Perchlorate Exposure in Pregnancy and Cognitive Outcomes in Children: It's Not Your Mother's Thyroid

高氯酸盐 甲状腺 甲状腺功能 激素 化学 内分泌学 内科学 医学 有机化学 离子
作者
Gregory A. Brent
出处
期刊:The Journal of Clinical Endocrinology and Metabolism [Oxford University Press]
卷期号:99 (11): 4066-4068 被引量:5
标识
DOI:10.1210/jc.2014-3673
摘要

Perchlorate (ClO−4) is utilized in manufacturing rocket fuel, fireworks, and airbag inflation systems as well as being formed naturally in the atmosphere (1). It is stable and soluble in water and has been detected in drinking water, vegetables, and even breast milk. Perchlorate is a direct inhibitor of iodine transport and is the best characterized toxicant with respect to mechanism of action, although a range of environmental toxicants have been identified that disrupt thyroid hormone synthesis, metabolism, and action (2). At a sufficient dose and duration of exposure, perchlorate can reduce thyroid hormone production by reducing iodine uptake into the thyroid. Iodine is essential for thyroid hormone production and must be derived from dietary sources (3). Perchlorate antagonism of iodine transport is additive with other inhibitors, such as thiocyanate, found in cigarette smoke. The impact of perchlorate on thyroid function, especially in pregnancy, has led to intense focus on determining acceptable levels of perchlorate and other iodine inhibitors in the water supply (4, 5).

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