The association between longterm PM2.5 exposure and latelife amyloid burden in the Atherosclerosis Risk in Communities (ARIC) study cohort
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AbstractBackgroundA number of studies show an association between longterm exposure to ambient particulate matter 2.5 um (PM2.5) and latelife cognitive impairment. Mechanistic models suggest that PM2.5 may influence cognitive health through promotion of Alzheimers disease, which is characterized by brain amyloid accumulation. However, the association between longterm PM2.5 exposure and brain amyloid deposition remains poorly characterized in epidemiological studies.MethodWe used data from the Atherosclerosis Risk in Communities (ARIC) study cohort. We used a chemical transport model with data fusion to estimate mean PM2.5 concentrations (ug/m3) in 36, 12, 4, and 1km grid cells in ARIC study areas. We linked the concentrations to geocoded participant addresses and calculated mean PM2.5 concentrations from 2000 to 2007. We estimated amyloid deposition using florbetapir amyloid positron emission tomography (PET) scans in 346 ARICPET participants with normal cognition or mild cognitive impairment in 20112014. We defined amyloid positivity as a global cortical standardized uptake value ratio (SUVR) the sample median of 1.2. We used logistic regression models to quantify the association between amyloid positivity and mean 20002007 PM2.5 concentration after adjusting for potential confounders. We additionally explored effect measure modification by APOE e4 allele status and tested whether effect estimates were consistent using alternate PM2.5 exposure methods.ResultAfter restricting to participants with nonmissing exposure and confounder data and excluding one participant with dementia, the analytic sample included 279 participants. At the time of amyloidPET scans, their mean age was 78 years, 56% were female, 42% were Black, and 26% had mild cognitive impairment. After adjusting for age, sex, education, and racestudy center, we found no significant association between brain amyloid positivity and longterm mean PM2.5 exposure. We also found no evidence of effect measure modification by APOE e4 allele status. Results were consistent when we used alternate PM2.5 estimation methods.ConclusionOur findings suggest that ambient PM2.5 may induce neurotoxic effects through nonamyloid, potentially vascular pathways, though we note the small sample size may have made us underpowered to detect a significant association.
Bennett, E. E., Xu, X., Lynch, K. M., Park, E. S., Ying, Q. i., Smith, R. L., ... Power, M. C.
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Bennett, Erin E||Xu, Xiaohui||Lynch, Katie M||Park, Eun Sug||Ying, Qi||Smith, Richard L||Stewart, James D||Whitsel, Eric A||Mosley, Thomas H||Yanosky, Jeff D||Wong, Dean F||Liao, Duanping||Gottesman, Rebecca F||Power, Melinda C
