Abstract

Early life exposure to air pollution poses a significant risk to brain development from direct exposure to toxicants or via indirect mechanisms involving the circulatory, pulmonary or gastrointestinal systems. In children, exposure to traffic related air pollution has been associated with adverse effects on cognitive, behavioral and psychomotor development. We aimed to determine whether childhood exposure to traffic related air pollution is associated with regional differences in brain volume and cortical thickness among children enrolled in a longitudinal cohort study of traffic related air pollution and child health. We used magnetic resonance imaging to obtain anatomical brain images from a nested subset of 12 year old participants characterized with either high or low levels of traffic related air pollution exposure during their first year of life. We employed voxel-based morphometry to examine group differences in regional brain volume, and with separate analyses, changes in cortical thickness. Smaller regional gray matter volumes were determined in the left pre- and post-central gyri, the cerebellum, and inferior parietal lobe of participants in the high traffic related air pollution exposure group relative to participants with low exposure. Reduced cortical thickness was observed in participants with high exposure relative to those with low exposure, primarily in sensorimotor regions of the brain including the pre- and post-central gyri and the paracentral lobule, but also within the frontal and limbic regions. These results suggest that significant childhood exposure to traffic related air pollution is associated with structural alterations in brain.

Highlights

  • Accumulating evidence suggests traffic-related air pollution (TRAP) is a contributor to both neurodegenerative diseases and neurodevelopmental disorders [1,2,3,4,5,6,7,8,9]

  • TRAP consists of a complex mixture of gaseous pollutants, fine and ultrafine particulate matter, heavy metals, elemental and organic carbon, polycyclic aromatic hydrocarbons, and other dynamic constituents [10]

  • ultrafine particulate matter (UFPM) can readily access the brain directly through the nasal olfactory mucosa via the olfactory bulb; this direct entry sets up a scenario for adverse structural consequences to occur in the brain due to the presence of TRAP despite a potentially low translocation rate from deposition in the nasal cavity [11,12,13]

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Summary

Introduction

Accumulating evidence suggests traffic-related air pollution (TRAP) is a contributor to both neurodegenerative diseases and neurodevelopmental disorders [1,2,3,4,5,6,7,8,9]. Diesel exhaust (DE) is a significant contributor to TRAP with a composition incorporating ultrafine particulate matter (UFPM;

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