Section of Endocrinology, Diabetes, and Nutrition, Boston University School of Medicine, 88 East Newton St., Boston, MA 02118, USA.
Thyroid. 2012 Sep;22(9):938-43. doi: 10.1089/thy.2012.0058. Epub 2012 Jul 24.
Breastfed infants rely on maternal iodine for thyroid hormone production required for neurodevelopment. Dietary iodine among women of childbearing age in the United States may be insufficient. Perchlorate (competitive inhibitor of the sodium/iodide symporter [NIS]) exposure is ubiquitous. Thiocyanate, from cigarettes and diet, is a weaker NIS inhibitor. Environmental perchlorate and thiocyanate exposures could decrease breast milk iodine by competitively inhibiting NIS in lactating breasts (thus impairing infants' iodine availability), and/or infants' thyroidal NIS to directly decrease infant thyroid function. The current study assessed the relationships between environmental perchlorate and thiocyanate exposures and infant serum thyroid function.
Iodine, perchlorate, and thiocyanate in breast milk, maternal and infant urine, and infant serum thyroid function tests were cross-sectionally measured in Boston-area women and their 1-3 month-old breastfed infants. Univariate and multivariable analyses assessed relationships between iodine, perchlorate, thiocyanate, thyroid-stimulating hormone (TSH), and free thyroxine (FT4) levels.
In 64 mothers and infants, median (range) iodine levels were 45.6 μg/L (4.3-1080) in breast milk, 101.9 μg/L (27-570) in maternal urine, and 197.5 μg/L (40-785) in infant urine. Median perchlorate concentrations were 4.4 μg/L (0.5-29.5) in breast milk, 3.1 μg/L (0.2-22.4) in maternal urine, and 4.7 μg/L (0.3-25.3) in infant urine. There were no correlations between infant TSH or FT4 and iodine, perchlorate, and thiocyanate levels in breast milk, maternal urine, and infant urine. In multivariable analyses, perchlorate and thiocyanate levels in breast milk, maternal urine, and infant urine were not significant predictors of infant TSH or FT4.
Boston-area mothers and their breastfed infants are generally iodine sufficient. Although environmental perchlorate and thiocyanate are ubiquitous, these results do not support the concern that maternal and infant environmental perchlorate and thiocyanate exposures affect infant thyroid function.
母乳喂养的婴儿依赖于母体碘来产生甲状腺激素，这对于神经发育是必需的。美国育龄妇女的饮食碘可能不足。高氯酸盐（钠/碘转运体 [NIS] 的竞争性抑制剂）的暴露是普遍存在的。来自香烟和饮食的硫氰酸盐是较弱的 NIS 抑制剂。环境高氯酸盐和硫氰酸盐的暴露可能通过竞争性抑制哺乳期乳房中的 NIS（从而损害婴儿的碘供应），和/或婴儿甲状腺中的 NIS 直接降低婴儿的甲状腺功能，从而降低母乳中的碘含量。本研究评估了环境高氯酸盐和硫氰酸盐暴露与婴儿血清甲状腺功能之间的关系。
在波士顿地区的妇女及其 1-3 个月大的母乳喂养婴儿中，对母乳、产妇和婴儿尿液以及婴儿血清甲状腺功能测试中的碘、高氯酸盐和硫氰酸盐进行了横断面测量。单变量和多变量分析评估了碘、高氯酸盐、硫氰酸盐、促甲状腺激素（TSH）和游离甲状腺素（FT4）水平之间的关系。
在 64 名母亲和婴儿中，母乳中碘的中位数（范围）为 45.6μg/L（4.3-1080），母亲尿液中为 101.9μg/L（27-570），婴儿尿液中为 197.5μg/L（40-785）。母乳中高氯酸盐的中位数浓度为 4.4μg/L（0.5-29.5），母亲尿液中为 3.1μg/L（0.2-22.4），婴儿尿液中为 4.7μg/L（0.3-25.3）。婴儿 TSH 或 FT4 与母乳、母亲尿液和婴儿尿液中的碘、高氯酸盐和硫氰酸盐水平之间没有相关性。在多变量分析中，母乳、母亲尿液和婴儿尿液中的高氯酸盐和硫氰酸盐水平并不是婴儿 TSH 或 FT4 的显著预测因素。
波士顿地区的母亲及其母乳喂养的婴儿通常碘充足。尽管环境高氯酸盐和硫氰酸盐普遍存在，但这些结果并不支持这样的担忧，即母亲和婴儿的环境高氯酸盐和硫氰酸盐暴露会影响婴儿的甲状腺功能。
