Prenatal and Early Life Air Pollution Exposure and Pubertal Development - The global population faces unhealthy air pollution levels. The onset of pubertal development, in both girls and boys, is occurring at younger ages, a concerning trend linked to adverse health outcomes throughout the life course. Early research suggests that early-life air pollution exposure may lead to early pubertal development and age at menarche. However, few studies have explored critical windows of exposure or had large enough sample sizes to examine moderating or mediating factors. The proposed research will address these gaps by investigating how air pollution exposure before conception, during pregnancy, and in early life is associated with pubertal development in girls and boys from large and generalizable populations. In the K99 phase, I will be trained by a multidisciplinary team of experts in the pathophysiology and clinical assessment of pubertal development; gestational diabetes (GDM) pathophysiology and management, and glycemic control; as well as air pollution exposure science and related statistical methods, including novel distributed lag models. I will leverage data of 8000+ mother-child pairs from 45 geographically varied sites included in the Environmental influences on Child Health Outcomes (ECHO) consortium. Aim 1 assesses whether air pollution exposure before pregnancy, during gestation, and in early childhood is associated with pubertal development and identifies susceptible windows of exposure. Aim 2 evaluates whether air pollution exposure before and during pregnancy is associated with GDM risk and whether GDM moderates or possibly mediates the air pollution-pubertal development association. In the R00 phase, I will use data from the electronic health records of 0.5 generalizable mother-child pairs in Kaiser Permanente Northern California, an integrated health care system. I will expand the range of air pollutants and include novel individual PM2.5 chemical components to examine whether exposure is associated with pubertal development and assess possible mediating and moderating factors. Specifically, Aim 3a): examines the primary associations between maternal air pollutant exposures before pregnancy and during gestation, and offspring air pollutant exposures in infancy/early childhood with early pubertal development; and identifies possible susceptible windows of exposure. Aim 3b) assesses the modifying or possibly mediating role of prenatal hyperglycemia and glycemic control trajectories; Aim 3c) assesses the mediation by child growth patterns and obesity; and Aim 3d) assesses modification by neighborhood deprivation. This research could inform policy decisions and air quality standards through the US EPA’s Integrated Science Assessments and guide clinical practice by developing interventions for children in regions with elevated air pollution and prenatal exposure to hyperglycemia. Results will support future R01 submissions and advance my career as an independent investigator in environmental epidemiology, examining how exposures impact pubertal development and long-term cardiometabolic health.
