RESEARCH PROJECT 1 ABSTRACT Eliminating racial/ethnic disparities in obesity is a national priority given the clinical and public health burden and costs of the adverse cardio-metabolic sequelae. The burden of obesity disproportionally affects the Hispanic population, with prevalence in excess of 21% nationally compared to 14% non-Hispanic whites. This obesity disparity is already present by preschool age, suggesting that it may have its origins in the earliest stages of life. A growing body of evidence suggests that environmental exposures during the in utero or early- life periods contribute to obesity and may be doing so by affecting food consumption, basal metabolism and patterns of adipose deposition. The biological driver behind these associations may be altered mitochondrial function ? one of the key players in metabolism ? which has also been associated with obesity and insulin resistance. Given that mitochondria are the primary energy producers for rapid fetal and postnatal growth, environmental exposure-induced mitochondrial dysfunction may affect early life health outcomes related to metabolic disease and may provide a plausible mechanism underlying increased childhood obesity risks. In California, the burden of exposures to multiple environmental chemicals is not evenly distributed in the population, with the Hispanic population carrying the greatest cumulative burden of harmful environmental exposures. Thus, the Hispanic population in California not only has one of the highest rates of obesity but also a disproportionate burden of multiple harmful environmental exposures. The cumulative effects of the disproportionate environmental exposures may be a primary driving factor underlying the disparities in obesity among Hispanic children. We propose to investigate how multiple chemical environmental exposures, coupled with other known psychosocial and behavioral risk factors for obesity, affect overall early childhood growth trajectories as well as infant feeding behaviors and metabolic efficiency. We will do so in a large longitudinal pregnancy cohort design, using cutting-edge technologies of cortisol assessment and fat depot quantification, state-of-the-art statistical methods, and novel methods for evaluating mitochondrial function. Project 1 will address the following aims: 1) To investigate the cumulative effects of multiple pre- and postnatal chemical exposures on birth weight and 12 month childhood height and weight growth trajectories for 750 low-income, primarily Hispanic infants; 2) to evaluate whether these environmentally-related birth and infant outcomes are larger in infants of mothers a) with high levels of psychosocial stress during pregnancy, b) who are overweight/obese before pregnancy or gain excess weight during pregnancy, and c) who have greater exposures to negative built and social environments; 3) to evaluate whether environmentally-related birth and infant outcomes are mediated through altered energy consumption and mitochondrial function; and 4) to examine the cumulative effects of prenatal environmental exposures and cortisol levels on abdominal fat depots of infants at <1 month of age using abdominal MRI scans in a subset of 40 infants.
| Alderete, T L; Song, A Y; Bastain, T et al. (2018) Prenatal traffic-related air pollution exposures, cord blood adipokines and infant weight. Pediatr Obes 13:348-356 |
| Felix, Janine F; Joubert, Bonnie R; Baccarelli, Andrea A et al. (2018) Cohort Profile: Pregnancy And Childhood Epigenetics (PACE) Consortium. Int J Epidemiol 47:22-23u |
| Alderete, Tanya L; Habre, Rima; Toledo-Corral, Claudia M et al. (2017) Longitudinal Associations Between Ambient Air Pollution With Insulin Sensitivity, ?-Cell Function, and Adiposity in Los Angeles Latino Children. Diabetes 66:1789-1796 |
