Environmental Mixtures, Cognitive Control and Reward Processes, and Risk for Psychiatric Problems in Adolescence

This study aims to examine the cognitive and neural pathways underlying the joint impact of chemical and social exposures on two aspects of cognitive function: cognitive control and reward processing. The investigators will use high resolution, multi-band resting state and task functional magnetic resonance imaging (fMRI) as well as neuromelanin stain MRI to identify pathways through which exposure to a mixture of prenatal chemical and early life social exposures alters brain function and behavior. Specifically, the investigators will leverage extant prenatal exposure data (N=550) from the Columbia Center for Children's Environmental Health (CCCEH) Mothers and Newborns (MN) birth cohort and study symptoms and brain function in adolescence.

Adolescence is a period of high risk for the emergence of psychiatric issues, particularly attention problems, substance abuse, and psychotic experiences. Risk for these problems likely originates in the prenatal period when the brain undergoes significant rapid change, making this a particularly vulnerable time for alterations in brain development. Few studies have examined risk from prenatal exposure to neurotoxicants that emerge in adolescence and the biological pathways that underlie these associations. Emerging findings suggest that prenatal exposure to environmental chemicals (e.g. environmental tobacco smoke (ETS), air pollutants such as polycyclic aromatic hydrocarbons (PAH)) is associated with behavioral symptoms of attentiondeficit/ hyperactivity disorder (ADHD), substance use disorders (SUD), and psychotic disorders (PD). These symptoms often emerge across adolescence, and frequently co-occur, suggesting shared underlying causes in the brain. Prenatal chemical exposures often co-occur with each other and with social exposures, such as early life stress (ELS) that are also associated with elevated behavioral symptoms. The joint contributions of these chemical and social exposures to these behavioral symptoms are understudied, as are the cognitive and neural pathways linking exposure to behavior.