Prenatal Exposure to Air Pollution and Childhood Social Anxiety Symptoms: Novel pathogenic pathways

ABSTRACT. Childhood social anxiety is highly prevalent and impairing; 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 social anxiety symptoms (SAS) in children who are most at risk. In animal models, prenatal exposure to polycyclic aromatic hydrocarbons (PAH) – a common class of neurotoxic air pollutants – causes increased avoidance behaviors, analogous to human behavioral inhibition (BI), a well-documented risk factor for SAS. Prenatal PAH exposure also alters children’s cognitive control, which in turn increases SAS 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 SAS 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 SAS. We will conduct our study in 200 Black and Latinx 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 factors (air pollution) that can be targeted to deliver maximally effective personalized prevention strategies. Future studies can leverage our findings to develop personalized prevention strategies targeted to help children from marginalized groups who are at greatest risk for exposure and poor mental health outcomes.