Food and Agricultural Organization of the United Nations PA N I S F I A T G u id e in e s o n fo o d fo r tific atio n w th m ic r o n u tr ie n ts Interest in micronutrient malnutrition has increased greatly over the last few years. One of the main reasons is the realization that micronutrient malnutrition contributes substantially to the global burden of disease. Furthermore, although micronutrient malnutrition is more frequent and severe in the developing world and among disadvantaged populations, it also represents a public health problem in some industrialized countries. Measures to correct micronutrient deficiencies aim at ensuring consumption of a balanced diet that is adequate in every nutrient. Unfortunately, this is far from being achieved everywhere since it requires universal access to adequate food and appropriate dietary habits. Food fortification has the dual advantage of being able to deliver nutrients to large segments of the population without requiring radical changes in food consumption patterns.

Guidelines on food fortification with micronutrients

Ozonation of drinking water: part II. Disinfection and by-product formation in presence of bromide, iodide or chlorine.

Oxidative treatment of bromide-containing waters: formation of bromine and its reactions with inorganic and organic compounds--a critical review.

A nonphotochemical generation of singlet oxygen (1O2) using potassium periodate (KIO4) in alkaline condition (pH > 8) was investigated for selective oxidation of aqueous organic pollutants. The generation of 1O2 was initiated by the spontaneous reaction between IO4– and hydroxyl ions, along with a stoichiometric conversion of IO4– to iodate (IO3–). The reactivity of in-situ-generated 1O2 was monitored by using furfuryl alcohol (FFA) as a model substrate. The formation of 1O2 in the KIO4/KOH system was experimentally confirmed using electron spin resonance (ESR) measurements in corroboration with quenching studies using azide as a selective 1O2 scavenger. The reaction in the KIO4/KOH solution in both oxic and anoxic conditions initiated the generation of superoxide ion as a precursor of the singlet oxygen (confirmed by using superoxide scavengers), and the presence of molecular oxygen was not required as a precursor of 1O2. Although hydrogen peroxide had no direct influence on the FFA oxidation process, th...

Singlet-Oxygen Generation in Alkaline Periodate Solution.

Disinfection by-products and their potential impact on the quality of water produced by desalination systems: a literature review.

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 1700 mg/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 1200 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 iodatespecific 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.

http://iodineresearch.com/files/burgi_2001_toxicology_of_iodate.pdf

T H Schaffner

Papers

The Toxicology of Iodate: A Review of the Literature