Ambient Pollution Components and Sources Associated with Hippocampal Architecture and Memory in Pre-Adolescents
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Background
Ambient air pollution poses significant risks to brain health. Hippocampal structure and function are particularly vulnerable, yet the extent to which they are associated with air pollution in children remains unclear. We therefore conducted multi-pollutant mixture analyses to examine how air pollution influences hippocampal architecture and memory performance in late childhood.
Methods
We used partial least squares correlation to explore cross-sectional associations between fifteen PM 2.5 components, six PM 2.5 source factors, NO₂, and ozone exposures, and measures of hippocampal microstructure and volume in children aged 9-11 years (n = 7,940) We adjusted for demographic, socioeconomic, and neuroimaging confounds. We also tested whether air pollutants were associated with hippocampal-dependent list-learning memory performance to examine functional implications of air pollution exposure. Shared variance refers to the proportion of total covariance between variable sets captured by each latent dimension in the multivariate relationship.
Findings
In the first latent dimension, greater exposure to organic carbon and ozone was associated with differential hippocampal diffusion (72% of shared variance), whereas the second latent dimension linked elemental carbon and iron to hippocampal diffusion (24% of shared variance). Source-based analyses identified biomass burning and traffic pollution as key contributors (61% and 32% variance, respectively). Volumetric analyses revealed higher copper and zinc exposure correlated with smaller hippocampal subregion volumes (left head, right body, tail; 77% variance), whereas lower nickel levels correlated with smaller right head volume (12% variance). Higher industrial and traffic pollutants were also associated with smaller hippocampal volumes (75% variance). We found two latent dimensions (67% and 23% variance, respectively) showing poorer learning, immediate recall, and mnemonic interference performance linked to higher calcium, elemental carbon, and zinc, and organic carbon, alongside lower copper exposure. Finally, hippocampal diffusion (higher free water/lower hindered extracellular diffusion; 83% variance) and smaller tail volumes (96% variance) were linked to poorer RAVLT recall.
Interpretation
These results underscore the complex relationship between air pollution exposure and hippocampal architecture and cautions that such structural changes may either presage or reflect subtle differences in neurocomputational mechanisms associated with learning and memory performance in children.
Funding
U.S. National Institute of Environmental Health Sciences
Research in Context
Evidence before this study
Using PubMed, we conducted a MeSH and text keyword search for air pollution (e.g., “Air Pollution” OR “Air Pollutant” OR “Air Pollutants” OR “Particulate Matter”) and structural MRI (“magnetic resonance image” OR “magnetic resonance images” OR “magnetic resonance imaging” OR “MRI”) among children and adolescents (<24 years-old), published until January 15, 2025, without language restrictions. Existing studies primarily focused on single pollutants or total hippocampal volume across various populations (children, adults, animals), leaving significant knowledge gaps regarding the specific impacts of PM 2.5 components and their sources on hippocampal structure during childhood. Previous research on hippocampal structure also generally lacked detailed exploration of hippocampal subregions and rarely employed advanced neuroimaging sensitive to microstructural changes. Existing evidence was inconsistent due to methodological differences and variations in pollutant types and exposure periods.
Added value of this study
This study significantly advances our understanding by explicitly linking specific PM 2.5 components and their source-specific mixtures to detailed hippocampal architecture differences in late childhood. Using advanced neuroimaging (restriction spectrum imaging and volumetric analyses), we identified precise microstructural and volumetric changes associated with exposure to organic carbon, metals, ozone, and pollutant sources such as biomass burning, traffic, industrial emissions, and agricultural pollution. Importantly, our findings also showed associations between PM 2.5 components and episodic memory performance, highlighting the neurodevelopmental impacts of complex air pollutant mixtures for the life course. This evidence underscores the necessity of targeting source-specific air pollution (e.g., biomass burning, traffic, and industrial emissions) during critical developmental windows to safeguard lifelong cognitive health.
Implications of all the available evidence
Factors in childhood profoundly shape the trajectory of neurocognitive aging, including risks for dementia and other age-related diseases. Our results support the concept that early-life environmental exposures significantly influence brain health, including cognitive function, and emphasize that preventive strategies must begin early. Future longitudinal studies should therefore address how childhood air pollution exposures, with particular focus on which sources, influence subsequent cognitive trajectories, neurodegeneration, and overall brain health in adulthood and older age. This approach will provide critical insights for targeted interventions and policymaking aimed at reducing early-life environmental exposures and promoting healthy aging from childhood into adulthood.
