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    Toxicological evaluation of some food
    additives including anticaking agents,
    antimicrobials, antioxidants, emulsifiers
    and thickening agents



    WHO FOOD ADDITIVES SERIES NO. 5







    The evaluations contained in this publication
    were prepared by the Joint FAO/WHO Expert
    Committee on Food Additives which met in Geneva,
    25 June - 4 July 19731

    World Health Organization
    Geneva
    1974

              

    1    Seventeenth Report of the Joint FAO/WHO Expert Committee on
    Food Additives, Wld Hlth Org. techn. Rep. Ser., 1974, No. 539;
    FAO Nutrition Meetings Report Series, 1974, No. 53.

    SORBITAN MONOESTERS OF PALMITIC AND STEARIC ACIDS
    AND TRIESTERS OF STEARIC ACID

    Explanation

         These compounds have been evaluated for acceptable daily intake
    by the Joint FAO/WHO Expert Committee on Food Additives (see Annex 1,
    Ref. No. 7) in 1963.

         Since the previous evaluation, additional data have become
    available and are summarized and discussed in the following monograph.
    The previously published monograph has been expanded and is reproduced
    in its entirety below.

    BIOLOGICAL DATA

    BIOCHEMICAL ASPECTS

         The fatty acid moiety of sorbitan monostearate has a coefficient
    of digestibility of 53.3% (Oser & Oser, 1957b).

         Experiments with 14C-labelled sorbitan monostearate showed that
    at least 90% of the emulsifier, when fed to rats in oily solution, was
    hydrolyzed to stearic acid and anhydrides of sorbitol. A significant
    fraction of the administered 14C was expired as CO2. When the
    labelled material was administered in water, 16-25% was recovered in
    the urine; when it was given in oil, 44 to 66% was so recovered. Of
    the ingested radioactivity, 3 to 7% was recovered in the tissues 48
    hours after feeding. Fractionation of the carcass fats showed that
    14C was incorporated into fatty acids, glycerol and a residue that
    did not sublime (Wick & Joseph, 1953).

         Sorbitan trioleate prepared with a 14C-label in the sorbitol
    or the oleicate moieties was administered orally to rats. After
    administration of sorbitan 14C-trioleate, the appearance of
    14C-CO2 in the expired air reached a peak at about 6 hours and
    amounted to 30 to 35% of administered label. The faeces and
    gastrointestinal tract contained about 42% of the 14C-label,
    indicating that it was incompletely absorbed, and 3% appeared in the
    urine; the liver contained about 3% and the carcass about 22%. After
    administration of the 14C-sorbitan labelled ester, less than 2% of
    the label was recovered as 14C-CO2; the proportions not absorbed
    were 24% from a water emulsion and 37% from a solution in oil; the
    proportions recovered of that absorbed were as follows: urine, 88%;
    expired air, 5%; liver, 1%; carcass, 6% (Treon et al., 1967).

    TOXICOLOGICAL STUDIES

    Acute toxicity

         The physical properties and low toxicity of the partial esters of
    sorbitan are such that formal acute toxicity tests are impracticable.

         Acute feeding tests on sorbitan monopalmitate have been conducted
    in the rat. No toxic symptoms were observed in 10 male rats, weighing
    100-175 g, using the ester as their sole ad libitum diet (except for
    water) for 24 hours, during which they consumed an average of 1.5 g
    per animal or approximately 10 g/kg bw (Krantz, 1947c).

         For 10 rats, sorbitan monostearate was mixed with a diet at a
    concentration of 50%. These animals weighed 175 to 250 g and, within
    10 hours, had ingested about 3 g of the ester. They all appeared
    unharmed after three days.

         No toxic symptoms were observed in any of 10 female rats,
    weighing 125 to 175 g, fed 10 ml/kg bw of sorbitan tristearate by
    stomach tube, in the form of 50% aqueous emulsion, and observed over a
    six-day period. Four of the 10 animals, all of which appeared normal,
    were sacrificed and gave normal histological findings in the livers
    and kidneys. In 10 female rats, weighing 125 to 175 g, intraperitoneal
    injection of sorbitan tristearate in doses of 10 ml/kg (50% aqueous
    emulsion form) produced two fatalities in 48 hours of observation; the
    other animals appeared normal (Krantz, 1947d).

         Sorbitan monopalmitate ("Spon 40"), sorbitan monostearate ("Spon
    60") and sorbitan tristearate ("Spon 65"), in the maximal orally
    administerable doses (15.9 g/kg) produced no mortality in rats
    (Brandner, 1973).

    Short-term studies

    Rat

         When groups of 10 young rats were fed for six weeks on diets
    containing 1% and 4% of sorbitan monostearate there was no effect on
    weight gain, nor were there any significant changes
    histopathologically in the liver, kidneys, intestine and bladder
    (Krantz, 1946).

         When sodium monostearate was added to diets designed to induce
    hepatic necrosis in rats, levels up to 10% tended to prolong the
    survival time and had no significant effect upon the hepatic changes
    over periods up to 120 days (György et al., 1958).

         Rats in groups of five receiving sorbitan monostearate in their
    diet for six weeks at levels of 5 and 15% showed no change in bile-
    duct size (Krantz, 1951).

    Dog

         Dogs were fed sorbitan monostearate in a semi-synthetic diet at a
    level of 5% for 19 to 20 months. There was no appreciable difference
    in food intake, weight, maintenance and longevity between control dogs
    and those fed sorbitan monostearate. The microscopic examination of
    the tissues showed ne changes attributable to the feeding of sorbitan
    monostearate, with the exception of some haemosiderosis of the liver
    (Fitzhugh et al., 1959).

    Monkey

         Two rhesus monkeys, fed daily with 0.7 to 0.8 g/kg bw of sorbitan
    monostearate for five weeks, appeared unharmed throughout. No damage
    to the liver and kidneys was seen post mortem (Krantz, 1946).

    Long-term studies

    Rat

         A life-span (two-year) study in 30 male rats given 5% sorbitan
    monopalmitate in their daily diet showed no alteration in the growth
    pattern or survival of the test rats, as compared with controls, and
    no abnormalities that could be attributed to the experimental diet.
    Blood studies and histopathological studies of the principal viscera
    were made during and at the end of the experiment. Examination of the
    brain, spleen, pancreas, thyroid, parathyroid, prostate, pituitary
    gland, salivary gland, adrenal gland, bladder, bone marrow, heart,
    lymph nodes, lung, testicle and muscle, revealed nothing of a
    pathological nature attributable to the experimental diet (Krantz.
    1947a)

         Thirty rats were fed on a diet containing 5% sorbitan
    monostearate for up to two years. Growth rate and survival were
    similar to those of the controls, nor were there any histological
    abnormalities post mortem that could be attributed to the diet
    (Krantz, 1947b).

         Studies made during and at the end of the experiment were similar
    to those reported for sorbitan monopalmitate (see above).

         Experiments were conducted over a period of two years on four
    generations of rats (30 rats in each group). At levels of 5 and 10% in
    the diet no effects were observed on growth, food efficiency,
    reproduction, lactation, metabolism, behaviour, mortality, or the
    gross and histopathological appearance of the tissues. At a level of
    20%, retardation of growth and impairment in lactation were noted, but
    mortality was not increased. The weight of the liver and kidneys was
    increased, but both appeared to be histologically normal (Oser & Oser,
    1956a, b; 1957a, b).

         Sorbitan monostearate was fed to groups of 24 rats at levels of
    2, 5, 10 and 25% in the diet for two years. Levels of 2 and 5% did not
    produce evidence of toxicity. The substance caused a significant
    increase in mortality at the 10 and 25% levels, with growth depression
    and enlargement of the liver and kidneys (Fitzhugh et al., 1959).

         A life-span (two-year) chronic feeding study was conducted on
    30 male rats, using 5% sorbitan tristearate in their diet. From this
    experiment it was concluded that there was no alteration in the growth
    pattern or survival of the test rats as compared to the controls, nor
    were there any abnormalities that could be attributed to the
    experimental diet (Krantz, 1947e).

         The investigations made were similar to those reported for
    sorbitan monopalmitate (see above).

    OBSERVATIONS IN MAN

         Sorbitan monostearate given to nine human subjects in doses of
    6 g/day for 28 days had no significant effect on the gastric activity,
    or on the activity of the gastrointestinal tract (Steigmann et al.,
    1953).

         Other experiments on 16 human subjects with the same doses and
    for the same period showed no deleterious effect. Blood chemistry
    (including cholesterol), other haematological findings, urine analyses
    and liver function tests were normal (Waldstein et al., 1954).

         In another study 4 g of sorbitan monostearate were fed daily to
    two children for 32 to 37 days without harmful effect (Preston et al.,
    1953).

    Comments:

         The partial esters of sorbitan have been thoroughly investigated
    in both short-term and long-term experiments. They have also been
    studied in man. From a toxicological point of view, the evidence can
    be taken to cover sorbitan mono- and tristearates and sorbitan
    monopalmitate.

    EVALUATION

    Level causing no toxicological effect

         Rat: 50 000 ppm (5%) in the diet equivalent to 2500 mg/kg bw.

    Estimate of acceptable daily intake for man

         0-25 mg/kg bw*

                 

    *    As total sorbitan esters.

    REFERENCES

    Brandner, J. D. (1973) Unpublished report submitted by ICI America
         Inc.

    Fitzhugh, O. G. et al. (1959) Toxicol. appl. Pharmacol., 1, 315

    György, P., Forbes, M. & Goldblatt, H. (1958) J. agric. food Chem., 6,
         139

    Krantz, J. C. jr (1946) Unpublished report No. WER-149-102 to the
         Atlas Chemical Co.

    Krantz, J., C. jr (1947a) Unpublished reports Nos WER-149-171/201/232/
         232A/232B to the Atlas Chemical Co.

    Krantz, J. C. jr (1947b) Unpublished reports Nos WER-149-187/245/245A
         to the Atlas Chemical Co.

    Krantz, J. C. jr (1947c) Unpublished report No. WER-149-126 to the
         Atlas Chemical Co.

    Krantz, J. C. jr (1947d) Unpublished report No. WER-149-145 to the
         Atlas Chemical Co.

    Krantz, J. C. jr (1947e) Unpublished reports Nos. WER-149-172/202/
         230/230A/230B to the Atlas Chemical Co.

    Krantz, J. C. jr (1951) Unpublished report No. WER-149-315 to the
         Atlas Chemical Co.

    Oser, B. L. & Oser, M. (1956a) J. Nutr., 60, 367

    Oser, B. L. & Oser, M. (1956b) J. Nutr., 60, 489

    Oser, B. L. & Oser, M. (1957a) J. Nutr., 61, 235

    Oser, B. L. & Oser, M. (1957b) J. Nutr., 61, 149

    Preston, E. et al. (1953) J. clin. Nutr., 1, 539

    Steigmann, F., Goldberg, E. N. & Schoolman, H. M. (1953) Amer. J. dig.
         Dis., 20, 380

    Treon, J. F. et al. (1967) Chemistry, Physics and Application of
         Surface Active Substances, Vol. III, pp. 381-395, Gordon &
         Breach, New York

    Waldstein, S. S., Schoolman, H. M. & Popper, H. (1954) Amer. J. dig.
         Dis., 21, 181

    Wick, A. W. & Joseph L. (1953) Food Res., 18, 79


    See Also:
       Toxicological Abbreviations