Environmental Lead, Thyroid Function & Neurodevelopment

产前甲状腺激素严重缺乏， 新生儿期与不良神经发育结果相关， 婴儿期和童年期。孕妇在怀孕期间缺碘导致 降低了活化的（即，碘化）甲状腺激素（T3）和 儿童中克汀病（伴有严重精神发育迟滞）的风险增加 孩子先天性甲状腺功能减退症和早产儿短暂性甲状腺功能减退症 与生命早期的认知缺陷有关。鉴于这些 观察，它是适当的，问是否次优产妇甲状腺 功能，特别是在怀孕的前半期， 对胎儿甲状腺激素的贡献最大，与 孩子的神经发育。最近的数据表明， 甲状腺功能“低正常”的人有认知能力小缺陷的风险 行为问题的报告也越来越多该项目的总体目标是 评估母体甲状腺功能轻度缺陷是否与 儿童神经发育不良，如果是这样， 生物学机制一种可能的机制是通过脉络膜的损伤 神经丛，脑特异性转运蛋白的产生部位， 甲状腺激素动物研究表明，脉络丛被破坏， 暴露于环境铅，提高了协会 铅暴露与儿童认知之间的关系是通过以下因素产生的： 铅会影响甲状腺激素向大脑的运输。 这项拟议中的研究利用了一项前瞻性研究的数据， 产前和产后铅暴露与儿童期 发展这一组约有300名儿童，出生于1984-1985年 在南斯拉夫科索沃的两个城镇，他们被跟踪到12岁。塞拉是 可用于测量母亲在怀孕中期和怀孕期间的甲状腺功能。 4岁、7岁和12岁的孩子。结果，包括认知、运动 功能，行为问题和人体测量，测量 在婴儿期和儿童期反复出现。该项目将扩大调查结果 南斯拉夫的研究，首先检查，是否产妇甲状腺功能， 怀孕的前半期与认知、行为和生长有关 第二，铅和这些结果之间的联系是否 通过暴露于甲状腺激素来调节。

Severe deficiency of thyroid hormone during the prenatal and neonatal periods is associated with adverse neurodevelopmental outcomes in infancy and childhood. Maternal iodine deficiency during pregnancy leads to a lowered production of activated (i.e., iodinated) thyroid hormone (T3) and an increased risk of cretinism (with associated severe mental retardation) in the child. Congenital hypothyroidism and transient hypothyroidism of prematurity are associated with deficits in cognition during early life. In light of these observations, it is appropriate to ask whether sub-optimal maternal thyroid function, particularly during the first half of pregnancy when maternal contribution to fetal thyroid hormone is maximal, is associated with neurodevelopment of the child. Recent data suggest that children of mothers with 'low-normal' thyroid function are at risk for small deficits in cognition and increased reports of behavior problems. The overall goal of this project is to assess whether mild deficiencies in maternal thyroid function are associated with adverse neurodevelopment in the child, and, if so, to elucidate possible biologic mechanism. One possible mechanism is through damage to the choroid plexus, the site of production of the brain-specific transport protein for thyroid hormone. Animal studies suggest that the choroid plexus is damaged by exposure to environmental lead, raising the possibility that associations between lead exposure and cognition in the child arise through an effect of lead on transport of thyroid hormone to the brain. The proposed study draws on data from a prospective study designed to examine the associations between pre- and post-natal lead exposure and childhood development. The cohort comprises approximately 300 children, born in 1984-1985 in two towns in Kosovo, Yugoslavia who were followed through age 12. Sera are available to measure thyroid function in the mothers at mid-pregnancy and in the children at ages 4, 7 and 12. Outcomes, including cognition, motor function, behavior problems and anthropometric measurements, were measured repeatedly during infancy and childhood. This project will expand the findings of the Yugoslavia study to examine first, whether maternal thyroid function in the first half of pregnancy is associated with cognitive, behavioral and growth outcomes and second, whether the associations between Pb and these outcomes are mediated by exposure to thyroid hormone.