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Abstract

Individuals living in large U.S. cities face a significant public health problem: exposure to high levels of air pollution. With recent literature suggesting the effect of children's exposure to air pollution on neurological development and cognition, it’s necessary to understand the biological mechanism by which this cognitive impairment is occurring. This study analyzed genome-wide DNA methylation from a large cohort of children in the Fragile Families and Child Wellbeing Study in the context of their cognitive abilities and their exposures to airborne neurotoxicants using census tract-level neurological hazard index data from the National Air Toxics Assessment. I identified a number of differentially methylated loci associated with exposure, several of which are found in genes and pathways which play a role in regulating the central nervous system. Further, regression modeling showed an association between epigenetic age acceleration (defined as the difference between DNA methylation age and chronological age) and both exposure and cognition—evidencing DNA methylation’s potential as a mediator of the association. These findings provide a critical step toward understanding the biological mechanism underlying the association between exposure to airborne neurotoxicants and cognitive impairment in children and may have significant policy implications regarding control of air quality in large cities, where many families of low socioeconomic status raise children.