Compared to the elemental form, potassium iodide has a median lethal dose (LD) that is relatively high in several animals: in rabbits, it is 10 g/kg; in rats, 14 g/kg, and in mice, 22 g/kg. The tolerable upper intake level for iodine as established by the Food and Nutrition Board is 1,100 µg/day for adults. The safe upper limit of consumption set by the Ministry of Health, Labor and Welfare in Japan is 3,000 µg/day.
The biological half-life of iodine differs between the various organs of the body, from 100 days in the thyroid, to 14 days in the kidneys and spleen, to 7 days in the reproductive organs. Typically the daily urinary elimination rate ranges from 100 to 200 µg/L in humans. However, the Japanese diet, high in iodine-rich kelp, contains 1,000 to 3,000 µg of iodine per day, and research indicates the body can readily eliminate excess iodine that is not needed for thyroid hormone production. The literature reports as much as 30,000 µg/L (30 mg/L) of iodine being safely excreted in the urine in a single day, with levels returning to the standard range in a couple of days, depending on seaweed intake. One study concluded the range of total body iodine content in males was 12.1 mg to 25.3 mg, with a mean of 14.6 mg. It is presumed that once thyroid-stimulating hormone is suppressed, the body simply eliminates excess iodine, and as a result, long-term supplementation with high doses of iodine has no additional effect once the body is replete with enough iodine. It is unknown if the thyroid gland is the rate-limiting factor in generating thyroid hormone from iodine and tyrosine, but assuming it is not, a short-term loading dose of one or two weeks at the tolerable upper intake level may quickly restore thyroid function in iodine-deficient patients.
Excessive iodine intake presents symptoms similar to those of iodine deficiency. Commonly encountered symptoms are abnormal growth of the thyroid gland and disorders in functioning, as well as in growth of the organism as a whole. Iodide toxicity is similar to (but not the same as) toxicity to ions of the other halogens, such as bromides or fluorides. Excess bromine and fluorine can prevent successful iodine uptake, storage and use in organisms, as both elements can selectively replace iodine biochemically.
Excess iodine may also be more cytotoxic in combination with selenium deficiency. Iodine supplementation in selenium-deficient populations is theoretically problematic, partly for this reason. Selenocysteine (abbreviated as Sec or U, in older publications also as Se-Cys) is the 21st proteinogenic amino acid, and is the root of iodide ion toxicity when there is a simultaneous insufficiency of biologically available selenium. Selenocysteine exists naturally in all kingdoms of life as a building block of selenoproteins.