Investigating the Role of Phthalates, Phenols, and Their Sources on Phenotypic Variability in Autism

About This Grant

PROJECT SUMMARY/ABSTRACT Autism is a neurodevelopmental disorder impacting 1 in 36 children in the US. Children with autism often experience multi-morbidity of other neurodevelopmental disorders (NDDs) and physical health outcomes like obesity and asthma at higher rates than typically developing peers. While prior work has observed associations between prenatal exposure to several classes of endocrine disrupting chemicals (EDCs) and autism, NDDs, obesity, and asthma, little is known regarding their associations with co-occurrence of these health outcomes. Phthalates and phenols are EDCs of particular concern, given their widespread occurrence in diet and personal care products, and strong potential to contribute to these outcomes in combination given shared mechanisms. Little work has considered how the sources of these chemicals may impact outcomes, limiting our ability to target exposure reduction strategies to optimize health for all children. I hypothesize that gestational exposure to phthalates and phenols will be associated with higher child health burdens and multi-morbidity in autism, and that patterns of maternal diet and personal care product use, as key exposure sources, contribute to differential chemical exposure among demographic subgroups and subsequent variability in child health outcomes across the population. In this proposal, I will use data from the Environmental Influences on Child Health Outcomes (ECHO) Program to address these gaps. ECHO is an NIH-funded consortium of longitudinal US-based cohort studies in which participants follow a common protocol and extant data is harmonized. In Aim 1, the K99 portion of this application, I will investigate how prenatal exposure to phthalates, phenols, and their mixtures drives phenotypic variability in autism and co-occurring NDDs, obesity, and asthma (n=4,250). In Aim 2, the R00 portion of this application, I will examine whether there are differences in measured biomarkers of these EDCs across the population according to diet and personal care product use source. Next, I will conduct mediation analyses to determine if demographic subgroups (e.g., rural versus urban dwelling) mediate associations between measured phthalate and phenol metabolites and exposure sources with child health outcomes (n=5,155). During the grant period, I will receive training in the autism phenotype, exposure science, and causal mediation analyses, guided by a mentorship team of experts in autism, epidemiology, and urban environmental health. Upon successful completion of the research and training included in this proposal, I will be well poised to develop and lead future projects focused on EDC exposure mitigation and interventions to reduce risk of child health outcomes related to gestational phthalate and phenol chemical exposure and their dietary and personal care product sources. This opportunity will prepare me well to achieve my goal of research independence.