Ethylmethylphenylglycidate (EMPG) was first evaluated for
acceptable daily intake by the Joint FAO/WHO Expert Committee on Food
Additives in 1967 and 1974 (see Annex I, Refs. 14 and 34). A
toxicological monograph was issued in 1968 (see Annex I, Ref. 15).
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.
In vitro experiments using simulated gastric juice showed over
80% cleavage of the epoxy linkage after one hour; with intestinal
fluid some 70% of the epoxy linkage was destroyed in three hours.
Ester hydrolysis occurred to only a minor degree (Oser, 1967).
Special studies on carcinogenicity
See under long-term studies.
Animal Route (mg/kg bw) Reference
Rat Oral 5 470 Jenner et al., 1964
Guinea-pig Oral 4 050 Jenner et al., 1964
In a 12-week study on 15 male and 15 female rats using mixed
esters, no adverse effect was noted at a level of 21 mg/kg/day (Oser,
1967). In another study lasting 16 weeks, groups of five male and five
female rats were fed 0 and 1% of ester in their diet. Growth
retardation, particularly of males, was observed, as well as
testicular atrophy (Hagan et al., 1967). In a one-year study on five
male and five female rats, the ester was fed at 0 and 0.25% in the
diet without any adverse effects on body weight gain, organ weights
and histology of major organs (Hagan et al., 1967).
A well-defined sample of EMPG was fed to groups of 15 male and 15
female rats at dietary levels of 0 (control), 0.02, 0.1 and 0.5% for
15 weeks and was found to have no effect on growth rate, food or water
consumption of the animals. There was no evidence of any impairment of
neuromuscular function. This finding was confirmed by histological
examination of the sciatic and brachial nerve and of the central
nervous system, no part of which showed any evidence of demyelination
or other changes. Similarly, no evidence of testicular damage, either
from the weight of the organs or from histological findings, was
The only effects observed were organ weight changes in animals
fed a dietary level of 0.5%. These changes consisted of increased
absolute and relative stomach, small intestine and caecum weights, and
increased relative liver and kidney weights in the female rats and
increases in absolute and relative kidney weight and relative liver
weight in male rats. Although none of these changes was associated
with any histological abnormalities, they cannot be disregarded. The
no-untoward-effect level in this study was, therefore, 0.1% EMPG. It
must be stressed that these findings are specific for the material
used for this study and cannot be applied generally to materials
termed "strawberry aldehyde" (Mason et al., 1978).
Groups of 20 male and 20 female rats were fed diets containing
various proportions of EMPG for two years. At the 0.5% level paralysis
of hindquarters was observed as well as demyelinating degenerative
changes in the sciatic nerve (Bär & Griepentrog, 1967).
Groups of 48 male and 48 female rats were given diets containing
0 (control), 0.02, 0.1 and 0.5% EMPG for two years. There was no
treatment-related effect on mortality, haematology, renal function,
serum chemistry or organ weights. General observations, tests of motor
coordination and histological examination of nerve tissues provided no
evidence of neuropathy. Histological change in the pancreas, adrenal
glands, lymph nodes and liver showed some increase in incidence in
treated animals, but the lesions were of types encountered in aging
rats. There was an increase of pituitary tumours in treated females
and of testicular interstitial cell tumours in the males, but
consideration of their background incidence in untreated rats and the
lack of any dose relationship in their occurrence in this study
indicated that these findings were unlikely to be related to
It is concluded, therefore, that this study did not demonstrate a
carcinogenic effect in rats given dietary levels of up to 0.5% EMPG
and that the no-untoward-effect level was 0.1% of the diet, providing
an EMPG intake of approximately 35 mg/kg/day in males and 60 mg/kg/day
in females (Dunnington et al., 1981).
Since the last evaluation, short- and long-term studies in the
rat have become available. In both studies there was no evidence of
any impairment of the neuromuscular function. Histological
examinations of nerve tissue did not confirm the findings of previous
studies in which demyelination was reported to occur (Griepentrog,
1969). The failure to show similar affects may be related either to
different strains of rats used or to differences in the specifications
of the test material.
The only effects observed were organ weight changes, lower body
weight in females and increased incidence of histological changes in
the lymph nodes, pancreas, adrenal glands and liver in rats fed a
dietary level of 0.5%. The no-untoward-effect level for
ethlymethylphenylglycidate from the studies considered was 0.1%.
No evaluation is possible at this time because clear
specifications of the test compound are not available.
Estimate of acceptable daily intake for man
Bär, F. & Griepentrog, F. (1967) Die Situation in der gesundheitlichen
Beurteilung der Aromatisierungsmittel für Lebensmittel, Med. u.
Ernähr., 8, 244-251
Dunnington, D. et al. (1981) Long-term toxicity study on ethyl
methylphenyl glycidate (strawberry aldehyde) in rat, Food
Cosmet. Toxicol., 19, 691-699
Griepentrog, F. (1969) Neurotoxische Wirkungen durch den Aromastoff
Athylmethylphenylglycidat ("Aldehyd C16") bei Ratten, Med. u.
Ernähr., 10, 89-90
Hagan, E. C. et al. (1967) Food flavourings and compounds of related
structure. II - Subacute and chronic toxicity, Food Cosmet.
Toxicol., 5, 141-157
Jenner, P. L. et al. (1964) Food flavourings and compounds of related
structure. I - Acute oral toxicity, Food Cosmet. Toxicol., 2,
Mason, P. L. et al. (1978) Studies on the purity and short-term
toxicity of ethyl methylphenyl glycidate (strawberry aldehyde) in
rat, Food Cosmet. Toxicol., 16, 331-336
Oser, B. L. (1967) Unpublished report