Influence of prenatal air pollutant and stress exposures on sleep outcomes in urban preschool-aged children

项目摘要/摘要 睡眠问题是年幼孩子的父母最常见的健康问题之一。足够 睡眠对正常的生长和发育很重要，持续的儿童早期睡眠问题会影响 一系列行为、认知和身体健康后果，具有潜在的终生后果。研究 在种族/少数民族，特别是非洲人中表现出更高的睡眠障碍发生率 美国人和拉美人与白人相比，不受社会经济地位的影响。睡眠的病因学 早期生活中出现的困难以及观察到的差异在很大程度上仍然是未知的。睡眠可以是 被概念化为“发育神经可塑性的复杂表型”。神经的发展 睡眠结构始于子宫，经历了一系列精心安排的阶段。当胎儿是 暴露于环境神经毒素，中枢神经系统编程，包括神经连接 参与睡眠调节的框架可能会被破坏，导致睡眠结构和效率的改变 童年早期。产前神经毒素与产后睡眠障碍之间的关系可能取决于 暴露的时间和剂量。候选神经毒素包括产前暴露于环境中的细颗粒物 颗粒物(PM2.5)与母体压力。此外，产前污染的影响可以通过以下方式增强 随之而来的暴露在压力之下。宫内暴露于周围空气污染物对神经发育的影响 被种族/民族或胎儿性别进一步修饰。早期的气质特征也是重要的决定因素 包括睡眠障碍在内的新出现的行为问题，研究表明， 对环境风险因素和睡眠行为之间的关联的缓和作用。我们利用 纵向城市多族裔妊娠队列(n=450对母子)，详细描述 产前暴露于周围环境PM2.5，母亲心理压力(一生和当前不良生活事件， 母体心理功能和生物应激反应(以母体毛发皮质醇为指标)，以及 婴儿的气质，开始检查这些因素与儿童睡眠结果之间的关系。 这一倡议将支持4-5岁儿童的睡眠表型，通过标准化的父母- 报告的睡眠问卷/日记、可穿戴加速计和家庭多导睡眠图(PSG) 目的：(1)研究产前PM2.5暴露与儿童睡眠不良结局之间的关系， 说明暴露的时间；(2)检查母亲的压力和心理生物学是否相关， 孕期评估，独立考虑和混合考虑，预测不良的儿童睡眠结果；(3) 研究PM2.5效应是否会因产前应激而改变；(4)探索这些关联是否 进一步通过i)种族/民族或ii)胎儿性别；和(5)检查产前空气污染和/或压力 影响被婴儿期难相处的气质所调节和/或改变。这些发现可能会开始阐明如何 社会和自然环境之间的相互作用导致了儿童早期睡眠差距。

Project Summary/Abstract 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.