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Hackman, D. A.

Publications and source records attributed to Hackman, D. A..

3 recordsLinked to original sources

Sources of outdoor air pollution exposure and child brain network development across the United States

Ambient fine particulate matter (PM2.5) pollution is a heterogeneous mixture of chemicals with documented neurotoxic effects. Developmental neuroimaging literature has linked childhood PM2.5 exposure to alterations in brain morphology, microarchitecture, and function, with implications for cognition and psychopathology. However, the extant literature remains largely cross-sectional and often considers PM2.5 a single pollutant, rather than a heterogeneous mixture of chemicals from different sources. This work addresses these gaps by leveraging estimates of exposure to six PM2.5 sources derived from positive matrix factorization, and longitudinal neuroimaging data from a large, geographically-diverse sample of Adolescent Brain Cognitive Development Study youth (N = 6,291) from across the United States (U.S.). To identify exposure-related differences in brain function and assess their geographical generalizability, we used a predictive modeling approach to assess both differences in functional brain network connectivity during childhood (9-11 years of age) and changes in functional brain network connectivity during the transition to adolescence (9-13 years of age) related to PM2.5 exposure. Childhood PM2.5 exposure from traffic emissions and industrial/residual fuel burning were linked to mixed patterns of both stronger and weaker connectivity of sensorimotor networks at ages 9-11 years. Conversely, childhood exposures to secondary pollutants (i.e., ammonium sulfates, nitrates) were linked to largely stronger connectivity of brain networks underlying higher-order cognition that decreased over the following two years. However, these patterns of exposure-related functional connectivity identified in youth across the U.S. better represented youth living in the northeast as compared to youth living in the west. Altogether, this work provides insights into the neurotoxicity of outdoor air pollution exposure in developing sensory and motor systems and potential for biomarkers of eventual psychopathology.

neuroscience↗

Ambient Pollution Components and Sources Associated with Hippocampal Architecture and Memory in Pre-Adolescents

BackgroundAmbient air pollution poses significant risks to brain health. The hippocampus may be particularly vulnerable, yet the extent to which it is impacted in children remains unclear. MethodsUsing partial least squares correlation, we cross-sectionally analyzed air pollution, brain, and cognitive data from the Adolescent Brain Cognitive Development Study to examine how multi-pollutant exposure influences hippocampal structure and memory in 9-11-year-olds (n= 7,940). Annual average air pollution exposures included PM2.5 (total mass, 15 components, and 6 source factors), NO2, and 8-hour maximum O3. Hippocampal outcomes included microstructure measured using Restriction Spectrum Imaging and hippocampus longitudinal-axis (i.e., head, body, tail) volumes. We examined hippocampal-dependent list-learning using the Rey Auditory Verbal Learning Test. Models were adjusted for demographic, socioeconomic, and neuroimaging factors. FindingsPM2.5 total mass was associated with hippocampal microstructure, but not long-axis volume or list-learning ability. Component and source analyses provided greater specificity: higher bromine, sulfate, and vanadium exposure was related to microstructure (72% shared variance), while higher copper and zinc exposure correlated with smaller left head and right body and tail volumes (75% shared variance). Source models implicated biomass burning and traffic pollution in microstructure (61% and 32% shared variance) and industrial and traffic sources in smaller hippocampal volumes (77% shared variance). Higher exposure to several components were also linked to poorer list-learning (67% shared variance). DiscussionCo-exposure to multiple pollutants is linked to differences in hippocampal structure and memory, showing that associations are driven not only by PM2.5 total mass but also by specific components and sources. This evidence underscores the necessity of targeting source-specific (e.g., biomass burning, traffic, and industrial emissions) and constituent components (e.g., metals) of air pollution during critical developmental windows to safeguard brain health.

neuroscience↗

Outdoor Air Pollution Relates to Amygdala Subregion Volume and Apportionment in Early Adolescents

BackgroundOutdoor air pollution is associated with an increased risk for psychopathology. Although the neural mechanisms remain unclear, air pollutants may impact mental health by altering limbic brain regions, such as the amygdala. Here, we examine the association between ambient air pollution exposure and amygdala subregion volumes in 9-10-year-olds. MethodsCross-sectional Adolescent Brain Cognitive DevelopmentSM (ABCD) Study(R) data from 4,473 participants (55.4% male) were leveraged. Air pollution was estimated for each participants primary residential address. Using the probabilistic CIT168 atlas, we quantified total amygdala and 9 distinct subregion volumes from T1- and T2-weighted images. First, we examined how criteria pollutants (i.e., fine particulate matter [PM2.5], nitrogen dioxide, ground-level ozone) and 15 PM2.5 components related with total amygdala volumes using linear mixed-effect (LME) regression. Next, partial least squares correlation (PLSC) analyses were implemented to identify relationships between co-exposure to criteria pollutants as well as PM2.5 components and amygdala subregion volumes. We also conducted complementary analyses to assess subregion apportionment using amygdala relative volume fractions (RVFs). ResultsNo significant associations were detected between pollutants and total amygdala volumes. Using PLSC, one latent dimension (LD) (52% variance explained) captured a positive association between calcium and several basolateral subregions. LDs were also identified for amygdala RVFs (ranging from 30% to 82% variance explained), with PM2.5 and component co-exposure associated with increases in lateral, but decreases in medial and central, RVFs. ConclusionsFine particulate and its components are linked with distinct amygdala differences, potentially playing a role in risk for adolescent mental health problems. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=123 SRC="FIGDIR/small/617429v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@e9f2ecorg.highwire.dtl.DTLVardef@14b677forg.highwire.dtl.DTLVardef@177f8daorg.highwire.dtl.DTLVardef@172dc0c_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗