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Background: Air pollution has been associated with cognitive decline among the elderly. Previous studies have not evaluated the simultaneous effect of neighborhood-level socioeconomic status (N-SES), which can be an essential source of bias. Objectives: We explored N-SES as a confounder and effect modifier in a cross-sectional study of air pollution and cognitive function among the elderly. Methods: We included 12,058 participants age 50+ years from the Emory Healthy Aging Study in Metro Atlanta using the Cognitive Function Instrument (CFI) score as our outcome, with higher scores representing worse cognition. We estimated 9-year average ambient carbon monoxide (CO), nitrogen oxides (NOx), and fine particulate matter (PM2.5) concentrations at residential addresses using a fusion of dispersion and chemical transport models. We collected census-tract level N-SES indicators and created two composite measures using principal component analysis and k-means clustering. Associations between pollutants and CFI and effect modification by N-SES were estimated via linear regression models adjusted for age, education, race and N-SES. Results: N-SES confounded the association between air pollution and CFI, independent of individual characteristics. We found significant interactions between all air pollutants and N-SES for CFI (p-values<0.001) suggesting that effects of air pollution differ depending on N-SES. Participants living in areas with low N-SES were most vulnerable to air pollution. In the lowest N-SES urban areas, interquartile range (IQR) increases in CO, NOx, and PM2.5 were associated with 5.4% (95%-confidence interval, -0.2,11.4), 4.9% (-0.4,10.4), and 9.8% (2.2,18.0) increases in CFI, respectively. In lowest N-SES suburban areas, IQR increases in CO, NOx, and PM2.5 were associated with higher increases in CFI, namely 13.4% (1.3,26.9), 13.4% (0.3,28.2), and 17.6% (2.8,34.5), respectively. Discussion: N-SES is an important confounder and effect modifier in our study. This finding could have implications for studying health effects of air pollution in the context of environmental injustice.

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 and traffic-related PM2.5and cerebrospinal fluid (CSF) biomarkers 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 in Georgia, USA. CSF biomarker concentrations of Aβ42, tTau, and pTau, were collected at enrollment (between 2016-2020) and analyzed with the Roche Elecsys system. Annual ambient and traffic-related residential PM2.5concentrations were estimated at a 1km and 250m resolution, respectively, and 3- and 5-year average exposures were computed for each participant based on time of specimen collection. Associations between PM2.5and CSF biomarker concentrations, considering continuous and dichotomous (dichotomized at clinical cut-offs for AD-biomarker positivity) outcomes, were estimated with multiple linear/logistic regression, respectively, controlling for potential confounders (age, gender, race/ethnicity, body mass index, and neighborhood socioeconomic status). 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, -0.00) ambient fine PM2.5exposures were negatively associated with Aβ42CSF concentrations. Associations between ambient PM2.5and Aβ42were similar for 5-year estimates, but not significant (β: -0.076; 95%-CI: -0.160, 0.005). Dichotomized CSF variables revealed similar and significant associations between ambient PM2.5and Aβ42. Associations with traffic-related PM2.5were similar but not significant. PM2.5exposures were not associated with tTau, pTau, tTau/Aβ42, or pTau/Aβ42levels at enrollment. Conclusion: In our cross-sectional study, PM2.5exposure was associated with a significant decrease in CSF Aβ42which suggests an accumulation of amyloid plaques in the brain and an increased risk of developing AD.