Prenatal Organochlorine Metabolites, Thyroid Function and Development

产前有机氯代谢物、甲状腺功能和发育

• 批准号: 7565810
• 负责人: Pam R Factor-Litvak
• 金额: $ 55.26万
• 依托单位: COLUMBIA UNIVERSITY HEALTH SCIENCES
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-15 至 2011-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7565810
• 关键词: 17 year old; Accounting; Adolescence; Adverse effects; Age; Age at Menarche; Animals; Antibodies; Award; Binding; Biological; Birth; Blood; Body mass index; California; Carrier Proteins; Child; Child health care; Childhood; Chlordan; Chlorinated Hydrocarbons; Cognition; Confounding Factors (Epidemiology); Consumption; Cretinism; Data; Development; Endocrine Disruptors; Enrollment; Environment; Environmental Pollution; Equation; Exposure to; Female; Folate; Follow-Up Studies; Foundations; Freezing; Functional disorder; Funding; Goals; Growth; Health; Health Planning; Height; Human; Hydrocarbons; Hydroxyl Radical; Hypothyroidism; Iodide Peroxidase; Knowledge; Lead; Life; Life Cycle Stages; Measures; Mental Retardation; Metabolism; Methods; Mothers; Neural Tube Defects; Neurodevelopmental Deficit; Outcome; Parents; Perinatal Exposure; Pesticides; Polychlorinated Biphenyls; Postpartum Period; Prealbumin; Pregnancy; Pregnant Women; Principal Investigator; Production; Properdin; Public Health; Publications; Research; Research Personnel; Research Project Grants; Schizophrenia; Second Pregnancy Trimester; Serum; Structure; Testing; Thyroid Function Tests; Thyroid Gland; Thyroid Hormones; Thyrotropin; Thyroxine; Time; United States National Institutes of Health; Weight; Woman; cognitive function; cohort; cost; design; early childhood; emerging adult; fetal; follow-up; girls; hormone deficiency; in utero; infancy; longitudinal analysis; neuropsychological; offspring; organochlorine exposure; postnatal; premature; prenatal; prenatal exposure; prenatal intervention; programs; public health relevance

DESCRIPTION (provided by applicant): The overall goal of this project is to assess whether exposure to metabolites of endocrine disrupting compounds during pregnancy is associated with a) adverse development (cognitive function, height, weight, weight for height, and for females, age at menarche) in the offspring at birth, early childhood, middle childhood, and adolescence, b) mild deficiencies in maternal thyroid function, and c) whether adverse developmental findings, if any, are attributed in part to deficiencies in exposure to maternal thyroid hormone in utero. We also aim to describe the relationships between the metabolites and parent compounds and to examine the associations between the metabolites and thyroid function in the pregnant women. The proposed study draws on data from the Child Health and Development Study, a longitudinal follow up of children born between 1959 and 1966 to mothers enrolled in the Oakland, California membership of the Kaiser Foundation Health Plan and expands upon previous NIH funded research. Prenatal sera has been appropriately frozen and stored, and are available to assess exposure to the metabolites of organochlorine compounds; exposure to organochlorine compounds and maternal thyroid function during pregnancy has already been measured. Serial measures of growth are available in the same children from birth to age 17 years, as are standardized developmental examinations at ages 5, 9-11, and 15-17. The proposed measures of organochlorine exposure and exposure to measures of maternal thyroid function (thyroid stimulating hormone, free thyroxine, and thyroid peroxidase antibodies). Statistical analyses will estimate associations taking advantage of the repeated measures structure of the data. The analyses will employ generalized estimating equations (GEE) methods for repeated measures, taking account of potentially confounding variables. We will distinguish effects of prenatal organochlorine metabolite exposures from infancy through adolescence. We will also investigate a specific mechanism: via maternal thyroid function. Results will fully describe the effects of prenatal exposure and will also further knowledge about the relation between subclinical maternal thyroid hormone deficiency and childhood development. This line of research could lead to prenatal interventions. PUBLIC HEALTH RELEVANCE: We will distinguish effects of prenatal organochlorine metabolite exposures from infancy through adolescence. We will also investigate a specific mechanism: via maternal thyroid function. Results will fully describe the effects of prenatal exposure and will also further knowledge about the relation between subclinical maternal thyroid hormone deficiency and childhood development. This line of research could lead to prenatal interventions.

描述(由申请人提供)：本项目的总体目标是评估怀孕期间接触内分泌干扰化合物的代谢物是否与a)出生时、幼儿早期、童年中期和青春期的后代发育不良(认知功能、身高、体重、身高体重以及女性的月经初潮年龄)有关，b)母亲甲状腺功能的轻度缺陷，以及c)不良发育结果是否部分归因于在子宫中接触母亲甲状腺激素的不足。我们还旨在描述代谢物和母体化合物之间的关系，并检查代谢物和孕妇甲状腺功能之间的关系。这项拟议的研究利用了儿童健康与发展研究的数据，该研究是对1959年至1966年出生的儿童的纵向跟踪，母亲在加利福尼亚州奥克兰参加了凯撒基金会健康计划，并在NIH资助的先前研究的基础上进行了扩展。产前血清已适当冷冻和储存，可用于评估接触有机氯化合物的代谢物；已对怀孕期间接触有机氯化合物和产妇甲状腺功能进行了测量。从出生到17岁的同一批儿童可以进行一系列的发育测量，5岁、9-11岁和15-17岁的标准化发育检查也是如此。建议的有机氯暴露措施和母亲甲状腺功能的暴露措施(促甲状腺激素、游离甲状腺素和甲状腺过氧化物酶抗体)。统计分析将利用数据的重复测量结构来估计关联。分析将使用广义估计方程(GEE)方法进行重复测量，并考虑潜在的混杂变量。我们将区分产前有机氯代谢产物暴露的影响，从婴儿期到青春期。我们还将研究一种特定的机制：通过母体甲状腺功能。结果将全面描述产前暴露的影响，并将进一步了解亚临床母亲甲状腺激素缺乏与儿童发育之间的关系。这一系列研究可能导致产前干预。公共卫生相关性：我们将区分产前有机氯代谢产物暴露的影响，从婴儿期到青春期。我们还将研究一种特定的机制：通过母体甲状腺功能。结果将全面描述产前暴露的影响，并将进一步了解亚临床母亲甲状腺激素缺乏与儿童发育之间的关系。这一系列研究可能导致产前干预。