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.
TARTARIC ACID AND ITS POTASSIUM, POTASSIUM-SODIUM AND
SODIUM SALTS
Explanation
These compounds have been evaluated for acceptable daily intake
by the Joint FAO/WHO Expert Committee on Food Additives (see Annex 1,
Refs Nos. 6, 7 and 8) in 1961, 1963 and 1964.
Since the previous evaluation, additional data have become
available and are summarized and discussed in the following monograph.
The previously published monographs have been expanded and are
reproduced in their entirety below.
BIOLOGICAL DATA
BIOCHEMICAL ASPECTS
Tartaric acid is metabolically inert in the human body (Underhill
et al., 1931a, b, c; 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.
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%).
Renal damage has been observed only after the intravenous
administration of tartaric acid in doses of 0.2 to 0.3 g in rabbits
and rats (Bodansky et al., 1942; Gold & Zahm, 1943).
TOXICOLOGICAL STUDIES
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 & 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).
Short-term studies
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).
Dog
Tartaric acid was administered in daily oral doses of 990 mg/kg
to each of four dogs for 90 to 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 gain of 30% to a loss of 32% (Krop & Gold, 1945).
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 & Nelson, 1947).
Comments:
The long-term study in rats showed no adverse effects at the
highest level tested and they have been used medicinally for long
periods. The evaluation is, therefore, based on the metabolic
inertness of three tartrates and the fact that they are normal
constituents of food.
EVALUATION
Estimate of acceptable daily intake for man
0-30* mg/kg bw.
* Calculated as L(+)-tartaric acid.
REFERENCES
Bodansky, O., Gold, H. & Zahm, W. (1942) J. Amer. pharm. Ass,,
sci. Ed., 31, 1
Finkle, P. (1933) J. biol. Chem., 100, 349
Fitzhugh, O, G. & Nelson, A. A. (1947) J. Amer. pharm. Ass., sci. Ed.,
36, 217
Gold, H. & Zahm, W. (1943) J. Amer. pharm. Ass., sci. Ed., 32, 173
Krop, S. & Gold, H. (1945) J. Amer. pharm. Ass., sci. Ed., 34, 86
Locke, A., Locke, R. B., Schlesinger, H. & Carr, H. (1942) J. Amer.
pharm. Ass., sci. Ed., 31, 12
Sourkes, T. L. & Koppanyi, T. (1950) J. Amer. pharm. Ass., sci. Ed.,
39, 275
Underhill, F. P., Leonard, C. S., Gross, E. G. & Joleski, T. C.
(1931b) J. Pharmacol. exp. Ther., 43, 359
Underhill, F. P., Peterman F. I., Joleski, T. C. & Leonard, C. S.
(1931c) J. Pharmacol. exp. Ther., 43, 381
Underhill, F. P., Peterman, F. I. & Krause, A. G. (1931a)
J. Pharmacol. exp. Ther., 43, 351