The Thyroid and Iodine

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Physiological Need for Stable Iodine

Iodine is an essential component of the iodine-containing thyroid hormones thyroxine (T4) and triiodothyronine (T3). Severe iodine deficiency (intake less than 50 |mg/day) causes mental retardation, cretinism, and endemic goiter. Even in developed countries such as Germany endemic goiter with thyroid enlarge ment and/or nodules is still prevalent in approximately 30% of the adult population [2]. The daily supply of iodine should amount to 90 |mg in children aged 0-7 years, 120 |mg in children aged 7-12 years, 150 |mg in adolescents and adults, and 200 | g in pregnant and nursing women ([3], In cases of iodine deficiency, the thyroid enlarges and more actively transports iodine from the bloodstream, thus allowing uptake of sufficient iodine for the maintenance of normal thyroid function. In contrast, when the iodine supply is excessive (more than 500 |mg/day) the sodium iodide sym-porter (NIS) of thyrocytes is downregulated, thus inhibiting iodide transport from the bloodstream into the thyroid gland (Wolff-Chaikoff effect, [4]). This effect leads to a transient decrease in thyroid hormone synthesis for about 48 hours; shortly thereafter, normal thyroid hormone synthesis resumes.

Exposure to Radioiodine

Medical Use

For more than 60 years, radioactive isotopes of iodine (mainly 131I as a b- and g-emitter with a physical half-life of 8 days) have been used for the diagnosis and treatment of thyroid disorders. Moreover, 131I has been employed extensively to study the biokinetics of iodine in healthy people and patients with disturbances of thyroid function. Thyroid radioiodine uptake is elevated in patients with hyperthyroidism and decreased in hypothyroid patients. In addition, it correlates inversely with the nutritional supply of stable iodine. Thus radioiodine uptake is high in iodine deficiency and low in case of iodine excess. In patients with hyperthyroi-dism, "toxic" nodular goiter, and differentiated thyroid cancer, 131I has been used effectively to normalize thyroid function and to ablate tumor tissue because high activities of 131I can cause cell death.

Nonmedical Use

Radioactive iodine is a byproduct of the fusion of uranium atoms. Minimal radioiodine is normally released into the environment from operating nuclear reactors, whether such reactors are operated for power production, for production of radioisotopes, for material testing or for research. In the case of nuclear power plants, the uranium fuel is contained in sealed metal tubes (fuel rods) and placed inside a steel reactor containment several inches thick, which itself is located inside a thick (several feet) concrete reactor building [1]. Before radioactive iodine from the nuclear fuel of a nuclear power plant can reach the environment, the fuel rods in the reactor core must be damaged, with additional damage to the containment enclosing the reactor. However, if the reactor construction does not fulfill usual safety standards, radioio-dine may be released into the environment if there is a nuclear emergency, such as the Chernobyl reactor catastrophe. On the other hand, radioiodine may be released into the environment when uranium is used as an explosive material in atomic bombs or if iodine isotopes were to be used as radioactive components of "dirty bombs" [1].

Radioiodine can exist in particulate form as sodium iodide or as radioiodine vapor. Radioiodine in the gaseous state can be inhaled into the lungs and enter the bloodstream thus reaching the thyroid gland. With normal nutritional iodine supply, a normally functioning thyroid gland will take up and store between 15% and 30% of the radioiodine to which it is exposed. After the Chernobyl reactor catastrophe, most of the dose to the thyroid of people living in the vicinity to the reactor plant was caused by the consumption of radioactive iodine-contaminated water and food, including milk [1].

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