Highlights of the American Thyroid Association Symposium - Thyroid Health and the Environment: Threats and Effects

March 24, 2006; Washington, DC

Kenneth D. Burman, MD

Disclosures

December 12, 2006

In This Article

Perchlorate

Perchlorate inhibits the thyroidal sodium iodide symporter; as a result, iodide uptake may be reduced with resulting inhibition of thyroid hormone synthesis and release.[1,8] This feature of perchlorate has allowed its use as a second-line treatment for thyrotoxicosis (especially when caused by amiodarone), although the adverse effects of aplastic anemia or agranulocytosis have diminished enthusiasm for this agent. These bone marrow side effects seem to be correlated with the dose administered, and occurred in 3% to 4% of patients taking 400-600 mg of perchlorate daily, and in 16% to 18% of patients taking 1000-2000 mg daily.[1,8]

There has been considerable discussion about the possible adverse effects of environmental perchlorate exposure.[9,10] On the basis of several studies, Cooper[1] estimated that chronic perchlorate exposure in normal, healthy individuals would have to exceed approximately 30 mg daily to alter thyroid function. Braverman[8] also summarized the clinical studies assessing perchlorate environmental exposure.

Perchlorate is used as an oxidizer in solid propellants for rockets and missiles used in the space program. It is also used in fireworks, road flares, matches, air bag inflation systems, and some commercial fertilizers. Perchlorate salts are highly soluble in water and can persist for decades in water or soil. Several US surveys have detected low levels (4 mcg/L) of perchlorate soil contamination. Perchlorate contamination has occurred in US lettuce samples, with parts per billion ranging from about 7 to 12.[8]

Braverman[8] studied the effect of perchlorate administration on thyroid function in healthy individuals. He administered 10 mg of perchlorate daily, which is approximately 300 times the maximum amount estimated to occur from water supply contamination. In these 14-day studies, he found no perchlorate-induced alterations in serum T4, T3, or TSH concentrations. Administering 0.5 or 3 mg perchlorate daily did not alter thyroid function tests either. Lastly, he showed that short-term occupational exposure (3 days) increased urine perchlorate concentration maximally to about 42 mcg/g creatinine, but serum TSH did not change prior to or during the exposure.

In summary, although further studies need to be performed, it appears that human environmental perchlorate contamination or exposure does not cause significant changes in thyroid hormone function. Nonetheless, further studies are warranted, and, obviously, efforts should be made to assess areas of environmental perchlorate contamination and to reduce human and animal exposure.

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