Air pollution associated with amyloid-β pathology in older adults with cognitive impairment
A cross-sectional study in >18,000 older adults with cognitive impairment finds an association between higher fine particulate matter (PM2.5) concentrations and brain amyloid-β (Aβ) plaques.
The study was a secondary analysis of data from the IDEAS (Imaging Dementia – Evidence for Amyloid Scanning) Study, which included 18,178 patients, of which 10,991 (60.5 percent) had mild cognitive impairment (MCI) and 7,187 (39.5 percent) had dementia (mean age, 75.8 years; female, 51.3 percent), who underwent a PET scan to assess brain Aβ accumulation (amyloid PET scan). Air pollution was estimated approximately 14 years (2002–2003 period) and 1 year (2015–2016) before the amyloid PET scan at the patient’s residence based on PM2.5 and ground-level ozone (O3) concentrations from the Environmental Protection Agency Downscaler model. [JAMA Neurol 2020, doi: 10.1001/jamaneurol.2020.3962]
“Living in areas with higher concentrations of PM2.5 was associated with an increase in the odds of amyloid PET scan positivity, with and without controlling for covariates,” wrote the researchers.
In adjusted models when considering 2002–2003 data, the odds of a positive amyloid PET scan were increased by a factor of 1.10 (odds ratio [OR], 1.10; 95 percent confidence interval [CI], 1.05 to 1.15; false discovery rate [FDR]-corrected p<0.001) for each 4 μg/m3 increase of estimated biennial PM2.5. Findings using 2015–2016 data were similar (OR, 1.15; 95 percent CI, 1.05 to 1.26; FDR-corrected p=0.003).
Considering 2002–2003 quartiles’ PM2.5 data, the most pronounced increase in the likelihood of amyloid PET scan positivity was observed in quartile 4 (Q4, locations with predicted PM2.5 >14.44 μg/m3) vs Q1 (reference group). For the 2015–2016 time window, the most pronounced increase was observed in Q3 (locations with predicted PM2.5 between 8.34 and 9.37 μg/m3) compared with Q1.
“The associations were statistically significant after adjusting for individualized covariates, and showed similar dose-response associations across the whole sample,” noted the researchers. “Complementary evidence from a recent neuroimaging study indicates that exposure to PM2.5 has an unfavorable association with episodic memory performance, an association mediated by volume loss in AD brain regions.” [Brain 2020;143:289-302]
On the other hand, exposure to higher O3 concentrations was not associated with amyloid PET scan positivity for either 2002–2003 or 2015–2016 periods. “Previous data on the associations between exposure to O3 and incidence of AD were inconsistent,” commented the researchers. [BMJ Open 2018;8:e022404; J Alzheimers Dis 2015;44:573-584] “Inhaled gaseous pollutants, such as O3, are less likely to reach the central nervous system and may trigger neurotoxic effects through indirect pathways, such as microglial activation and priming through O3-induced peripheral circulating proinflammatory factors.” [Curr Environ Health Rep 2017;4:166-179; FASEB J 2016;30:1880-1891]
“Higher PM2.5 concentrations appeared to be associated with brain Aβ plaques, a signature of AD. Adverse effects of airborne toxic pollutants associated with Aβ pathology should be considered in public health policy decisions and should inform individual lifetime risk of developing AD and dementia,” concluded the researchers.