Fragrance raw materials monographs 821

METHYL SALICYLATE
S!VIO~IJVII:Methyl o-hydroxybenzoate.
Structure: H0.CgHQ.0C0.CH3.
Descriprion and physical properties: Merck Index (1976).
Occurrence: Found in wintergreen oil, Gaulrheria procumbens and birch, tuberose, Dianrhus caryo-
phyllus L., Acacia caoenia Hook. and Am., ylang-ylang and several fruit jufces, including cherry,
apple and raspberry (Fenarolis Handbook of Flavor Ingredients, 1975).
Preparation: By esterification of salicylic acid with methanol (Merck Index, 1976).
Loses: In public use since the 1930s. Use in fragrances in the USA amounts to approximately 90,000
Ib/yr.
Concentration in final product (/n):
Soap Detergent Creams, lotions Perfume
Usual 0.03 0.003 0.01 0.05
Maximum 0.3 0.03 0.15 0.8
Analyfical data: Gas chromatogram, RIFM no. 73-29: infra-red curve, RIFM no. 73-29.

Status
Methyl salicylate was given GRAS status by FEMA (1965) and the Council of Europe listed
it with an ADI of 0.5 mg/kg. The Joint FAO/WHO Expert Committee on Food Additives (1967)
has published a monograph and specifications for methyl salicylate. giving it an unconditional AD1
of O-O.5 mg/kg, and there is also a monograph in the Food Chemicals Codex (1972). Liquid prep-
arations containing more than 5% (w/w) methyl salicylate, other than those packaged in pressurized
spray containers, are required in the USA to be packaged in accordance with the Poison Prevention
Act of 1970 (21 CFR 295.3). CAS Registry No. 119-36-8.

Biological data
Acute toxicity. The oral LD5,, was reported to be lllOmg/kg in mice (Davison, Zimmerman
& Smith, 1961), 887 mg/kg (Jenner;Hagan, Taylor, Cook & Fitzhugh, 1964) and 1250 mg/kg (Giroux,
Granger & Monnier, 1954) in rats, 1060 mg/kg (Jenner ef al. 1964) and 700 mg/kg (Fassett, 1963)
in guinea-pigs, 1300 mg/kg (Castagnou, Larceban & Queyment, 1952) and 2800 mg/kg (Fassett,
1963) in rabbits and 2100 mg/kg (Fassett, 1963) in dogs. Administration of 0.5 ml methyl salicylate
to rats by gavage caused some slight redness and irritation of the stomach mucosa (Strom & Jun.
1974). The minimum lethal SC dose in guinea-pigs was reported as 15OOmg/kg by Houghton (1905),
while Spector (1955) gave figures of 2700-2750, 4250-4350 and 2250mg/kg for the lethal SC dose
for the guinea-pig, rabbit and dog, respectively. The acute dermal LDSo value in rabbits was reported
as exceeding 5 g/kg (Moreno, 1973).
Administration of 06-4.7 g methyl salicylate/kg by intubation into the stomach and duodenum
of four conscious dogs caused primary nausea. vomiting, intense hyperpnoea. excitation of the central
nervous system and diarrhoea (Lacroix & Ferragne, 1964). Two dogs recovered and two died, after
8 and I8 hr. In three anaesthetized dogs given 0.65 g/kg, an increase in the respiratory amplitude
without modification of the arterial pressure was observed (Lacroix & Ferragne, 1964). Oral adminis-
tration of 700mg methyl salicylate/kg to dogs produced a drop in blood pressure and cardiac
output, accompanied by a slight increase in heart rate within 5 hr (Ojiambo, 1974). The myocardial
failure produced by this dose has been related to hyperkalaemic cardiomyopathy and inhibition
of high-energy phosphate production as a result of uncoupling of oxidative phosphorylation
(Ojiambo, 1972 & 1975; Ojiambo, Petrie. Dusek & Klassen, 1972). Elevated creatine-phosphokinase
levels in the coronary effluent, an increase in arterial lactate, potassium ion and oxygen consumption
(Ojiambo, 1971a) and an increase in arterial epinephrine and norepinephrine were noted (Ojiambo,
197lb). Following infusion of 700 mg methyl salicylate/kg into the hindlimb muscle of dogs, similar
effects were noted (Ojiambo, 1971~).
Subacute and chronic toxicity. The maximum tolerated dose defined as the maximum single dose
tolerated by all of five mice given six ip injections over a 2-wk period, was found to be 500 mg/kg
(Stoner, Shimkin, Kniazeff, Weisburger, Weisburger & Gori, 1973). Methyl salicylate fed to rats
at a dietary level of 1% for 13 days did not affect body or liver weights but caused pronounced
alterations of microbodies in the hepatocytes (Hruban, Swift & Slesers, 1966).
The feeding of methyl salicylate to rats for 2 yr at levels of 0.1, 0.5, I.0 and 2% of the diet
produced statistically significant growth retardation in the rats on the 1 and 2% diets (Webb &
Hansen, 1963). All rats on the 2% diet died by wk 50. There was an increase in cancellous bone
in all bones examined from the rats on the 2% diet; this was less pronounced in degree and incidence
in the rats on the 1% diet. Another 2-yr feeding study in rats revealed no bone changes or other
adverse effects up to a level of 0.21% in the diet (Packman, Abbott, Wagner & Harrison, 1961).
A lo-wk feeding study, showed an increase in cancellous bone in the femur and tibia of rats receiving
a22 D. L. J. OPDYKE

20,000 or 11,250 ppm methyl salicylate, but not of those given 9000. 6330, 3550 or 2000 ppm
(Harrison, Abbott & Packman, 1963).
The oral administration of methyl salicylate to dogs in doses ranging from 50 to 1200 mg/kg/day
on 6 days/wk for up to 59 days resulted in weight loss and death in all dogs on doses of 500
mg/kg/day or more. The livers of the dogs receiving 1200 or 800 mg/kg/day showed moderate
to marked degrees of fatty metamorphosis (Webb & Hansen, 1963). In dogs given orally 50, 150
or 350 mg/kg/day for 2yr, there were no effects at the 50-mg level but at the two higher dose
levels enlarged livers and an increase ain the size of the hepatic cells were observed. The dogs on
350 mg/kg/day lost weight and showed growth retardation: those on 150 mg/kg/daily showed growth
retardation but no weight loss (Webb & Hansen, 1963).
Rabbits inuncted with 40 ml methyl saIicylate/kg/day for 90 days showed early deaths and kidney
damage, while rabbits given lower doses appeared predisposed to spontaneous nephritis and mild
hepatitis (Webb & Hansen, 1963).
Human toxicity. Ingestion of relatively small amounts of methyl salicylate may cause severe poison-
ing and death. Signs of poisoning include nausea, vomiting, acidosis, pulmonary oedema. pneumonia
and convulsions (Merck Index, 1976). Numerous cases of methyl salicylate poisoning have been
reported with a 5060% mortality rate (Graham, 1961; Jacobziner & Raybin, 1962; Kloss & Boeck-
man, 1967). From 4 to 8 ml methyl salicylate is considered a lethal dose for children, the signs
common to all such poisonings being excitation of the central nervous system, abnormally rapid
breathing, fever, high blood pressure and increased heartbeat, generalized convulsions and coma.
Death results from respiratory failure after a period of unconsciousness (Adams, Bigier & Green,
1957; Winek, Collom & Voldeng. 1973). Levels of lactate dehydrogenase, glutamic-oxalacetic trans-
aminase, glutamic-pyruvic transaminase and creatine phosphokinase were increased in a 2-yr-old
male with severe metabolic acidosis due to ingestion of approximately log methyl salicylate (De
Virgiliis, Cao & Falorni, 1968). The enzyme changes were attributed to the acid-base equilibrium.
salicylate rather than to cellular changes resulting from alterations of the acid-base equilibrium.
Inhalarion. After twenty 7-hr exposures to saturated (120 ppm, 700mg/m3) methyl salicylate
vapour, rats showed no toxic signs and no organ abnormalities (Gage, 1970).
Irritation. Methyl salicylate, incorporated into most topically applied pain relievers, has been
evaluated as being a moderate irritant, eliciting necrosis and intradermal and subcutaneous haemor-
rhage when applied in various vehicles to the shaved skin of rabbits in concentrations as low
as 1% (Yankell, 1972). It has also been reported to be severely irritating to guinea-pig skin and
eye (Fassett, 1963). Applied full strength to intact or abraded rabbit skin for 24 hr under occlusion,
it was moderately irritating (Moreno, 1973). but tested at. 8% in petrolatum, it produced no irritation
after a 48-hr closed-patch test on human subjects (Epstein, 1973).
Skin absorption. The percutaneous absorption of methyl salicylate was determined in rabbits and
the compound was detected in muscle 1 hr after administration (Takahashi & Iwatsubo. 1963). It
was absorbed at all pH values through intact rat skin (Siddiqi & Ritschell, 1972), but such absorption
was reported to be slow (Valette & Cavier, 1954).
Sensitization. A maximization test (Kligman, 1966; Kligman & Epstein, 1975) was carried out
on 27 volunteers. The material (RIFM no. 73-29) was tested at a concentration of 8% in petrolatum
and produced no sensitization reactions (Epstein, 1973).
Mefabolisw. Methyl salicylate is converted to a considerable extent to salicylic acid in the body.
Much hydrolysis of the ester occurs in the intestine after oral administration; in dogs about 0.2-05%
of an oral dose of Q2 g/kg appears in the urine as the ester, whereas after intramuscular injection
14% of the ester appears unchanged in the urine (Williams. 1959). A comparison of the fate of
methyl salicylate in man and the dog has been made (Oiiambo, 1971a-c). A dose of 700 mg/kg
administered intragastrically was completely hydrolysed after 1.5 hr in the dog, while 21% of the
ingested amount was still circulating in human patients showing myocardial failure after accidental
ingestion of 1-30~ oil of wintergreen. Lethal concentrations of total circulating plasma salicylate
in man were 2-3 times higher than those in the dog at the time of death. Lack of adequate detoxifica-
tion mechanisms in man led to freely circulating methyl ester, which was lethal. The level of total
plasma salicylate resulting in death was lower in female than in male dogs because of the formers
higher fat content.
Plasma analysis for methyl salicylate after oral administration to rats and dogs shows complete
hydrolysis shortly after administration, but hydrolysis is slower in man (Davison er al. 1961). In
the rabbit, the ester gives rise to an ethereal sulphate (Williams, 1938). Certain steroids known
to induce hepatic microsomal drug-metabolizing enzymes prevented severe systemic poisoning with
methyl salicylate in rats (Selye, 1972). These steroids included pregnenolone-Hia-carbonitrile,. ethyl-
estrenol, spironolactone and norbolethone. Phenobarbitone offered slight protection, but prednisolone
acetate, triamcinolone and thyroxine were either without effect or enhanced the toxicity of methyl
salicylate. The major site of hydrolysis of the ester in the rat, rabbit, dog and monkey is the liver,
although the intestine, kidneys, pancreas and spleen may play minor roles (Davison et al. 1961).
With rat diets containing initially 1% methyl salicylate and kept under normal laboratory condi-
tions for 1 wk, comparison of the recovery of the ester from the diet before and after storage
demonstrated a 35% loss (Jones, Taylor & Hagan. 1962).
 Fragrance raw materials monographs 823

Carcinogenicity. In male and female strain A mice given 24 ip injections of methyl salicylate,
at the maximum tolerated dose and at 20% of this dose, over 8 wk and killed after 24 wk. the
incidence of lung tumours was not increased over that in controls (Stoner et al. 1973).
Teraroyenicir?~. Female rats given 0.1 ml methyl salicylate ip on days 10 and 11 of pregnancy
gained less weight, had fewer and smaller offspring and had more resorptions and malformed young
than controls (Woo & Hoar, 1972). Methyl salicylate retarded renal development, particularly the
growth of the renal papillae, and increased the number of both transient grid permanent renal
abnormalities in rat foetuses near term (Woo & Hoar, 1972). Administered subcutaneouslyto preg-
nant rats on day 9 or 10 of pregnancy, the ester was found to induce cardiovascular malformations
in the young (Takacs & Warkany, 1968). Teratogenic anomalies of the palate and tail, together
with an increase in foetal resorption and a decrease in survival rate and body weights of foetuses.
were noted in litters of pregnant rats receiving methyl salicylate SC on day 7, 9 or 11 (Pyun, 1970).
Methyl salicylate fed to rats at 500, 1500, 3000 or 5000 ppm for three generations did not decrease
the fertility index at any dose, but at the 3000- and 5000-ppm levels significant decreases were
seen in average litter size and in the average numbers of live-born progeny, survivors to day 4
and survivors to weaning (Collins, Hansen & Keeler, 1971). The decreases were greatest in the
second generation. External examination and autopsy of newborn and weanling rats revealed no
visible abnormalities.
Wilson (1973) reported that a significantly greater percentage of women delivering defective babies
had taken a sahcylate preparation during the first trimester of pregnancy than had women delivering
normal babies, a finding of possible relevance to methyl salicylate in view of its metabolism to
salicylic acid.
Pharmacology. Methyl salicylate in a dose of 2OOmg/kg was found to be inactive in inhibiting
the permeability of the peritoneal blood vessels of the mouse to plasma proteins (Northover, 1963).
Cyrotoxicity. A 50% inhibition of the growth of HeLa cells and Bacillus subrilis cultures was
effected by 2.8 and 6.5 rnhl-methyl salicylate, respectively (Sheu, Salomon, Simmons, Sreevalsan
& Freese, 1975). In concentrations of 1, 10 or lOO~g/ml, methyl salicylate was not toxic to HeLa
cells (Silyanovska. Stoichev. Zolotovich & Nachev, 1967).
References
Adams. J. T., Bigler. J. A. SCGreen, 0. C. (1957). A case of methyl salicylate intoxication treated by exchange
transfusion. J. Ajar. rued. Ass. 165, 1.563.
Castagnou. R.. Larceban, S. & Queyment, A. (1952). Bull. Sac. Phann. Marseille 3, 30.
Collins, T. F. X., Hansen, W. H. & Keeler. H. V. (1971). Elect of methyl salicylate on rat reproduction.
Toxic. appl. Phamac. 18. 755.
Council of Europe (1974). Natural Flavouring Substances, Their Sources. and Added Artificial Flavouring
Substances. Partial Agreement in the Social and Public Health Field. List I. no. 433, o. 214. Strasboure.
Davison, C., Zimmerman, E. F. & Smith, P. K. (1961). Expl Ther. 132, 207.
De Virailiis, S.. Cao A. e Falorni. A. (1968). Su alcune modificazioni enzimatiche in un case di avvelenamento
acuto da sahcilato di metile. Minerca daediat. 20, 1650.
Ejystein. W. L. (1973). Report to RIFM, 26 November.
Fassett, D. W. (1963). Esters. In Industrial Hygiene and Toxicology. 2nd Ed. Edited by F. A. Patty. Vol.
II, p. 1897. lnterscience Publishers, New York.
Fenarol?s Handbook o/ Flatlor Ingredients (1975). Edited by T. E. Furia and N. Bellanca. 2nd Ed. Vol. II.
p. 406. CRC Press. Cleveland, OH.
Flavoring Extract Manufacturers Association (1965). Survey of flavoring ingredient usage levels. No. 2745.
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Gage, J. C. (1970). The subacute inhalation toxicity of 109 industrial chemicals. Er. .I. ind. Med. 27, I.
Giroux, J.. Granger. R. & Monnier, P. (1954). Trac. Sot. Pharm. Monrpellier 14, 383.
Graham, D. C. (1961). Methyl salicylate: A lethal hazard in the home. Can. wed. Ass. J. 84, 960.
Harrison, J. W. E., Abbott, D. D. & Packman, E. W. (1963). fedn. Proc. Fedn Am. Sots. exp. Biol. 22.
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Houghton. E. M. (1905). Am. J. Physiol. 13. 331.
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Jenner. P. M.. Hagan. E. C.. Taylor, J. M., Cook, E. L. & Fitzhugh, 0. G. (1964). Food flavourings and
compounds of related structure. I. Acute oral toxicity. Fd Comet. Toxicol. 2, 327.
Joint FAO/WHO Expert Committee on Food Additives (1967). Toxicological Evaluation of Some Flavouring
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Jones, W. I., Taylor, J. M. & Hagan, E. C. (1962). The loss of food flavors from laboratory animal diets.
J. Ass. ofl agric. Chem. 45, 781.
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824 D. L. J. OPDYKE

Kloss, J. L. & Boeckman, C. R. (1967). Methyl salicylate poisoning. Ohio 51. rued. J. 63, 1064.
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NJ.
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Ojiambo. H. P. (197la). Certain aspects of metabolism in myopathies induced by methylsalicylate intoxication
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Ojiambo, H. P. (1971 b). Catecholamine metabolism in methylsalicylate myopathies. E. Air. rtred. J. 48. 236.
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Ojiambo, H. P. (1972). Myocardial mechanics, metabolism and energetics in hyperkalaemic cardiomyopathy
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Vol. 1, p. 97. E. African Literary Bureau. Nairobi.
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dog. Recent Adr. Srud. Card. Srrucr. Merab. 1. 579.
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essential oils. C.r. Acad. bulg. Sci. 20, 1337.
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Test for carcinogenicity of food additives and chemotherapeutic agents by the pulmonary tumor response
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Valette, G. & Cavier, R. (1954). Hydrocarbons, alcohols and esters. Archs inr Pharrnacodyn. Thh. 97, 232.
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in dogs, rats and rabbits. Toxic. appl. Pharmac. 5, 576.
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Yankell. S. L. (1972). The effects of various vehicles on absorption rates in skin. AdD. Bioi. Skin 12, 511.

Additional references

Isolated enzymes and tissues

McNabb, T.. Sproul, J. & Jellinck, P. H. (1975). Effects of phenols on the oxidation of estradiol by uterine
peroxidase. Can. J. Biochem. 53, 855.
Ottoson, D. & von Sydow. E. (1964). Electrophysiological measurements of the odor of single components
of a mixture separated in a gas chromatograph. L@ Sci. 3, II I I.
Insects
Beadles, M. L., Drummond, R. 0. & Whetstone. T. M. (1973). Tropical horse tick. Effects of solvents on
oviposition. J. econ. Ent. 66. 125.
Camin, J. H., Clark, G. K., Goodson. L. H. & Shuyler, H. R. (1964). Control of the snake mite, Ophionyssus
natricis, in captive reptile collections. Zooiogica 49(2), 65.
Dabrowski, Z. T. 8c Rodriguez, J. G. (1971). Resistance OTstrawberries to mites. 3. Preference and nonprefer-
ence responses of Terranychus urticae and I: rurkestani to essential oils of foliage. J. econ. Em. 64, 387.
Dodson. C. H., Dressler, R. L., Hills, H. G.. Adams, R. M. & Williams. N. H. (1969). Biologically active
compounds in orchid fragrances. Science, N.l! 164, 1243.
 Fragrance raw materials monographs 825

Kamorzina. 1. G.. Karpov. G. A. & Knyarena, K. S. (1966). Aromatic products as deodorants for insecticides
and repellents. Khirrr. Se/. Kho:. 4, 499.
Rodriguez, J. G.. Kemp. T. R. & Dabrowski. 2. T. (1976). Behavior of Ferronrchus urricae toward essential
oil mixtures from strawberry foliage. J. cherrr. Ecol. 2, 221.
Rudnev, D. F., Karasev. V. S.. Kuznetsov. N. V. & Mirsina. G. A. (1972). Toxicity of some components
of essential oils of willows and poplars for leaf insects. Zoshch. Rosr., Kiev 16, 27.

Micro-organisms
Burwood, R. & Spencer. D. M. (1970). Metabolism by phytopathogenic fungi. Degradation of hydromybenzoic
acids by Glomrrella cingulara. Phyrodwmisrry 9. 333.
Muenzing. H. P. & Schels. H. (1972). Possibihties of replacement of preservative in cosmetics by essential
oils. J. Sot. COSIIIF~. Chem. 23. 841.
Munzig H. P. & Schels, H. (1974). Essential oils as possible preservatives in cosmetics. Tlusx:r. Srodki
Pioraw. Kosmrr. 18. 355.

F.C.T. 16 ,a PP. I l--m