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    FAO Nutrition Meetings
    Report Series No. 40A,B,C
    WHO/Food Add./67.29




    TOXICOLOGICAL EVALUATION OF SOME
    ANTIMICROBIALS, ANTIOXIDANTS, EMULSIFIERS,
    STABILIZERS, FLOUR-TREATMENT AGENTS, ACIDS AND BASES





    The content of this document is the result of the deliberations of the
    Joint FAO/WHO Expert Committee on Food Additives which met at Rome,
    13-20 December, 19651 Geneva, 11-18 October, 19662




                   

    1 Ninth Report of the Joint FAO/WHO Expert Committee on Food
    Additives, FAO Nutrition Meetings Report Series, 1966 No. 40; 
    Wld Hlth Org. techn. Rep. Ser., 1966, 339

    2 Tenth Report of the Joint FAO/WHO Expert Committee on Food
    Additives, FAO Nutrition Meetings Report Series, 1967, in press; 


    Food and Agriculture Organization of the United Nations
    World Health Organization
    1967


    POTASSIUM IODATE

    Chemical name                Potassium iodate

    Empirical formula            KIO3

    Molecular weight             214.00

    Definition                   Potassium iodate contains not less than
                                 99 per cent. and not more than the
                                 equivalent of 101 per cent. of KIO3
                                 after drying.

    Description                  Potassium iodate occurs as a white,
                                 crystalline powder and may have a slight
                                 odour.

    Use                          As a rapid oxidizing agent used for
                                 strengthening flour.

    Biological Data

    Biochemical aspects

         It is presumed that the oxidizing effects of potassium iodate on
    flour proteins are essentially similar to those caused by other
    oxidizing agents; in addition, the formation or some halogenated
    compounds might be expected. The main residue is iodide, but some
    iodate may be present (London et al., 1965). In the rat the inhibiting
    effect of iodine on the functional activity of the thyroid is
    intensified by deficiency of dietary protein or by an excessive
    proportion of vegetable protein or of vegetable and animal fat in the
    diet (Shtenberg and Plotnikova, 1960).

    Acute toxicity

                                                                       

    Animal                 Route     LD50             References
                                     (mg/kg 
                                     body-weight)
                                                                       

    POTASSIUM IODATE

    Mouse (fasting)        oral      531 ± 211        Webster et al.,
                                                      1957
    Mouse (fed)            oral      1 177 ± 61       Webster et al.,
                                                      1957
    Mouse                  i.p.      136 ± 5          Webster et al.,
                                                      1957
    Guinea-pig (fasting)   oral      <400             Webster, 1954
                                                                       

    (continued)
                                                                       

    Animal                 Route     LD50             References
                                     (mg/kg 
                                     body-weight)
                                                                       

    POTASSIUM IODIDE

    Mouse (fasting)        oral      1 862 ± 100      Webster et al.,
                                                      1957
    Mouse (fed)            i.p.      2 068 ± 140      Webster et al.,
                                                      1957
    Mouse                  i.p.      1 117 ± 30       Webster et al.,
                                                      1957
                                                                       

    Daily intravenous injection of high doses (45 mg/kg) of potassium
    iodate for up to 6 days in rabbits has produced retinopathy (Cucco,
    1954).

    Short-term studies

         Mouse. Groups of 9 or 10 mice were given water to which has
    been added 0, 0.05, 0.1, 0.25, 0.5 or 0.75 per cent. potassium iodate;
    a group also received water containing potassium iodide equivalent to
    a potassium iodate content of 0.84 per cent. Observation was continued
    for 16 weeks. Reduction of water intake and weight gain was observed
    in the groups receiving 0.5 per cent. and 0.75 per cent. potassium
    iodate. Three mice on the highest level of intake of potassium iodate
    died within the first week; the remainder survived for 16 weeks. No
    changes were found grossly or microscopically, except at the 0.5 per
    cent and 0.75 per cent. levels of intake. In these animals some
    haemolysis had occurred, resulting in reduced haemoglobin levels and
    haemosiderin deposits in the kidneys. Increased susceptibility to
    iodate was not demonstrable (Webster et al., 1959).

         Guinea-pig. Three groups of 6 male and 6 female guinea-pigs
    received water containing 0, 0.05, 0.25 and 0.5 per cent. of potassium
    iodate for 2 weeks. Except for reduced rate of weight gain and fluid
    intake in the two highest intake groups, no other significant
    abnormalities were observed (Webster et al., 1959).

         Rabbit. Fourteen rabbits received daily amounts of sodium
    iodate equivalent to 0.3099 mg/kg body-weight of potassium iodate for
    4-14 months without ill effect (Murray, 1953).

         Sheep. Groups of 2 male and 2 female lambs were fed on diets
    containing 0, 50, 100 and 500 ppm of potassium iodate for 45 days
    without demonstrable ill effect (Penick, 1955).

         Fowl. Groups of 9 male and 10 female day-old chicks were fed a
    basal diet containing 1.3 ppm of iodine with 1.2, 6, 30 and 150 ppm of
    added potassium iodate for 10 weeks. Weight gain, efficiency of food
    utilization, haemoglobin and methaemoglobin levels, blood cell counts
    and mortality were unaffected (Brumbaugh et al., 1959).

         Man. There is wide experience of therapeutic administration of
    iodides and iodates to human subjects (Stacpoole, 1953).

    Long-term studies

         No data are available on animals.

         Man. Iodized table salt at a level of 10 ppm has been used for
    many years for prophylaxis against endemic goitre. No ill affects have
    been reported. The intake of water with a high level of iodine (up to
    50 µg/1) did not appear to have any significant deleterious effects on
    general health, and provided some prophylaxis against thyroid
    enlargement (Medical Research Council, 1948; WHO, 1958).

    Comments

         There is a paucity of information on the effect of iodates on the
    nutritional value of flour and no long-term, studies appear to have
    been carried out on iodate-treated flour or bread made from it.

    Evaluation

         Amounts of iodine of the order of a few micrograms per litre in
    the drinking water have been shown to be prophylactic against thyroid
    enlargement in children. Calculations show that the use of iodate as a
    flour-maturing agent might well result in a daily intake of about 2000
    µg, which exceeds considerably the normal daily requirement of iodine
    (100-200 µg). It is undesirable for use as a food additive,
    particularly in a staple food, since it has an important physiological
    action.

    REFERENCES

    Brumbaugh, J. H., Mehring, A. L. jr & Titus, H. W. (1959) Poultry
    Sci., 38

    Cucco, G. (1954) Arm. ottal., 80, 102

    London, W. T., Vought, R. L. & Brown  F. A. (1965) New Eng. J. med.,
    273, 381

    Medical Research Council (1948) Memorandum No. 18, H.M.S.O., London

    Murray, M. M. (1953) Bull. Wld Hlth Org., 9 211

    Penick & Co. (1953) Unpublished Report from Univ. Pennsylvania

    Stacpoole, H. H. (1953) Bull. Wld Hlth Org., 9, 283

    Webster, S. H. (1954) Unpublished information

    Webster, S. H., Rice, M. E., Highman, B. & von Oettingen, W. F. (1957)
    J. Pharmacol. exp. Therap., 120, 171

    Webster, J. H, Rice, M. E., Highman, B. & Stohlman, E. F. (1959)
    Toxicol. appl. Pharmacol., 1, 87

    WHO (1958) Bull. Wld Hlth Org., 18, No. 1-2
    


    See Also:
       Toxicological Abbreviations