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.
ARABIC GUM
Explanation
This substance has been evaluated for acceptable daily intake by
the Joint FAO/WHO Expert Committee on Food Additives (See Annex 1,
Ref. No. 20) in 1969.
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
Arabic gum is almost completely digested by guinea-pigs (O'Dell
et al., 1957).
At dietary levels of less than 10%, arabic gum is fully absorbed
with a caloric equivalent of four calories per gram (Shue et al.,
1962)
TOXICOLOGICAL STUDIES
Acute toxicity
No data available. Sensitivity reactions have been reported in
man, e.g. asthma in printers (Brown & Crepea, 1947; Bohner et al.,
1941; Sprague, 1942; Fowler, 1952).
Gum sensitization is an occupational risk for predisposed
persons. In the case of inhalation, respiratory symptoms predominate
(Gelfand, 1943). Allergenic reaction can also occur following the
ingestion of arabic gum (Gelfand. 1949).
Short-term studies
Rat
Groups of rats were fed 0% or 154 arabic gum in their diet for 62
days. A cathartic effect was observed but weight gain, food
efficiency, haematological findings and organ weights were normal
(Booth et al., 1963).
Guinea-pig
Groups of 10 and 20 guinea-pigs were fed 15% powdered arabic gum
for six weeks. Controls received no bulk food in their diet. Weight
gain was improved in the test groups (Booth et al., 1949).
Rabbit
A group of four rabbits was given 20% arabic gum in a casein diet
for four weeks. Weight gain improved significantly in the test groups
(Hove & Herndon, 1957).
Dog
Three dogs were given 32 to 35 intravenous injections of acacia
over a period of 76 days at a total cumulative dosage ranging from
15.7 to 47.7 g/kg. The dog on the largest dose died with an enlarged
liver but unexplained cause of death four months after its last
injection. The other two dogs remained in good condition; biopsy
showed acacia present in their livers 26 months after their last
injections (Smalley et al., 1945).
Long-term studies
None available.
OBSERVATIONS IN MAN
Nine patients with nephrotic oedema received one to six
intravenous injections of acacia over periods up to eight weeks, with
total doses ranging from 80-325 g. There were no signs or symptoms of
liver enlargement, and no other complications. Five of these patients
excreted in the urine 5.5% to 38% of a single dose during periods
ranging from 10 to 30 days, respectively (Johnson & Newman, 1945).
Comments:
This gum has a traditional use in foods and pharmaceutical
preparations. The biochemical information available is sparse but it
has been demonstrated in the rat that this gum is completely
metabolized when it comprises less than 10% of the diet. Allergenic
reactions have been reported in man following ingestion of the
substance. Studies of the metabolic fate in man and potential body
storage are desirable.
EVALUATION
Estimate of acceptable daily intake for man
Not limited.*
FURTHER WORK OR INFORMATION
Desirable
Studies of the metabolic fate in man as well as more adequate
studies in animals. Studies on the allergenic reactions reported
following ingestion in men.
REFERENCES
Bohner, C. B., Sheldon, J. M. & Trenis, J. W. (1941) J. Allergy, 12,
290
Booth, A. N., Hendrickson, A. P. & De Eds, F. (1963) Toxicol. appl.
Pharmacol., 5, 478
Booth, A. N., Elvehjem, C. A. & Hart, E. B. (1949) J. Nutr., 37, 263
Brown, E. B. & Crepea, S. B. (1947) J. Allergy, 18, 214
Fowler, P. B. S. (1952) Lancet, 2, 755
Gelfand, H. H. (1943) J. Aller., 14, 203
Gelfand, H. H. (1949) J. Aller., 20, 311
Hove, E. L. & Herndon, F. J. (1957) J. Nutr., 63, 193
Johnson, J. B. & Newman, L. H. (1945) Arch. intern. Med., 76, 167
O'Dell, B. L. et al. (1957) J. Nutr., 63, 65
Shue, G. M., Douglass, C. D. & Friedman, L. (1962) Fed. Proc., 21(2),
91
Smalley, R. E. et al. (1945) Arch. intern. Med., 76, 39
Sprague, P. H. (1942) Canad. med. Ass. J., 47, 253
* See relevant paragraph in the seventeenth report, pages 10-11.