Long-term environmental exposure to perchlorate through drinking water and thyroid function during pregnancy and the neonatal period.

We have conducted a longitudinal epidemiologic study among pregnant women from three cities in northern Chile: Taltal with 114 microg/L, Chañaral with 6 microg/L, and Antofagasta with 0.5 microg/L perchlorate in the public drinking water. We tested the hypothesis that long-term exposure to perchlorate at these levels may cause a situation analogous to iodine deficiency, thus causing increases in thyrotropin (TSH) and thyroglobulin (Tg) levels and decreased levels of free thyroxine (FT4), in either the mother during the early stages of gestation or the neonate at birth, or in the fetus cause growth retardation. We found no increases in Tg or TSH and no decreases in FT4 among either the women during early pregnancy (16.1 +/- 4.1 weeks), late pregnancy (32.4 +/- 3.0 weeks), or the neonates at birth related to perchlorate in drinking water. Neonatal birth weight, length, and head circumference were not different among the three cities and were consistent with current U.S. norms. Therefore, perchlorate in drinking water at 114 microg/L did not cause changes in neonatal thyroid function or fetal growth retardation. Median urinary iodine among the entire cohort was 269 microg/L, intermediate between that of pregnant women in the United States at National Health and Nutrition Examination Survey (NHANES) I and at NHANES III and consistent with current World Health Organization (WHO) recommendations. Median breast milk iodine was not decreased in the cities with detectable perchlorate. Analysis of maternal urinary perchlorate excretion indicates an additional dietary source of perchlorate.