title: The toxicology of iodate: a review of the literature.
abstract: Because it is more stable than iodide, most health authorities preferentially recommend iodate as an additive to salt for correcting iodine deficiency. Even though this results in a low exposure of at most 1,700 microg/d, doubts have recently been raised whether the safety of iodate has been adequately documented. In humans and rats, oral bioavailability of iodine from iodate is virtually equivalent to that from iodide. When given intravenously to rats, or when added to whole blood or tissue homogenates in vitro or to foodstuff, iodate is quantitatively reduced to iodide by nonenzymatic reactions, and thus becomes available to the body as iodide. Therefore, except perhaps for the gastrointestinal mucosa, exposure of tissues to iodate might be minimal. At much higher doses given intravenously (i.e., above 10 mg/kg), iodate is highly toxic to the retina. Ocular toxicity in humans has occurred only after exposure to doses of 600 to 1,200 mg per individual. Oral exposures of several animal species to high doses, exceeding the human intake from fortified salt by orders of magnitude, pointed to corrosive effects in the gastrointestinal tract, hemolysis, nephrotoxicity, and hepatic injury. The studies do not meet current standards of toxicity testing, mostly because they lacked toxicokinetic data and did not separate iodate-specific effects from the effects of an overdose of any form of iodine. With regard to tissue injury, however, the data indicate a negligible risk of the small oral long-term doses achieved with iodate-fortified salt. Genotoxicity and carcinogenicity data for iodate are scarce or nonexisting. The proven genotoxic and carcinogenic effects of bromate raise the possibility of analogous activities of iodate. However, iodate has a lower oxidative potential than bromate, and it did not induce the formation of oxidized bases in DNA under conditions in which bromate did, and it may therefore present a lower genotoxic and carcinogenic hazard. This assumption needs experimental confirmation by proper genotoxicity and carcinogenicity data. These in turn will have to be related to toxicokinetic studies, which take into account the potential reduction of iodate to iodide in food, in the intestinal lumen or mucosa, or eventually during the liver passage.
authors.affiliation: International Council for the Control of Iodine Deficiency Disease, Solothurn, Switzerland. buergi@smile.ch
authors.forename: H
authors.initials: H
authors.lastname: Bürgi
authors.forename: T H
authors.initials: TH
authors.lastname: Schaffner
authors.forename: J P
authors.initials: JP
authors.lastname: Seiler
mesh_terms: D002273:Carcinogens; D005503:Food Additives; D006801:Humans; D007452:Iodates / Q000008:administration & dosage / Q000737:chemistry / Q000493:pharmacokinetics / Q000506:poisoning*; D007455:Iodine; D007881:Legislation, Food; D009153:Mutagens; D018673:Nutrition Policy; D017673:Sodium Chloride, Dietary; D014481:United States
chemical_list: D002273:Carcinogens; D005503:Food Additives; D007452:Iodates; D009153:Mutagens; D017673:Sodium Chloride, Dietary; C034024:iodized salt; D007455:Iodine