In the body, iodine (I) is involved primarily in the synthesis of 2 thyroid hormones, thyroxine (T4) and triiodothyronine (T3).
(See also Overview of Mineral Deficiency and Toxicity.)
Iodine occurs in the environment and in the diet primarily as iodide. In adults, about 80% of the iodide absorbed is trapped by the thyroid gland. Most environmental iodine occurs in seawater as iodide; a small amount enters the atmosphere and, through rain, enters ground water and soil near the sea.
Fortifying table salt with iodide (typically 70 mcg/g) helps ensure adequate intake (150 mcg/day). Requirements are higher for pregnant (220 mcg/day) and lactating (290 mcg/day) women.
Chronic toxicity may develop when intake is > 1.1 mg/day. Most people who ingest excess amounts of iodine remain euthyroid. Some people who ingest excess amounts of iodine, particularly those who were previously deficient, develop hyperthyroidism (Jod-Basedow phenomenon). Paradoxically, excess uptake of iodine by the thyroid may inhibit thyroid hormone synthesis (called Wolff-Chaikoff effect). Thus, iodine toxicity can eventually cause iodide goiter, hypothyroidism, or myxedema.
Very large amounts of iodide may cause a brassy taste in the mouth, increased salivation, gastrointestinal irritation, and acneiform skin lesions. Patients frequently exposed to large amounts of iodine-containing radiographic contrast dyes or the drug amiodarone need to have their thyroid function monitored.
Diagnosis of iodine toxicity is usually based on results of thyroid function testing and imaging, which are correlated with clinical data. Iodine excretion may be more specific but is not usually measured.
Treatment of iodine toxicity consists of correcting thyroid abnormalities and, if intake is excessive, dietary modification.
Hypothyroidism due to iodine toxicity usually resolves in a few weeks after ingestion of excessive amounts is stopped; however, some patients remain permanently hypothyroid and require ongoing replacement of thyroid hormone.
