Fine particulate matter and neuroanatomic risk for Alzheimer’s disease in older women

Objective: To examine whether late-life exposure to PM2.5 (particulate
matter with aerodynamic diameters <2.5-µm) contributes to
progressive brain atrophy predictive of Alzheimer’s disease (AD) using a
community-dwelling cohort of women (aged 71-89) with up to two brain MRI
scans (MRI-1: 2005-6; MRI-2: 2010-11). Methods: AD pattern similarity
(AD-PS) scores, developed by supervised machine learning and validated
with MRI data from the AD Neuroimaging Initiative, was used to capture
high-dimensional gray matter atrophy in brain areas vulnerable to AD
(e.g., amygdala, hippocampus, parahippocampal gyrus, thalamus, inferior
temporal lobe areas and midbrain). Based on participants’ addresses and
air monitoring data, we employed a spatiotemporal model to estimate 3-year
average exposure to PM2.5 preceding MRI-1. General linear models
were used to examine the association between PM2.5 and AD-PS scores
(baseline [n=1365] and 5-year standardized change [n=712]), accounting for
potential confounders and white matter lesion volumes. Results: There was
no association between PM2.5 and baseline AD-PS score in cross-sectional
analyses. Longitudinally, each interquartile range increase of PM2.5
(2.82-µg/m3) was associated with increased AD-PS scores during the
follow-up, equivalent to a 24% (hazard ratio=1.24; 95% CI: 1.14, 1.34)
increase in AD risk over 5-years. This association remained after
adjustment for socio-demographics, intracranial volume, lifestyle,
clinical characteristics, and white matter lesions, and was present with
levels below US regulatory standards (<12-µg/m3). Conclusions:
Late-life exposure to PM2.5 is associated with increased neuroanatomical
risk of AD, which may not be explained by available indicators of
cerebrovascular damage.