Biology subjects

Rosario, M. A.

Publications and source records attributed to Rosario, M. A..

3 recordsLinked to original sources

bioRxiv2026

Air Pollution, Early Adversity, and Amygdala: Environmental Correlates of Psychopathology in Preadolescents

Early life adversity (ELA) and ambient fine particulate matter (PM2.5) are hypothesized to be environmental risk factors for altered brain structure and psychopathology, but their unique and interactive effects in childhood remain unclear. This study examines the interactive associations of ELA and annual average residential PM2.5 exposure (total mass and 15 components) on total amygdala and basolateral amygdala subregion volumes and psychopathology symptoms in a subset of children (N=3,601, 45% assigned female at birth, 9-10 years) from the Adolescent Brain Cognitive Development Study. Linear mixed-effects models, adjusting for sociodemographic factors, co-pollutants, and neuroimaging covariates, showed that ELA was associated with greater bifactor model-defined general, specific internalizing, and specific externalizing symptoms of psychopathology. PM2.5 moderated ELA associations with specific externalizing symptoms, with greater symptoms in those exposed to higher ELA and higher PM2.5 exposures. Among youth with higher ELA, smaller basolateral paralaminar volumes were linked to greater general and specific externalizing symptoms. These findings underscore the importance of considering psychosocial and physical environmental co-exposures when identifying children at risk for psychopathology.

neuroscience↗

bioRxiv2025

Outdoor Air Pollution, Perivascular Space Morphology, and Cognition in Preadolescence

BackgroundAmbient air pollution exposure is associated with structural brain differences and poorer cognition in children; however, mechanisms of toxicity remain unclear. Perivascular spaces (PVS), key for brain waste clearance, may play a role in the neurotoxicity of air pollution. This study explored associations between air pollution exposure, PVS morphology, and cognition in preadolescents. MethodsWe analyzed cross-sectional Adolescent Brain Cognitive DevelopmentSM (ABCD) Study(R) data from 6,949 9-10-year-old participants. Annual average exposures to PM2.5, O3, NO2, and 15 PM2.5 components were estimated using spatiotemporal models mapped to residential addresses. PVS count and volume were derived from T1w and T2w MRI, and cognition was estimated using NIH Toolbox scores. Linear mixed-effects models examined independent associations between air pollution, PVS, and cognition; weighted quantile sum regression assessed co-exposure effects of PM2.5 mixtures. FindingsLinear models revealed that exposures to Zn, NH4 +, and Br were positively associated with PVS count in several regions. Higher PVS count in five key regions was associated with poorer cognitive performance across several NIH Toolbox domains. Higher Ca, Zn, and NH 4 + exposures were associated with poorer cognition (PFDR < 0.01). Higher frontal lobe PVS count mediated the association between Zn exposure and poorer total cognition (P < 0.01). Co-exposure models revealed that PM2.5 mixtures were associated with higher temporal and cingulate PVS count, and poorer working memory and crystallized intelligence (P < 0.01). InterpretationOutdoor air pollution was associated with higher PVS count and reduced cognition, suggesting that brain clearance may be a novel mechanism linking pollution to neurodevelopmental harm in preadolescents. FundingThis work was supported by the National Institutes of Health (NIH) National Institute of Environmental Health Sciences (NIEHS) (Grant Nos. R01ES032295 and R01ES031074 [to MMH]; T32ES013678 [to JM]; P30ES07048 [to JM and MAR]; 3P30ES000002-55S [to MAR]), National Institute of Mental Health (NIMH) (Grant RF1MH123223 [to JC]), National Institute of Neurological Disorders and Stroke (Grant R01NS128486 [to JC]), and EPA grants (Grant Nos. 83587201 and 83544101 [to JS]).

neuroscience↗

bioRxiv2025

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↗