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    INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

    WORLD HEALTH ORGANIZATION



    SUMMARY OF TOXICOLOGICAL DATA OF CERTAIN FOOD ADDITIVES



    WHO FOOD ADDITIVES SERIES NO. 12






    The data contained in this document were examined by the
    Joint FAO/WHO Expert Committee on Food Additives*
    Geneva, 18-27 April 1977




    Food and Agriculture Organization of the United Nations
    World Health Organization



    * Twenty-first Report of the Joint FAO/WHO Expert Committee on Food
    Additives, Geneva, 1977, WHO Technical Report Series No. 617

    L(+) AND DL - TARTARIC ACID

    Explanation

         Tartaric acid and its potassium, potassium-sodium and sodium
    salts have been evaluated for acceptable daily intake by the Joint
    FAO/WHO Expert Committee on Food Additives (see Annex I, Ref. Nos. 6,
    7, 8 and 33) in 1961, 1963, 1964 and 1973.

         The previous monographs have been expanded and are reproduced
    below.

    EVALUATION FOR ACCEPTABLE DAILY INTAKE

    BIOLOGICAL DATA

    BIOCHEMICAL ASPECTS

         L(+)-tartaric acid was reported to be inert in the human body
    (Finkle, 1933).

         When taken by mouth, only about 20% of ingested tartrate is
    eliminated in the urine; the remainder is not absorbed as such since
    it is destroyed in the intestinal tract by bacterial action (Underhill
    et al., 1931; Finkle, 1933).

         Contrary to the two above-mentioned studies a study has been
    published where the percentages of both L(+) and D(-)-tartarte acids
    eliminated in urine after intramuscular injection to one man were only
    slightly greater than that after oral administration (Bauer and
    Pearson, 1957).

         The excretion of L(+)-tartaric acid in the urine after p.o.
    administration was investigated in the rat, guinea-pig, dog and
    rabbit. In the rat 68% (61-85) of a 400 mg/kg bw dose was recovered.
    In the guinea-pig 13-27% of the dose was recovered from doses ranging
    from 100 to 800 mg/kg bw. In the dog doses less than 600 mg/kg bw were
    totally excreted in the urine (83-100%), but with higher doses
    (600-1500 mg/kg) the recovery diminished to 50-60% and was associated
    with slight renal changes. In the rabbit 90-99% of a dose of 50 mg/kg
    bw was recovered. When the dose was raised to 100, 200 and 300 mg/kg
    bw 21-23%, 15-26% and 2-3% were found in urine, respectively.
    Histological studies revealed an increasing degree of kidney damage in
    parallel with the decreasing excretion (Underhill et al., 1931).

         Sodium tartrate in daily doses of up to 10 or even 20 g has been
    used in medical practice as a laxative. It has been tested for this
    action in a clinical study involving the application of daily doses of

    10 g of sodium tartrate to 26 patients for an average of 11.8 doses,
    giving laxative responses in 66% of the subjects. The only side-
    effects noticed were nausea or vomiting (1.6%) and abdominal cramps
    (2.1%) (Gold and Zahm, 1943). Following a single oral dose of
    400 mg/kg monosodium (14C) L(+) tartrate to rats, 70% of the
    radioactivity was excreted in urine, 16% in expired air and 14% in the
    faeces within 48 hours. Most of the labelled material was excreted by
    eight hours, the half-life for elimination from urine being 4.6 and
    4.8 hours in male and female rats respectively. Comparison with
    intravenous administration indicated that the portion of radioactivity
    expired resulted from metabolism of the tartrate salt to 14Co2 by
    the rat, about half of which occurred in the gut (HRC, 1975).

         With monosodium (14C) L(+) tartrate given at a daily dose of
    2.73 g/kg for seven consecutive days, the concentration of label in
    blood and bone was maximal one hour after administration of the last
    dose. Half-lives for elimination were 5.9 and nine days respectively
    for blood and bone. By contrast, peak label concentrations in blood
    and bone following the same dose of monosodiom (14C)DL(-) tartrate
    occurred at three and 12 hours respectively while the half-lives were
    6.5 and 2.5 days respectively for these organs. Labelled material in
    bone was not associated with the mineralized fraction. Repeated doses
    of 2.73 g/kg for seven days of monosodium (14C)DL(-) tartrate to rats
    produced an increased kidney/body weight ratio compared to controls
    while monosodium (14C)L(+)-tartrate produced no such change.
    Autoradiographic studies demonstrated that after repeated oral
    administration of monosodium (14C)DL-tartrate, radioactivity was
    associated with the gastrointestinal tract, liver, kidneys and bone
    during 24 hours; after 48 hours and eight days radioactivity was
    associated only with bone and with granular deposits in the kidneys
    (HRC, 1975).

    TOXICOLOGICAL STUDIES

    Reproductive and teratology studies

         Teratology studies have been conducted in rats, mice, hamsters
    and rabbits. Tartaric acid administered during the period of
    organogenesis did not produce terata in either soft or skeletal
    tissues of the highest dose tested which was hamsters, 225 mg/kg/day -
    five days; rabbits, 215 mg/kg/day - 13 days; rats, 181 mg/kg/day - 10
    days; mouse, 274 mg/kg/day - 10 days. Likewise no effects were noted
    on nidation or on maternal or foetal survival rats (FDRL, 1973).

    Acute toxicity

         In the mouse, the LD50 of the sodium salt administered by mouth
    was found to be 4360 mg/kg bw (Locke et al., 1942).

         Tartaric acid administered by stomach tube in a dose of
    5000 mg/kg was fatal to a dog (Sourkes and Koppanyi, 1950).

         Three out of seven male rabbits died following oral
    administration of disodium tartrate in an average dose of 5290 mg/kg;
    while six male rabbits survived an average oral dose of 3680 mg/kg
    (Locke et al., 1942). Renal damage has been observed only after the
    intravenous administration of tartaric acid in doses of 0.2-0.3 g in
    rabbits and rats (Bodansky et al., 1942; Gold and Zahm, 1943).

         A fatal case of tubular nephropathy in man following accidental
    ingestion of 30 g tartaric acid has been reported (Robertson and
    Lönnell, 1968).

    Short-term studies

    Cat

         Sodium tartrate was injected subcutaneously three times a week
    for a total of 45 doses to two, one, two and two cats in doses of 0,
    50, 75 and 100 mg/kg, respectively. The weights of the kidneys were
    essentially the same for the treated and the control groups, and the
    kidneys appeared similar on gross examination. The kidneys of four
    animals were examined histologically. The sections of the two control
    animals were normal, while those of the two animals on the 100 mg/kg
    dose level showed considerable tubular degeneration (Gold and Zahm,
    1943).

    Dog

         Tartaric acid was administered in daily oral doses of 990 mg/kg
    bw to each of four dogs for 90-114 days. Casts appeared in the urine
    of three dogs; the blood chemistry remained normal except in one dog
    in which azotaemia developed with death in 90 days. Weight changes
    varied from a weight gain of 30% to a loss of 32% (Krop and Gold,
    1945).

    Rabbit

         Three rabbits survived 17 consecutive daily feedings of disodium
    tartrate in an average dosage of 1150 mg/kg; whereas, average dosages
    of 3680 mg/kg killed three out of six rabbits in six to 19 consecutive
    daily feedings (Locke et al., 1942).

         A study in which 15 male New Zealand rabbits were fed 7.7% sodium
    tartrate in the diet for 22 weeks produced no evidence of toxicity
    either in terms of body and organ weight (testes and thyroid) changes
    or pathology (Packman et al., 1963).

    Long-term studies

    Rat

         Groups of 24 rats (12 of each sex) were fed diets containing
    0.1%, 0.5%, 0.8% and 1.2% of tartaric acid for a period of two years.
    A group of 48 rats served as controls. No significant toxic effects
    were observed in any of the groups as determined by growth rate (for
    the first year), mortality throughout the experiment, and gross and
    microscopic findings at the end of the two-year period. An
    exceptionally thorough microscopic pathological examination was
    carried out (Fitzhugh and Nelson, 1947).

         Groups of 35 male and 35 female Sprague-Dawley rats were
    administered diets containing 0, 2.56, 4.22, 6.02 or 7.68% monosodium
    L(+) tartrate for 104 weeks. A dosage related reduction in body weight
    gain, food intake and efficiency of food utilization recorded in
    treated rats during the first 26 weeks of treatment. Thereafter, rats
    receiving 2.56% had body weight gains and food intake values similar
    to those of controls. Other treated rats continued to show body weight
    gains and food intake values which were lower than those of the
    controls. A treatment related reduction in mortality incidence was
    recorded which was probably associated with the reduced food intake.
    Urinalysis, haematology, blood chemistry and organ weight data
    revealed no adverse reactions to treatment with monosodium L(+)
    tartrate. Histopathology revealed no evidence of treatment related
    change, and in particular, there was no indication of an untoward
    effect on the spontaneous tumour profile of the rat (HRC, 1976).

    REFERENCES

    Bauer, C. W. and Pearson, R. W. (1957) J. Amer. Pharm. Ass.
    Sci. Ed., 46, 575-578

    Bodansky, O., Gold, H. and Zahm, W. (1942) J. Amer. Pharm. Ass.
    Sci. Ed., 31, 1

    Finkle, P. (1933) J. Biol. Chem., 100, 349

    Fitzhugh, O. G. and Nelson, A. A. (1947) J. Amer. Pharm. Ass.
    Sci. Ed., 36, 217

    Gold, R. and Zahm, W. (1943) J. Amer. Pharm. Ass. Sci. Ed., 32,
    173

    Krop, S. and Gold, H. (1945) J. Amer. Pharm. Ass. Sci. Ed., 34, 86

    Locke, A., Locke, R. B., Schlesinger, H. and Carr, H. (1942)
    J. Amer. Pharm. Ass. Sci. Ed., 31, 12

    Packman, E. W., Abbott, D. D. and Harrisson, J. W. E. (1963)
    Toxicol. and Appl. Pharmacol., 5, 163-167

    Robertson, B. and Lönnell, L. (1968) Act. path. microb. Scand.,
    74, 305-310

    Sourkes, T. L. and Koppanyi, T. (1950) J. Amer. Pharm. Ass.
    Sci. Ed., 39, 275

    Underhill, F. P., Leonard, C. S., Gross, E.G. and Joleski, T. C.
    (1931) J. Pharmacol. Exp. Ther., 43, 359

    Unpublished reports (1973) Food and Drug Research Laboratories Inc.

    Unpublished report (1975) Huntingdon Research Centre

    Unpublished report (1976) Huntingdon Research Centre


    See Also:
       Toxicological Abbreviations