A growing body of evidence suggests that prenatal and early-life exposures to environmental stressors play a role in the etiology of multiple childhood health outcomes including childhood obesity and metabolic dysfunction. One pervasive exposure of concern is particulate air pollution. Prenatal exposure to air pollution has been associated with adverse fetal growth outcomes, including decreased biparietal diameter, head and abdominal circumference, femur length, and low birth weight. At the same time, prenatal air pollution has also been associated with increased risk for childhood obesity. One explanation for this apparent paradox is a fetal programming hypothesis, which holds that a maladaptive intrauterine environment leads to an adaptive response that alters the fetal metabolic and hormonal milieu designed for intrauterine survival. Thus, growth restriction in utero is associated with greater catch-up growth in infancy and obesity risk later in life. A more sophisticated metric of fetal development?the Doppler ultrasound assessment of umbilical venous perfusion of the fetal liver?also influences fetal growth by prioritizing nutrient allocation for prenatal fat deposition when essential nutrients are plentiful. Moreover, the adipokines leptin and adiponectin play key roles in fetal- maternal metabolism. We hypothesize that air pollution decreases fetal growth and negatively alters fetal liver blood flow which in turn increases the risk of catch-up growth and obesity in later childhood. We further hypothesize that adiponectin and leptin may mediate these observed effects. We will investigate these hypotheses in a subset of 500 participants in the longitudinal pregnancy cohort of low income, predominantly Hispanic, pregnant women known as the Maternal And Developmental Risks from Environmental and Social Stressors (MADRES) Cohort.
The specific aims i nclude investigating the effects of personal prenatal air pollution (NO2, BC, BrC, PM2.5 mass, its components and sources) exposure on 1) ultrasound-derived fetal growth measures and 2) childhood adiposity and early childhood growth trajectories from 0 - 2 years, 3) whether associations are modified by maternal BMI, GDM, and infant sex, and 4) whether protein levels of leptin and adiponectin in maternal serum, placenta, and cord blood mediate associations between air pollutant exposures and infant growth and adiposity. This proposal addresses a critical gap in our current understanding of the etiology of childhood obesity risk by investigating the specific role of prenatal environmental exposures to air pollution, and specific constituents of air pollution, using state-of-the-art personal monitoring to reduce exposure measurement error and innovative phenotyping of fetal growth (fetal liver blood flow).
A growing body of evidence suggests that prenatal and early-life exposures to environmental stressors play a role in the etiology of multiple childhood health outcomes including childhood obesity and metabolic dysfunction. This proposal addresses a critical gap in our current understanding of the etiology of childhood obesity risk, by investigating the role of prenatal air pollution exposure and its specific constituents, using a personal monitoring approach to reduce exposure measurement error, on fetal and infant growth trajectories. In addition, we will test whether leptin and adiponectin levels in maternal serum, cord blood, and placenta mediate the effects of air pollution on fetal and infant growth.
