Endocrine Disrupting Chemicals, Thyroid Hormones, and Child Neurobehavior

内分泌干​​扰化学物质、甲状腺激素和儿童神经行为

• 批准号: 8887432
• 负责人: Joseph M Braun
• 金额: $ 68.56万
• 依托单位: BROWN UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-06-01 至 2019-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8887432
• 关键词: 2 year old; 3 year old; 8 year old; Address; Adverse effects; Affect; Attention deficit hyperactivity disorder; Behavior; Biological Markers; Birth; Brain; Chemical Exposure; Chemicals; Child; Child Behavior; Childhood; Chronic; Cognition; Data; Development; Disease; Endocrine Disruptors; Endocrine system; Environment; Environmental Health; Epoxy Resins; Exposure to; Feces; Health; Hormonal; Impulsivity; Individual; Infant; Learning; Learning Disabilities; Life; Link; Maternal Exposure; Measurement; Measures; Meconium; Mediating; Metabolism; Methodology; Modeling; Mothers; Nature; Newborn Infant; Outcome; Outcome Measure; Pattern; Perinatal Exposure; Plastics; Play; Polyvinyl Chloride; Pregnancy; Pregnancy Trimesters; Pregnant Women; Primary Prevention; Psyche structure; Psychometrics; Public Health; Research; Research Personnel; Risk; Risk Factors; Role; Sampling; Self Care; Serum; Signal Transduction; Statistical Methods; Testing; Thyroid Function Tests; Thyroid Hormones; Thyrotropin; Thyroxine; Time; Toxic effect; Triclosan; Triiodothyronine; Umbilical Cord Blood; Urine; Visuospatial; antimicrobial; base; bisphenol A; clinical risk; cognitive ability; cohort; consumer product; early life exposure; environmental chemical; environmental chemical exposure; executive function; fetal; inattention; infancy; innovation; man; modifiable risk; monomer; neurobehavior; neurobehavioral; neurobehavioral disorder; neurodevelopment; novel; phthalates; polycarbonate plastic; postnatal; prenatal; prenatal exposure; prospective; public health intervention; public health relevance; spatial memory

 DESCRIPTION (provided by applicant): Neurodevelopment is dependent on the action of thyroid hormones, and disruption of this hormonal axis during sensitive periods of development could increase the risk of clinical disorders like attention- deficit/hyperactivity disorder or learning disabilities. Phthalate, triclosan, and bisphenol A (BPA) exposures are nearly universal in pregnant women and children, and could adversely affect thyroid hormones and brain development. No studies have prospectively linked these exposures to both thyroid hormones and neurodevelopment to determine if and when the developing fetal or child brain is more sensitive to these early life exposures. We will address this gap using an existing prospective cohort of 356 mother-child pairs who have been followed from the 2nd trimester of pregnancy until their child is ~8 years old. We will comprehensively assess pre- and postnatal phthalate, triclosan, and BPA exposure using infant meconium samples, two pregnancy urine samples, and up to six urine samples from infancy/childhood. Child cognitive abilities and behavior have been repeatedly assessed from 1-8 years of age and thyroid hormone levels will be measured during pregnancy, at birth, and 1, 3, 5, and ~8 years of age. These data will be systematically investigated to: 1) determine if and when early life phthalate, triclosan, and BPA exposures have an adverse effect on children's cognitive abilities and behavior between 1-8 years of age and 2) investigate the association between early life phthalate, triclosan, and BPA exposure and maternal/child thyroid hormone concentrations to determine if thyroid hormones mediate the associations between chemical exposures and neurobehavioral outcomes. Innovative features of this project include detailed prospective exposure assessment using meconium biomarkers to directly assess fetal exposure and up to 8 urine samples during gestation and childhood, repeated neurobehavioral assessments, hormonal intermediates that are essential for neurodevelopment and potentially sensitive to these chemical exposures, and sophisticated statistical methods to pinpoint the period of maximum sensitivity to these chemicals. These data will inform public health agencies about the toxicity of highly prevalent and potentially modifiabl environmental chemical exposures and help target effective public health interventions aimed at reducing exposure during the most sensitive periods of brain development.

 描述（由申请人提供）：神经发育依赖于甲状腺激素的作用，在发育敏感时期破坏该激素轴可能会增加患注意力缺陷/多动障碍或学习障碍等临床疾病的风险。孕妇和儿童几乎普遍接触双酚 A (BPA)，并且可能对甲状腺激素和大脑发育产生不利影响。目前尚无研究前瞻性地将这些接触与这两种甲状腺激素联系起来。我们将利用现有的 356 对母子队列来解决这一差距，这些母子对从妊娠第二个月一直进行跟踪。我们将使用婴儿胎便样本、两份妊娠尿液样本以及最多六份婴儿/儿童时期的尿液样本，全面评估产前和产后邻苯二甲酸盐、三氯生和 BPA 的暴露情况。对 1-8 岁的行为和行为进行了反复评估，并将在怀孕期间、出生时以及 1、3、5 和 ~8 岁期间测量甲状腺激素水平。将对这些数据进行系统研究，以：1)。确定生命早期接触邻苯二甲酸盐、三氯生和 BPA 是否以及何时对 1-8 岁儿童的认知能力和行为产生不利影响，2) 调查生命早期邻苯二甲酸盐、三氯生和 BPA 之间的关联BPA 暴露和母婴甲状腺激素浓度，以确定甲状腺激素是否介导化学品暴露和神经行为结果之间的关联，该项目的创新特征包括使用胎粪生物标志物进行详细的前瞻性暴露评估，以直接评估胎儿暴露和妊娠期间最多 8 个尿液样本。和儿童期、重复的神经行为中间评估、对神经发育至关重要且对这些化学物质潜在敏感的激素评估，以及精确确定对这些化学物质最敏感时期的复杂统计方法。将向公共卫生机构通报高度普遍且可能可改变的环境化学物质暴露的毒性，并帮助制定有效的公共卫生干预措施，旨在减少大脑发育最敏感时期的暴露。