Human Exposures to Iodine Uptake-Inhibitors ClO4-, SCN- and NO3- are common.

Common anions (ClO4-, SCN- and NO3-) reduce production of TH through competitive inhibition at the Sodium Iodide Symporter (NIS). The NIS is the transport molecule that normally transfers iodine into the thyroid gland for incorporation into T4 and T3. Perchlorate is the most powerful THD with a 30x greater affinity for the NIS than does its normal target, iodine. It is about ten times as powerful as SCN- in this respect. Nitrate is a relatively weak inhibitor of iodine uptake and is believed to be 300x lower than ClO4-. However, concentrations in drinking water may be magnitudes higher. There appears to be no synergistic mechanism, and total exposure of each anion will be additive once the relative differences in strength are taken into account. All have been associated with altered TSH in infants.

The normal response to low T4/T3 is to stimulate hypothalamic release of TRH which prompts release of TSH. In a healthy individual, free of auto-immune or other thyroid disease, concentrations of TSH and T4/T3 are markers of low iodine intake, or of exposure to THDs. An individual with low iodine intake and/or high THD-exposure would be expected to have elevated TSH and/or diminished T4/T3. TSH is significantly elevated in perchlorate-exposed women and infants (BLOUNT). Any change in thyroid hormone concentrations is considered an indication of adverse effect for thyroid-hormone disrupting chemicals. Altered thyroid hormone status is, at present, the most important indicator of adverse effect in humans for thyroid-disrupting chemicals.

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