Dataset Information

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

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 (PM_2.5, PM₁₀, PM_2.5-10, PM_{2.5absorbance}, NO₂, 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). 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

PM_2.5 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.

SUBMITTER: Parra KL

PROVIDER: S-EPMC8976829 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature

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Publications

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

Parra Kimberly L KL Alexander Gene E GE Raichlen David A DA Klimentidis Yann C YC Furlong Melissa A MA

Environmental research 20220208

<h4>Background</h4>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.<h4>Objectives</h4>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 b ...[more]

PMID: 35149105

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Project description:ImportanceFine particulate matter air pollution (PM2.5) has been consistently associated with cardiovascular disease, which, in turn, is associated with an increased risk of dementia. As such, vascular dysfunction might be a mechanism by which PM2.5 mediates dementia risk, yet few prior epidemiological studies have examined this potential mechanism.ObjectiveTo investigate whether hypertension and stroke serve as mediators and modifiers of the association of PM2.5 with incident dementia.Design, setting, and participantsAs part of the Environmental Predictors of Cognitive Health and Aging (EPOCH) Project, this cohort study used biennial survey data collected between 1998 and 2016 from respondents of the Health and Retirement Study (HRS), a nationally representative, population-based, cohort in the US. Eligible participants were those over 50 years of age who were free of dementia at baseline and had complete exposure, mediator, outcome, and demographic data from the HRS. Data analysis was conducted from August to November 2022.ExposuresExposure to PM2.5, calculated for the 10 years preceding each person's baseline examination according to residential histories and spatiotemporal models.Main outcomes and measuresIncident dementia was identified using a validated algorithm based on cognitive testing and informant reports. The 4-way decomposition causal mediation analysis method was used to quantify the degree to which hypertension and stroke mediated or modified the association of PM2.5 with incident dementia after adjustment for individual-level and area-level covariates.ResultsAmong 27 857 participants (mean [SD] age at baseline, 61 [10] years; 15 747 female participants [56.5%]; 19 249 non-Hispanic White participants [69.1%]), 4105 (14.7%) developed dementia during the follow-up period (mean [SD], 10.2 [5.6] years). Among participants with dementia, 2204 (53.7%) had a history of hypertension at baseline and 386 (9.4%) received a diagnosis of hypertension during the follow up. A total of 378 participants (9.2%) had a history of stroke at baseline and 673 (16.4%) developed stroke over the follow-up period. The IQR of baseline PM2.5 concentrations was 10.9 to 14.9 μg/m3. In fully adjusted models, higher levels of PM2.5 (per IQR) were not associated with increased risk of incident dementia (HR, 1.04; 95% CI, 0.98 to 1.11). Although there were positive associations of prevalent stroke (HR, 1.67; 95% CI, 1.48 to 1.88) and hypertension (HR, 1.15; 95% CI, 1.08 to 1.23) with incident dementia compared with those free of stroke and hypertension during follow-up, there was no statistically significant association of PM2.5 with stroke (odds ratio per IQR increment in PM2.5, 1.08; 95%CI, 0.91 to 1.29) and no evidence of an association of PM2.5 with hypertension (odds ratio per IQR increment in PM2.5, 0.99; 95%CI, 0.92 to 1.07). Concordantly, there was no evidence that hypertension or stroke acted as mediators or modifiers of the association of PM2.5 with incident dementia. Although the nonmediated interaction between PM2.5 and hypertension accounted for 39.2% of the total excess association (95% CI, -138.5% to 216.9%), the findings were not statistically significant.Conclusions and relevanceThese findings suggest that although hypertension may enhance the susceptibility of individuals to air pollution, hypertension and stroke do not significantly mediate or modify the association of PM2.5 with dementia, indicating the need to investigate other pathways and potential mediators of risk.

Project description:Human exposure to particulate air pollution (e.g., PM2.5) can lead to adverse health effects, with compelling evidence that it can increase morbidity and mortality from respiratory and cardiovascular disease. More recently, there has also been evidence that long-term environmental exposure to particulate air pollution is associated with type-2 diabetes mellitus (T2DM) and dementia. There are many occupations that may expose workers to airborne particles and that some exposures in the workplace are very similar to environmental particulate pollution. We conducted a cross-sectional analysis of the UK Biobank cohort to verify the association between environmental particulate air pollution (PM2.5) exposure and T2DM and dementia, and to investigate if occupational exposure to particulates that are similar to those found in environmental air pollution could increase the odds of developing these diseases. The UK Biobank dataset comprises of over 500,000 participants from all over the UK. Environmental exposure variables were used from the UK Biobank. To estimate occupational exposure both the UK Biobank's data and information from a job exposure matrix, specifically developed for UK Biobank (Airborne Chemical Exposure-Job Exposure Matrix (ACE JEM)), were used. The outcome measures were participants with T2DM and dementia. In appropriately adjusted models, environmental exposure to PM2.5 was associated with an odds ratio (OR) of 1.02 (95% CI 1.00 to 1.03) per unit exposure for developing T2DM, while PM2.5 was associated with an odds ratio of 1.06 (95% CI 0.96 to 1.16) per unit exposure for developing dementia. These environmental results align with existing findings in the published literature. Five occupational exposures (dust, fumes, diesel, mineral, and biological dust in the most recent job estimated with the ACE JEM) were investigated and the risks for most exposures for T2DM and for all the exposures for dementia were not significantly increased in the adjusted models. This was confirmed in a subgroup of participants where a full occupational history was available allowed an estimate of workplace exposures. However, when not adjusting for gender, some of the associations become significant, which suggests that there might be a bias between the occupational assessments for men and women. The results of the present study do not provide clear evidence of an association between occupational exposure to particulate matter and T2DM or dementia.

Project description:BackgroundWorldwide, the prevalence of dementia is increasing and diet as a modifiable factor could play a role. Meat consumption has been cross-sectionally associated with dementia risk, but specific amounts and types related to risk of incident dementia remain poorly understood.ObjectiveWe aimed to investigate associations between meat consumption and risk of incident dementia in the UK Biobank cohort.MethodsMeat consumption was estimated using a short dietary questionnaire at recruitment and repeated 24-h dietary assessments. Incident all-cause dementia comprising Alzheimer disease (AD) and vascular dementia (VD) was identified by electronic linkages to hospital and mortality records. HRs for each meat type in relation to each dementia outcome were estimated in Cox proportional hazard models. Interactions between meat consumption and the apolipoprotein E (APOE) ε4 allele were additionally explored.ResultsAmong 493,888 participants included, 2896 incident cases of all-cause dementia, 1006 cases of AD, and 490 cases of VD were identified, with mean ± SD follow-up of 8 ± 1.1 y. Each additional 25 g/day intake of processed meat was associated with increased risks of incident all-cause dementia (HR: 1.44; 95% CI: 1.24, 1.67; P-trend < 0.001) and AD (HR: 1.52; 95% CI: 1.18, 1.96; P-trend = 0.001). In contrast, a 50-g/d increment in unprocessed red meat intake was associated with reduced risks of all-cause dementia (HR: 0.81; 95% CI: 0.69, 0.95; P-trend = 0.011) and AD (HR: 0.70; 95% CI: 0.53, 0.92; P-trend = 0.009). The linear trend was not significant for unprocessed poultry and total meat. Regarding incident VD, there were no statistically significant linear trends identified, although for processed meat, higher consumption categories were associated with increased risks. The APOE ε4 allele increased dementia risk by 3 to 6 times but did not modify the associations with diet significantly.ConclusionThese findings highlight processed-meat consumption as a potential risk factor for incident dementia, independent of the APOE ε4 allele.

Dataset Information

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

Background

Objectives

Methods

Results

Discussion

Publications

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

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