Environmental Lead, Thyroid Function & Neurodevelopment

产前和产后甲状腺激素严重缺乏 新生儿期与不良神经发育结局有关 婴儿期和儿童期。孕妇孕期缺碘导致 活化的(即，碘化的)甲状腺激素(T3)和AN的生成减少 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和一过性早产儿甲状腺功能减退 与早期生活中的认知缺陷有关。鉴于这些， 观察，我们应该问一问，母亲的甲状腺是否处于次优状态 功能，特别是在怀孕的前半段，当孕妇 对胎儿甲状腺激素的贡献最大，与 儿童的神经发育。最近的数据表明，母亲的孩子 甲状腺功能低常者有轻微认知缺陷的风险 并增加了对行为问题的报告。这个项目的总体目标是 评估母亲甲状腺功能轻度缺陷是否与 儿童神经发育不良，如果是这样的话，来阐明可能的 生物机制。一种可能的机制是通过脉络膜的损伤 神经丛，是产生大脑特异性运输蛋白的部位 甲状腺激素。动物研究表明，脉络丛受到 暴露在环境铅中，增加了 儿童的铅暴露和认知之间的关系是通过一种 铅对甲状腺激素向大脑的运输有影响。 这项拟议的研究利用了一项前瞻性研究的数据，该研究旨在检查 出生前和产后铅暴露与儿童的关系 发展。这一队列包括大约300名出生于1984-1985年的儿童 在南斯拉夫科索沃的两个城镇，他们一直被跟踪到12岁。 可用于测量孕中期和年内母亲的甲状腺功能 4、7和12岁的儿童。结果，包括认知、运动 对功能、行为问题和人体测量进行测量 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，母亲的甲状腺功能是否在 怀孕的前半段与认知、行为和发育有关。 第二，铅与这些结果之间的关联是否 通过接触甲状腺激素来调节。

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.