Association between Fine Particulate Matter Exposure and Cerebrospinal Fluid Biomarkers of Alzheimer’s Disease among a Cognitively Healthy Population-based Brain Cohort Restricted; Files & ToC

Casey, Emma (Spring 2023)

Permanent URL: https://etd.library.emory.edu/concern/etds/nz8061140?locale=zh
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Abstract

Background: Epidemiological evidence suggests air pollution adversely affects cognition and increases the risk of Alzheimer’s disease (AD), but little is known about the biological effects of fine particulate matter (PM2.5) on early predictors of future disease risk.

 

Objectives: We investigated the association between 1, 3, and 5-year exposure to ambient or traffic-related PM2.5 and cerebrospinal fluid biomarkers (CSF) of AD.

 

Methods: We conducted a cross-sectional analysis using data from 1,113 cognitively healthy adults (aged 45-75 years) from the Emory Healthy Brain Study (EHBS) in Georgia. CSF biomarker concentrations of Aβ42, tTau, and pTau, were collected from participants at enrollment (between 2016-2020) and analyzed with the Roche Elecsys system. Annual ambient and traffic-related residential PM2.5 exposures were estimated at a 1 km and 250 m resolution respectively, and 3- and 5-year exposures were computed as averages of the time before specimen collection. Associations between PM2.5 and CSF biomarker concentrations in addition to AD positive cut-offs were estimated with multiple linear/logistic regression respectively, controlling for potential confounders (age, sex, race/ethnicity, BMI, and neighborhood socioeconomic status (N-SES)).

 

Results: Interquartile range (IQR; IQR=0.845) increases in 1-year [β: -0.101; 95% confidence interval (CI): -0.18, -0.02] and 3-year [β: -0.078; 95% CI: -0.15, -0.006] residential ambient fine PM2.5 exposures were negatively associated with Aβ42 CSF concentrations. Associations between ambient PM2.5 and Aβ42 were similar for 5-year estimates, but not significant (β: -0.076; 95% CI: -0.160, 0.005). AD CSF portfolio positive cut-offs revealed similar and significant associations between ambient PM2.5 and Aβ42. PM2.5 exposures were not associated with tTau, pTau, tTau/Aβ42, or pTau/Aβ42 levels at enrollment.

 

Conclusion: In our study, PM2.5 exposure, was associated with a significant decrease in CSF Aβ42 which suggests an increased risk of developing AD. Longitudinal analyses will clarify the effects of PM2.5 on AD progression. 

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