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.

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发育发现（如果有的话）部分归因于子宫内甲状腺激素暴露的缺陷。我们还旨在描述代谢产物与家长化合物之间的关系，并检查孕妇中代谢物与甲状腺功能之间的关联。拟议的研究借鉴了儿童健康与发展研究的数据，这是对1959年至1966年之间出生的儿童的纵向随访，授予了加利福尼亚州奥克兰的Kaiser Foundation Health计划成员资格，并根据先前的NIH资助研究扩展。产前血清已适当冷冻并储存，可用于评估暴露于有机氯化合物的代谢物；已经测量了在怀孕期间暴露于有机氯化合物和母体甲状腺功能。从出生到17岁的同一名儿童，同一儿童的生长序列度量以及5、9-11和15-17岁的标准化发展检查。提出的有机氯暴露和暴露于母体甲状腺功能的度量（甲状腺刺激激素，游离甲状腺素和甲状腺过氧化物酶抗体）。统计分析将估计关联利用数据的重复度量结构。分析将考虑到潜在的混淆变量，采用一般估计方程（GEE）方法进行重复测量。我们将区分产前有机氯代谢物的影响与青春期至青春期的影响。我们还将研究一种特定的机制：通过母体甲状腺功能。结果将充分描述产前暴露的影响，并将进一步了解亚临床母甲状腺激素缺乏症与儿童发育之间的关系。这项研究可能会导致产前干预。公共卫生相关性：我们将区分产前有机氯代谢物的影响，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。结果将充分描述产前暴露的影响，并将进一步了解亚临床母甲状腺激素缺乏症与儿童发育之间的关系。这项研究可能会导致产前干预。