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Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity
Published on: October 25, 2016
Ambient air pollution and neurotoxicity on brain structure: Evidence from women's health initiative memory study
Jiu-Chiuan Chen1, Xinhui Wang1, Gregory A Wellenius2
1Department of Preventive Medicine, University of Southern California, Keck School of Medicine, Los Angeles, CA.
Objective:
The aim of this study was to examine the putative adverse effects of ambient fine particulate matter (PM2.5 : PM with aerodynamic diameters <2.5microm) on brain volumes in older women.
Methods:
We conducted a prospective study of 1,403 community-dwelling older women without dementia enrolled in the Women's Health Initiative Memory Study, 1996-1998. Structural brain magnetic resonance imaging scans were performed at the age of 71-89 years in 2005-2006 to obtain volumetric measures of gray matter (GM) and normal-appearing white matter (WM). Given residential histories and air monitoring data, we used a spatiotemporal model to estimate cumulative PM2.5 exposure in 1999-2006. Multiple linear regression was employed to evaluate the associations between PM2.5 and brain volumes, adjusting for intracranial volumes and potential confounders.
Results:
Older women with greater PM2.5 exposures had significantly smaller WM, but not GM, volumes, independent of geographical region, demographics, socioeconomic status, lifestyles, and clinical characteristics, including cardiovascular risk factors. For each interquartile increment (3.49microg/m(3) ) of cumulative PM2.5 exposure, the average WM volume (WMV; 95% confidence interval) was 6.23cm(3) (3.72-8.74) smaller in the total brain and 4.47cm(3) (2.27-6.67) lower in the association areas, equivalent to 1 to 2 years of brain aging. The adverse PM2.5 effects on smaller WMVs were present in frontal and temporal lobes and corpus callosum (all p values <0.01). Hippocampal volumes did not differ by PM2.5 exposure.
Interpretation:
PM2.5 exposure may contribute to WM loss in older women. Future studies are needed to determine whether exposures result in myelination disturbance, disruption of axonal integrity, damages to oligodendrocytes, or other WM neuropathologies.
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