Bürgi H, Schaffner T H, Seiler J P
International Council for the Control of Iodine Deficiency Disease, Solothurn, Switzerland.
Thyroid. 2001 May;11(5):449-56. doi: 10.1089/105072501300176408.
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.
由于碘酸盐比碘化物更稳定，大多数卫生当局优先推荐将碘酸盐作为食盐添加剂，用于纠正碘缺乏。尽管这样导致的最高暴露量很低，至多为1700微克/天，但最近有人质疑碘酸盐的安全性是否有充分的文献记载。在人和大鼠中，碘酸盐中碘的口服生物利用度实际上与碘化物中的相当。当给大鼠静脉注射碘酸盐，或在体外将其添加到全血或组织匀浆中，或添加到食物中时，碘酸盐通过非酶反应定量还原为碘化物，从而以碘化物的形式被人体利用。因此，除了胃肠道黏膜外，组织对碘酸盐的暴露可能极少。静脉注射更高剂量（即超过10毫克/千克）时碘酸盐对视网膜具有高毒性。人类仅在接触到每人600至1200毫克的剂量后才出现眼毒性。几种动物经口接触高剂量碘酸盐（比强化盐中的人类摄入量高出几个数量级）后，出现了胃肠道腐蚀作用、溶血、肾毒性和肝损伤。这些研究不符合当前的毒性测试标准，主要是因为它们缺乏毒代动力学数据，且未将碘酸盐特异性效应与任何形式碘过量的效应区分开来。然而，就组织损伤而言，数据表明碘酸盐强化盐产生的小剂量长期口服风险可忽略不计。关于碘酸盐的遗传毒性和致癌性数据很少或不存在。溴酸盐已证实的遗传毒性和致癌作用增加了碘酸盐具有类似活性的可能性。然而，碘酸盐的氧化电位低于溴酸盐，在溴酸盐能诱导DNA中氧化碱基形成的条件下，碘酸盐并未诱导这种形成，因此它可能具有较低的遗传毒性和致癌风险。这一假设需要通过适当的遗传毒性和致癌性数据进行实验证实。反过来，这些数据必须与毒代动力学研究相关联，毒代动力学研究要考虑到碘酸盐在食物中、肠腔或黏膜中，或最终在肝脏代谢过程中还原为碘化物的可能性。
