Prenatal Exposure to Air Pollution and Childhood Social Anxiety Symptoms: Novel pathogenic pathways - Childhood social anxiety disorder is a highly prevalent and impairing condition; in severe cases it can lead to school refusal and social isolation and is often comorbid with other mental and physical health problems posing a significant public health burden. Although exposure to environmental toxicants have not commonly been thought of as contributors to mental health problems, epidemiologic studies have linked prenatal exposure to ambient air pollution with increased risk for anxiety symptoms and disorders. Children living in the context of economic disadvantage are at disproportionately higher risk for anxiety and exposure to air pollution. This proposal integrates findings from environmental health sciences and developmental psychology/neuroscience and proposes a novel framework detailing the pathway through which prenatal exposure to air pollution contributes to SADS in those children most at risk. In animal models, prenatal exposure to polycyclic aromatic hydrocarbons (PAH), a common and neurotoxic class of air pollutants, causes increased avoidance behaviors, analogous to human behavioral inhibition (BI), a well-documented risk factor for SADS. Prenatal PAH exposure also alters children’s cognitive control, which in turn increases SADS risk in children with BI. We have linked prenatal exposure to PAH with BI-like behaviors in infants and children and with internalizing symptoms and altered cognitive control. We now propose to test the overarching hypothesis that (1) prenatal PAH exposure is linked with SADS via effects on BI-like behaviors and (2) that prenatal PAH exposure alters neural function underlying cognitive control, and (3) moderates the association between PAH, BI, and SADS. We will conduct the study in 200 children living in the context of economic disadvantage who are followed in a prospective longitudinal birth cohort at the Columbia Center for Children’s Environmental Health. Using EEG to measure alterations in brain function associated with PAH exposure will allow us to show effects of air pollution on children's task-related brain function (versus structure) for the first time and at very early time points (preschool age) when intervention and prevention may be most effective. Findings will identify modifiable inflection points in developmental cascades that can be targeted to deliver maximally effective personalized intervention strategies. In addition, working collaboratively with implementation scientists and public health agencies, our findings can be used to develop personalized prevention strategies targeted to help children who are at risk for exposure and poor mental health outcomes.
