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
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.
ACETIC ACID AND ITS POTASSIUM AND SODIUM SALTS
These substances have been evaluated for acceptable daily intake
by the Joint FAO/WHO Expert Committee on Food Additives (see Annex 1,
Ref. No. 11) in 1965.
Since the previous evaluation, additional data have become
available and are summarized and discussed in the following monograph.
The previously published monograph has been revised and is reproduced
in its entirety below.
Acetate enters naturally into the metabolism of the body. It is
absorbed from the gastrointestinal tract and is completely utilized in
oxidative metabolism or in anabolic syntheses. Isotope experiments
have shown acetates to be utilized in the formation of glycogen,
intermediates of carbohydrates and fatty acid synthesis as well as
cholesterol synthesis. In addition it participates in the acetylation
of amines and may be converted to alanine by transamination and thence
incorporated into proteins of plasma, liver, kidney, gut mucosa,
muscle and brain (Documenta, Geigy, 1970).
Animal Route (mg/kg bw) References
(free acid) 4 960 Woodard et al., 1941
(free acid) 3 310 Woodard et al., 1941
(sod. acetate) 3 530 Smyth, 1951
Rabbit Rectal 1 200
(free acid) (LD, 1 hour) Dreyfus, 1920
s.c. 1 200
(free acid) (LD, 48 hours) Dreyfus, 1920
Oral 1 200
(free acid) (LD, 6 days) Dreyfus, 1920
Toxic effects of acetic acid are due not only to its irritant
properties but also to its effect on the central nervous system and
kidneys. Large oral doses cause narcotic CNS depression and death in
rats and mice (Woodard et al., 1941).
The immediate toxic effects of glacial acetic acid are due to its
corrosive acid action and to dehydration of tissues with which it
comes into contact. Ingestion results in severe pain and the formation
of white plaques and ulcers of mucosal surfaces, and may be followed
by haematemesis (Martindale, 1972).
Groups of three to six rats were given 0.01, 0.1, 0.25 and 0.5%
acetic acid in drinking-water for periods of from nine to 15 weeks.
Fluid intake was the same in all groups; at the 0.5% level there was
immediate progressive reduction in body weight gain, loss of appetite
and fail in food consumption to 27%. Mortality rate was unaffected
(Sollmann, 1921). In another experiment groups of three to four
rats survived 14 days when given 1800 mg/kg bw per day free acid
intragastrically or 4200-4800 mg/kg bw sodium acetate, but only three
to five days on daily intragastric 2400 mg/kg bw free acid. Animals
lost weight before death and showed blistered paws and reddened noses.
No autopsies were done (Hemmingway & Sparrow, 1942). Intragastric
intubation of 3 ml of 10% solution acetic acid to rats for 90 days
produced a drop in haemoglobin concentration and erythrocyte count
Four groups of two young pigs were fed daily diets containing 0,
240, 720, 960 and 1200 mg/kg bw per day for successive 30-day periods
to a total of 150 days. There were no significant differences in
growth rate, weight gain, early morning urinary ammonia and terminal
blood pH between controls and test groups. No autopsies were done
(Lamb & Evvard, 1919).
No animal studies are available.
About 1 g/day of acetic acid present in vinegar and other items
of food and drink has been consumed by man for centuries apparently
without causing any adverse effects. However, continued ingestion of
large doses has been regarded as a contributory factor in the
development of Laennec type of liver cirrhosis (Singer, 1936).
In evaluating the acceptance of acetic acid, emphasis is placed
on its established metabolic pathways and its consumption by man as a
normal constituent of the diet.
Estimate of acceptable daily intake for man
Documenta, Geigy, ]970, 7th ed. (J. R. Geigy S.A., Basle)
Dreyfus, L. (1920) Compt. rend. soc. biol., 83, 136
Hemmingway, A. & Sparrow, A. (1942) Proc. Soc. exper. Biol. Med., 51,
Lamb, A. R. & Evvard, M. J. (1919) J. Biol. Chem., 37, 317
Martindale's Extra Pharmacopoeia, 1972, 26th ed. (The Pharmaceutical
Singer, L. (1936) Munch. med. Wschr., 83, 1288
Sollmann, T. (1921) J. Pharm. Exp. Therap., 16, 463
Woodard, G. et al. (1941) J. Ind. Hyg. Toxic., 23, 78
Wysokinska, Z. (1952) Roczniki Panstwowego Zakladu Hig., 3, 273
* See relevant paragraph in the seventeenth report (pages 10-11).