Perchlorate and thiocyanate exposure and thyroid function in first-trimester pregnant women.

Abstract

Thyroid hormone, requiring adequate maternal iodine intake, is critical for fetal neurodevelopment. Perchlorate decreases thyroidal iodine uptake by competitively inhibiting the sodium/iodide symporter. It is unclear whether environmental perchlorate exposure adversely affects thyroid function in pregnant women. Thiocyanate, derived from foods and cigarette smoke, is a less potent competitive sodium/iodide symporter inhibitor than perchlorate. Our objective was to determine whether environmental perchlorate and/or thiocyanate exposure is associated with alterations in thyroid function in pregnancy. We conducted a cross-sectional study at health centers in Cardiff, Wales, and Turin, Italy. During 2002-2006, 22,000 women at less than 16 wk gestation were enrolled in the Controlled Antenatal Thyroid Screening Study. Subsets of 261 hypothyroid/hypothyroxinemic and 526 euthyroid women from Turin and 374 hypothyroid/hypothyroxinemic and 480 euthyroid women from Cardiff were selected based on availability of stored urine samples and thyroid function data. Urinary iodine, thiocyanate, and perchlorate and serum TSH, free T(4) (FT(4)), and thyroperoxidase antibody were measured. Urinary iodine was low: median 98 microg/liter in Cardiff and 52 microg/liter in Turin. Urine perchlorate was detectable in all women. The median (range) urinary perchlorate concentration was 5 microg/liter (0.04-168 microg/liter) in Turin and 2 microg/liter (0.02-368 microg/liter) in Cardiff. There were no associations between urine perchlorate concentrations and serum TSH or FT(4) in the individual euthyroid or hypothyroid/hypothyroxinemic cohorts. In multivariable linear analyses, log perchlorate was not a predictor of serum FT(4) or TSH. Low-level perchlorate exposure is ubiquitous but did not affect thyroid function in this cohort of iodine-deficient pregnant women.