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Air pollution relates to altered intracellular microstructure in prefrontal white matter in children across the U.S.

Wed, April 7, 11:35am to 1:05pm EDT (11:35am to 1:05pm EDT), Virtual

Abstract

Introduction:
Fine particulate matter (aerodynamic diameter<2.5 μm; PM2.5) is ubiquitous in urban areas and is emerging as a novel neurotoxicant that may impact cognitive, psychomotor, and behavioral development. Moreover, initial human MRI and animal studies suggest that PM2.5 may especially impact white matter and increase neuroinflammation. The goal of the current study was to examine how PM2.5 exposure relates to prefrontal white matter microstructure in a large, diverse sample of children.

Hypothesis:
We hypothesized that higher levels of ambient PM2.5 exposure would be related to differences in white matter microstructure as indexed by tractography white matter bundle volumes and altered microarchitecture in intracellular and extracellular spaces.

Study Population:
The 2.0.1 data release of the ABCD study was used to collect baseline data for 11,875 children, aged 9-10, from 21 study sites across the United States. After exclusion for missing data and abnormal MRI findings, the final study population includes 8,193 children.

Methods:
Yearly ambient PM2.5 exposure estimates were assigned to the primary residential address at the study inception using an ensemble-based model. Multi-band diffusion weighted images (96 directions; 7 b=0; 4 b-values; 1.7 mm isotropic voxels) were collected for each child. Major white matter tracts were estimated using TrackAtlas and a Restriction Spectrum Imaging model was used to estimate isotropic restricted diffusion in white matter. Linear mixed effects models, fit with natural cubic splines, were used to analyze the relationship between annual PM2.5 exposure and white matter structural connectivity and isotropic restricted diffusion in 9-10 year-old children. Models were fit for the left and right hemispheres separately. Annual ambient PM2.5 exposure and potential confounders – selected based on prior knowledge and empirical data – were included in the models as fixed effects. To account for within-site clustering in ABCD sites and clustering within families, random intercepts were included for ABCD sites, and nested random intercepts were included for families.

Results:
In the left hemisphere, natural cubic splines modeling the association between ambient PM2.5 exposure and white matter isotropic restricted diffusion reflect consistent and statistically significant relationships between the exposure and altered white matter microstructure in six of the eight white matter fiber tracts analyzed. Among these six tracts, as annual PM2.5 exposure increased from 0 ug/m3 to 10 ug/m3, isotropic restricted diffusion increased, on average, by 1.21% (95% CI: 0.91%-1.52%). Around an exposure level of 10 ug/m3, the trend shifted, and, as annual PM2.5 exposure increased from 10 ug/m3 to 15 ug/m3, isotropic restricted diffusion increased, on average, by 2.96% (95% CI: 2.32%-3.60%). A similar, less pronounced relationship was observed in the right hemisphere tracts.

Summary:
Higher levels of fine particulate air pollution may impact restricted isotropic diffusion, which suggests increases in the number or size of support cells in these white matter tracts during late-childhood. Although human MRI cannot detect the exact biological mechanisms at play, our findings are congruent with previous literature showing chronic exposure to high concentrations of air pollution is linked to upregulation or activation of infiltrating monocytes or resident microglia cells (Calderón-Garcidueñas et al. 2008).

Authors