Search

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 (PM 2.5 , PM 10 , PM 2.5-10 , PM 2.5absorbance , NO 2 , NO X ) 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 PM 2.5 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). NO 2 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: PM 2.5 and NO 2 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., (Published by Elsevier Inc.)

Air pollution has consistently been associated with cardiometabolic outcomes, although associations with obesity have only been recently reported. Studies of air pollution and adiposity have mostly relied on body mass index (BMI) rather than body fat percentage (BF%), and most have not accounted for noise as a possible confounder. Additionally, it is unknown whether genetic predisposition for obesity increases susceptibility to the obesogenic effects of air pollution. To help fill these gaps, we used the UK Biobank, a large, prospective cohort study in the United Kingdom, to explore the relationship between air pollution and adiposity, and modification by a polygenic risk score for BMI. We used 2010 annual averages of air pollution estimates from land use regression (NO 2 , NO X , PM 2.5 , PM 2.5absorbance , PM 2.5-10 , PM 10 ), traffic intensity (TI), inverse distance to road (IDTR), along with examiner-measured BMI, waist-hip-ratio (WHR), and impedance measures of BF%, which were collected at enrollment (2006-2010, n = 473,026) and at follow-up (2012-2013, n = 19,518). We estimated associations of air pollution with BMI, WHR, and BF% at enrollment and follow-up, and with obesity, abdominal obesity, and BF%-obesity at enrollment and follow-up. We used linear and logistic regression and controlled for noise and other covariates. We also assessed interactions of air pollution with a polygenic risk score for BMI. On average, participants at enrollment were 56 years of age, 54% were female, and 32% had completed college or a higher degree. Almost all participants (~95%) were white. All air pollution measures except IDTR were positively associated with at least one continuous measure of adiposity at enrollment. However, NO 2 was negatively associated with BMI but positively associated with WHR at enrollment, and IDTR was also negatively associated with BMI. At follow-up (controlling for enrollment adiposity), we observed positive associations for PM 2.5-10 with BMI, PM 10 with BF%, and TI with BF% and BMI. Associations were similar for binary measures of adiposity, with minor differences for some pollutants. Associations of NO X , NO 2 , PM 2.5absorbance , PM 2.5 and PM 10 , with BMI at enrollment, but not at follow-up, were stronger among individuals with higher BMI polygenic risk scores (interaction p <0.05). In this large, prospective cohort, air pollution was associated with several measures of adiposity at enrollment and follow-up, and associations with adiposity at enrollment were modified by a polygenic risk score for obesity., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare., (Copyright © 2020 Elsevier Inc. All rights reserved.)