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It is well known that sudden exposure to high levels of iodide can disrupt thyroid function.
This can lead to exposure to perchlorate in nursing infants, while at the same time leading to lower levels of iodide in breast milk.
This has been demonstrated in rats where perchlorate exposure to nursing dams resulted in decreased levels of iodide in milk (Clewell et al. 2003).
Baseline uptake may be high in those with induced levels of iodide transporter in response to suboptimal iodide intake (Dohan et al. 2003).
Pigeons and rabbits were exposed for 3 months to diets containing high (950 ppb) or low (300 ppb) levels of iodide and to drinking water containing two levels of chlorine.
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Iodine-oxidizing bacteria were isolated directly from brine waters, but were only isolated from seawater after enrichment in the presence of 1 mM iodide (however, it was shown that KI does not influence the levels of iodide-oxidizing activity in the isolates).
Results do not confirm a consistent, significant reduction in the plasma level of iodide in rabbits and pigeons exposed to chlorinated water and the low-iodide diet.
By 2 hr after dosing, the thyroid gland has sequestered radiolabeled iodide, but circulating levels of the iodide remain in the body and are available for sequestration into the thyroid gland.
The perchlorate exposure thresholds for changes of these hormones are likely to depend on dietary iodide intake level, amount of iodide stored in the thyroid, preexisting stress on the thyroid, exposure to other goitrogens, and age.
Some level of iodine (applied as iodide) sorption was observed in nearly all samples (K d = 0 - 0.99 mL/g).
There was one sample each from two individuals in which perchlorate levels exceeded those of iodide.
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