The NAS Committee stated “it is unlikely that perchlorate poses a risk of cancer in humans.” (See page 145 of the NAS report, “Health Implications of Perchlorate Ingestion.”)
“There are no reports of the appearance of a new thyroid disorder, thyroid nodules or thyroid carcinoma in any patient treated with potassium perchlorate for hyperthyroidism. Iodide deficiency in the thyroid gland, a possible consequence of perchlorate administration or exposure, is not associated with an increase in thyroid cancer … In hyperthyroid patients treated with antithyroid drugs, there was no increase in thyroid cancer mortality” (See page 62 of the NAS report, “Health Implications of Perchlorate Ingestion.”).
“The committee concludes that the thyroid tumors in the (rat) offspring were most likely treatment related but that thyroid cancer in humans resulting from perchlorate exposure is unlikely because of the hormonally mediated mode of action and species differences in thyroid function.” (see page 12)
“In addition, EPA’s science policy document on the assessment of thyroid follicular-cell tumors notes that although there may be some qualitative similarities, there is evidence that “humans may not be as sensitive quantitatively to thyroid cancer development of thyroid-pituitary disruption as are rodents. The increased sensitivity may be due to marked species differences in the physiology of the thyroid gland. The EPA and IARC documents provide guidance for the evaluation of thyroid follicular-cell tumors based on mode of action (for example, tumors secondary to hormone imbalance).” (see page 145)
One of the animal studies of perchlorate looked at two generations of rats that were exposed to perchlorate in drinking water. A certain type of thyroid tumor known as a follicular cell tumor was identified in two of the rats given perchlorate. On page 145 of the report, the NAS Committee indicates that these types of tumors are not unexpected in rats when they are exposed to agents that affect the thyroid because “spontaneous thyroid follicular-cell adenomas can occasionally be observed in control rats of this strain and age.” In other words, thyroid tumors occur often in rats (especially Sprague Dawley rats as were studied here) even when they are not exposed to anything. The committee also notes that, in this regard, rats are much different than humans, stating “humans may not be as sensitive quantitatively to thyroid cancer development of thyroid-pituitary disruption as are rodents…The increased sensitivity may be due to marked species differences in the physiology of the thyroid gland.”
Rats are known to respond much more rapidly and to a greater extent to agents that affect their thyroid than do humans because of many physiological differences. When a rat is exposed to an agent that affects the thyroid, more thyroid stimulating hormone (TSH) is produced than in a human at a comparable dose, which causes a much more rapid production of thyroid cells. When cells multiply rapidly, the likelihood that cellular mutations will occur increases, which can lead to tumors. Since TSH levels are not affected in humans at equivalent doses, stimulation of the thyroid to produce more cells does not occur. The NAS states that these agents “can be assumed not to be carcinogenic in humans in concentrations that do not lead to alterations in thyroid hormone homeostasis.” (See page 145 of the NAS report, “Health Implications of Perchlorate Ingestion.”)