Childhood obesity is a major public health issue in the U.S. with widening racial/ethnic gaps and health consequences across the life course. Inequalities in childhood obesity can be traced to as early as infancy, signifying the prenatal period as potentially a critical window during which differences in environmental exposures may program disparities in offspring obesity risk. Racial/ethnic minorities are disproportionately burdened by adverse environmental conditions, such as neighborhood-level psychosocial stressors and air pollutants, which may act synergistically to impact childhood risk of obesity. Disentangling the effects of prenatal environmental exposures and better understanding the mechanisms through which these exposures influence cardiometabolic risk factors, such as childhood obesity, may lead to improved chronic disease risk assessment and more effective intervention strategies, particularly among vulnerable populations who are more likely to experience adverse environments. Epigenetic mechanisms?changes to the genome that do not modify the DNA sequence?are sensitive to environmental exposures during critical periods and may serve as a putative link to early life disparities in childhood obesity. Previous studies have found that prenatal psychosocial stressors and environmental toxicants are associated with epigenetic modifications, particularly in DNA methylation, and offspring obesity risk, but have not considered the joint effect of these environmental exposures and the underlying biological mediators are not well understood. The proposed research will investigate whether environmental stressors during pregnancy influence offspring obesity risk through modifications in DNA methylation using data from a racially diverse birth cohort study with follow-up into childhood. Through the Pathway to Independence Award, the candidate will gain additional training in environmental exposures, biomarkers and epigenetic mechanisms, bioinformatics, and professional development to successfully transition into an independent research career focused on the early life origins of chronic disease. The skills acquired during the training phase will be used to: 1) Estimate the impact of prenatal neighborhood psychosocial stressors (concentrated poverty, deprivation, racial residential segregation, and violent crime) and air pollution exposure on offspring birth weight, growth trajectory in the first 12 months, and risk of overweight and obesity at 3-5 years of age; 2) Examine the effect of prenatal neighborhood psychosocial stressors and air pollution on offspring DNA methylation marks in umbilical cord blood; and 3) Examine the association between environmental stressor-related DNA methylation marks identified in Aim 2 and risk of childhood overweight or obesity. Completion of the training and research aims will result in scientific presentations and publications, preliminary data to successfully compete for R01 funding, and uniquely position the candidate to make significant contributions to the study of epigenetic profiles relating environmental stressors to childhood obesity risk.
Racial inequalities in childhood obesity can be traced to early infancy, signifying the prenatal period as a potential window during which differences in environmental exposures may program early disparities. Critical research gaps exist regarding the effects of exposure to adverse prenatal social environments and air pollution on offspring obesity risk. This study will investigate whether prenatal neighborhood psychosocial stressors and air pollution exposure are associated with offspring risk of obesity through modifications in DNA methylation.
