Air Pollution Exposure and Prefrontal Connectivity in Early Adolescence
Megan M. Herting1, Elisabeth Burnor1, Hedyeh Ahmadi1, Sandrah P. Eckel1, Kiros Berhane2, Rob McConnell1, Joel Schwartz3, Wesley K. Thompson4, Chun Chan4, Jiu-Chiuan Chen1
1University of Southern California; Los Angeles, CA, USA; 2Columbia University; New York City, NY, USA; 3Harvard University; Cambridge, Massachusetts, USA; 4University of California San Diego; San Diego, CA, USA
Background. We aim to investigate whether annual average ambient PM2.5 exposure at 9-10 years is associated with 1) prefrontal connectivity in youth ages 9-10 and 2) subsequent mental health problems and risk for neuropsychiatric disorders at ages 10-11 years.
Methods. The current study uses data from the nationwide Adolescent Brain Cognitive Development (ABCD) study℠ (N=11,873), with diffusion weighted imaging data collected at 9-10 years and longitudinal emotional health outcomes at 9-10 and 11-12 years. Using residential address information provided by the caregiver at ages 9-10, we use a novel hybrid spatiotemporal exposure model to estimate the annual ambient exposure to PM2.5 at the child’s home. The current study will also explore corresponding associations with annual NO2 exposure. Using diffusion tensor imaging (DTI), we are currently assessing the association between annual ambient PM2.5 exposure and white matter microstructure in prefrontal white matter tracts of interest. In addition, we are also assessing the association between PM2.5 exposure and dimensional emotional outcomes, as reported by the caregivers based on the Child Behavioral Checklist (CBCL), as well as mental health diagnoses as determined by DSM-V criteria on the computerized Schedule for Affective Disorders and Schizophrenia for School-Aged Children (K-SADS-COMP).
Results. The mean annual PM2.5 concentration of residential exposure for ABCD participants across the 21 study sites was 7.66 µg/m3 (SD: 1.56; Range: 1.72 – 8.66) in 2016-2018. Preliminary findings of our study suggested that associations between PM2.5 exposure and DTI measures vary significantly by hemisphere for both fractional anisotropy (FA) and mean diffusivity (MD). In hemisphere-specific models, significant, nonlinear associations were observed between annual ambient PM2.5 exposure and MD in the right anterior thalamic radiations and the right corticospinal tract. These associations indicated that, as PM2.5 exposure increases, MD increases in a nonlinear pattern, with more pronounced increases in MD occurring at PM2.5 exposures above 8 µg/m3. These findings suggest even relatively low levels of PM2.5 exposure may impact white matter microstructure in fronto-thalamic and motor tracts at 9-10 years of age. Regarding emotional outcomes on the CBCL, we found PM2.5 to relate to internalizing, externalizing, and total problem behaviors at the 1-year follow-up, albeit these observed effects were negligible (beta coefficients ranging from -0.08 to -0.14 for t-scores with a mean=50 and SD=10). Current efforts include examining the primary pollutant models for NO2 on our outcomes as well as estimating and adjusting for any potential prenatal exposure effects.
Conclusions. Although our findings are still preliminary, PM2.5 exposure levels in our current study are largely below the standards set by the U.S. and World Health Organization. Our study’s eventual conclusions may provide important epidemiologic data on developmental neurotoxicity at low exposure levels that are critical to the continuing review and risk assessment for the National Ambient Air Quality Standard.