in the UK Biobank

Background: Air pollution may cause inflammatory and oxidative stress damage to the brain, leading to neuro-degenerative disease. The association between air pollution and dementia, and modification by apolipoprotein E genotype 4 (APOE-epsilon 4) 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-epsilon 4 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 in-tervals (95% CI) were calculated to estimate the association of air pollutants and incident dementia, and modification of these associations by APOE-epsilon 4.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 de-mentia (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-epsilon 4 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-epsilon 4. 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.