Dataset Information

Incident dementia and long-term exposure to constituents of fine particle air pollution: A national cohort study in the United States.

ABSTRACT: Growing evidence suggests that fine particulate matter (PM_2.5) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. Here, we conducted a nationwide population-based cohort study (2000 to 2017) by integrating the Medicare Chronic Conditions Warehouse database and two independently sourced datasets of high-resolution PM_2.5 major chemical composition, including black carbon (BC), organic matter (OM), nitrate (NO₃^-), sulfate (SO₄^2-), ammonium (NH₄⁺), and soil dust (DUST). To investigate the impact of long-term exposure to PM_2.5 constituents on incident all-cause dementia and Alzheimer's disease (AD), hazard ratios for dementia and AD were estimated using Cox proportional hazards models, and penalized splines were used to evaluate potential nonlinear concentration-response (C-R) relationships. Results using two exposure datasets consistently indicated higher rates of incident dementia and AD for an increased exposure to PM_2.5 and its major constituents. An interquartile range increase in PM_2.5 mass was associated with a 6 to 7% increase in dementia incidence and a 9% increase in AD incidence. For different PM_2.5 constituents, associations remained significant for BC, OM, SO₄^2-, and NH₄⁺ for both end points (even after adjustments of other constituents), among which BC and SO₄^2- showed the strongest associations. All constituents had largely linear C-R relationships in the low exposure range, but most tailed off at higher exposure concentrations. Our findings suggest that long-term exposure to PM_2.5 is significantly associated with higher rates of incident dementia and AD and that SO₄^2-, BC, and OM related to traffic and fossil fuel combustion might drive the observed associations.

SUBMITTER: Shi L

PROVIDER: S-EPMC9910468 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature

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Incident dementia and long-term exposure to constituents of fine particle air pollution: A national cohort study in the United States.

Shi Liuhua L Zhu Qiao Q Wang Yifan Y Hao Hua H Zhang Haisu H Schwartz Joel J Amini Heresh H van Donkelaar Aaron A Martin Randall V RV Steenland Kyle K Sarnat Jeremy A JA Caudle W Michael WM Ma Tszshan T Li Haomin H Chang Howard H HH Liu Jeremiah Z JZ Wingo Thomas T Mao Xiaobo X Russell Armistead G AG Weber Rodney J RJ Liu Pengfei P

Proceedings of the National Academy of Sciences of the United States of America 20221227 1

Growing evidence suggests that fine particulate matter (PM<sub>2.5</sub>) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. Here, we conducted a nationwide population-based cohort study (2000 to 2017) by integrating the Medicare Chronic Conditions Warehouse database and two independently sourced datasets of high-resolution PM<sub>2.5</sub> major chemical composition, including black carbon (BC), organic matter (OM), nitrate (N ...[more]

PMID: 36574646

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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:BackgroundAir 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.ObjectivesTo 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.MethodsThe 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.ResultsOur 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.DiscussionPM2.5 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.

Dataset Information

Incident dementia and long-term exposure to constituents of fine particle air pollution: A national cohort study in the United States.

Publications

Incident dementia and long-term exposure to constituents of fine particle air pollution: A national cohort study in the United States.

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