Abstract
In the case of a nuclear power plant accident, repetitive/prolonged radioiodine release may occur. Radioiodine accumulates in the thyroid and by irradiation enhances the risk of cancer. Large doses of non-radioactive iodine may protect the thyroid by inhibiting radioiodine uptake into the gland (iodine blockade). Protection is based on a competition at the active carrier site in the cellular membrane and the Wolff–Chaikoff effect, the latter being, however, only transient (24–48 h). Perchlorate may alternatively provide protection by a carrier competition mechanism only. Perchlorate has, however, a stronger affinity to the carrier than iodide. Based on an established biokinetic–dosimetric model developed to study iodine blockade, and after its extension to describe perchlorate pharmacokinetics and the inhibition of iodine transport through the carrier, we computed the protective efficacies that can be achieved by stable iodine or perchlorate in the case of an acute or prolonged radioiodine exposure. In the case of acute radioiodine exposure, perchlorate is less potent than stable iodine considering its ED50. A dose of 100 mg stable iodine has roughly the same protective efficacy as 1000 mg perchlorate. For prolonged exposures, single doses of protective agents, whether stable iodine or perchlorate, offer substantially lower protection than after acute radioiodine exposure, and thus repetitive administrations seem necessary. In case of prolonged exposure, the higher affinity of perchlorate for the carrier in combination with the fading Wolff–Chaikoff effect of iodine confers perchlorate a higher protective efficacy compared to stable iodine. Taking into account the frequency and seriousness of adverse effects, iodine and perchlorate at equieffective dosages seem to be alternatives in case of short-term acute radioiodine exposure, whereas preference should be given to perchlorate in view of its higher protective efficacy in the case of longer lasting radioiodine exposures.
Highlights
Large amounts of radioactive materials may be released in the case of a nuclear emergency, including fission products, activation products, uranium, plutonium, and transuranic elements (Wohni 1995)
The biokinetics of iodine was described as previously reported by a simple two-compartment model (Rump et al 2019) derived from the iodine model introduced by Riggs (1952) and widely used in radiation protection by the International Commission for Radioprotection (ICRP) (ICRP 1994, 1997) (Fig. 1)
As we are interested in the competition of radioiodine and stable iodine, we did not consider the kinetics of iodine integrated with thyroid hormones being secreted from the thyroid and their elimination, and the corresponding compartments were deleted
Summary
Large amounts of radioactive materials may be released in the case of a nuclear emergency, including fission products, activation products, uranium, plutonium, and transuranic elements (Wohni 1995). In the case of radioiodine uptake, this leads to an irradiation of the tissue, which may cause destruction and hypothyroidism at very high activities, or stochastic damages with an increased incidence of thyroid cancers on the long run. This occurred following the Chernobyl accident with an increase in the frequency of thyroid cancers among the population who had been exposed to radioiodine as children (Lomat et al 1997; Henriksen et al 2014). The elimination of iodine that has not been taken up into the gland out of the body occurs through the kidney with a clearance between 30 and 50 ml/min (Geoffroy et al 2000)
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