Sleep problems are one of the most common health concerns among parents of young children. Adequate sleep is important to normal growth and development and persistent early childhood sleep problems impact a host of behavioral, cognitive, and physical health outcomes, with potential lifelong consequences. Studies demonstrate a higher prevalence of sleep disturbances in racial/ethnic minorities, particularly African Americans and Latinos when compared to whites, independent of socioeconomic status. The etiology of sleep difficulties emerging in early life, as well as observed disparities, remain largely unknown. Sleep can be conceptualized as ?a complex phenotype of developmental neural plasticity?. Development of the neural architecture of sleep begins in utero, through a sequence of carefully orchestrated stages. When the fetus is exposed to environmental neurotoxins, central nervous system programming, including the neural connectivity framework involved in sleep regulation, can be disrupted resulting in altered sleep architecture and efficiency in early childhood. Associations between prenatal neurotoxins and postnatal sleep disorders may depend on timing of exposure as well as dose. Candidate neurotoxins include prenatal exposure to ambient fine particulate matter (PM2.5) and maternal stress. Moreover, effects of prenatal pollution can be enhanced by concomitant exposure to stress. Neurodevelopmental effects of in utero exposure to ambient air pollutants can be further modified by race/ethnicity or fetal sex. Early life temperament traits are also important determinants of emerging behavior problems including disordered sleep, with studies showing both mediating and moderating effects on associations between environmental risk factors and sleep behaviors. We leverage a longitudinal urban multi-ethnic pregnancy cohort (n=450 mother-child pairs), with detailed characterization of prenatal exposure to ambient PM2.5, maternal psychological stress (lifetime and current adverse life events, maternal psychological functioning, and biological stress response indexed by maternal hair cortisol), and infant temperament, to begin to examine associations among these factors and childhood sleep outcomes. This initiative will support sleep phenotyping at age 4-5 years, ascertained through standardized parent- reported sleep questionnaires/diaries, wearable accelerometers, and in-home polysomnography (PSG) in order to: (1) examine associations between prenatal PM2.5 exposure and adverse child sleep outcomes, accounting for timing of exposure; (2) examine whether maternal stress and psychobiological correlates, assessed in pregnancy, considered independently and as mixtures, predict adverse child sleep outcomes; (3) examine whether PM2.5 effects are modified by prenatal stress; (4) explore whether these associations are further modified by i) race/ethnicity or ii) fetal sex; and (5) examine whether prenatal air pollution and/or stress effects are mediated and/or modified by difficult temperament in infancy. Findings may begin to elucidate how interactions among social and physical environments contribute to early childhood sleep disparities.
Starting in utero, central nervous system (CNS) processes and networks, including the neural connectivity framework involved in sleep regulation, are vulnerable to environmentally induced programming by both ambient particulate matter and psychosocial stress. This prospective longitudinal study will be first to examine associations among prenatal air pollution, chronic maternal stress and state-of-the-art sleep phenotypes in lower-income, ethnically mixed preschool-aged children, and whether these associations differ based on fetal sex, race/ethnicity, and/or early life temperament. Identifying factors contributing to poor sleep in early life can inform intervention strategies that promote optimal development, which may have lifelong health implications.
