Benzyl acetate

log Kow = 1.96

1.96

1.96

PEAR-LIKE ODOR

CHARACTERISTIC FLOWERY (JASMINE) ODOR

Powerful but thin, sweet floral fresh, fresh and light, fruity odor reminiscent of Jasmin, Gardenia, Muguet, Lily and other flowers.

1.04 (USCG, 1999) - Denser than water; will sink

1.050 @ 25 °C/4 °C

Relative density (water = 1): 1.1

1.049-1.059

1.04

1.05 @25 °C

This chemical does not meet GHS hazard criteria for 32.5% (779 of 2397) of reports.

H412 (62.6%): Harmful to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]

P273, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 2397 reports by companies from 19 notifications to the ECHA C&L Inventory.

Danger

H227: Combustible liquid [Warning Flammable liquids]

Chemical: Acetic acid, phenylmethyl ester

Commission Regulation (EC) No 1565/2000 (Repealed by Com. Implementing Reg. (EU) No 872/2012)

Acetic acid, phenylmethyl ester is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Acetic acid, phenylmethyl ester are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 01-12-2022 https://echa.europa.eu/registration-dossier/-/registered-dossier/14570

Benzyl acetate: Does not have an individual approval but may be used under an appropriate group standard

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

This chemical is combustible. (NTP, 1992)

Combustible. Above 90 °C explosive vapour/air mixtures may be formed.

Causes respiratory tract irritation in the range of 50-160 ppm; [CHEMINFO] Has anesthetic effects at high concentrations in animal studies; [ChemIDplus] Included in list of fragrance substances with negative human data, i.e. patch tests of patients with suspected contact allergy to fragrance ingredients which yielded negative results.; [EC: Scientific Committee on Consumer Safety: Fragrance allergens in cosmetic products (2011)] An irritant; May cause smarting and reddening of skin if spilled and allowed to remain on clothes; [CHRIS] Vapor causes eye and respiratory tract irritation; May cause effects on the CNS and kidneys; [ICSC] Safe when used as a flavoring agent in food; Acceptable daily intake (ADI) of 0-5 mg/kg; [JECFA] A skin and strong eye irritant; May cause CNS depression; Targets nerves and kidney; [Sigma-Aldrich MSDS]

Benzyl acetate is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) when intended for use in or on food it is of appropriate food grade and is prepared and handled as a food ingredient. Synthetic flavoring substances and adjuvants incl benzyl acetate may be safely used in foods.

DHHS/NTP; Toxicology & Carcinogenesis Studies of Benzyl Acetate in F344/N Rats and B6C3F1 Mice (Gavage Studies) Technical Report Series No. 250 (1986) NIH Publication No. 86-2506

WHO/IPCS; Toxicological Evaluation of Certain Food Additives and Contaminants WHO Food Additives Series 32 (1993)

BENZYL ACETATE is an ester. Esters react with acids to liberate heat along with alcohols and acids. Strong oxidizing acids may cause a vigorous reaction that is sufficiently exothermic to ignite the reaction products. Heat is also generated by the interaction of esters with caustic solutions. Flammable hydrogen is generated by mixing esters with alkali metals and hydrides. This chemical is incompatible with strong oxidizing agents. It is also incompatible with acids, bases and reducing agents. (NTP, 1992)

Fire Extinguishing Agents: Water spray, carbon dioxide, dry chemical, alcohol foam. (USCG, 1999)

Use water spray, powder, alcohol-resistant foam, carbon dioxide.

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Do NOT induce vomiting. Give one or two glasses of water to drink. Rest. Refer for medical attention .

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. Then, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 280(SRC), determined from a log Kow of 1.96(2) and a regression-derived equation(3), indicates that benzyl acetate is expected to have moderate mobility in soil(SRC). Volatilization of benzyl acetate from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.1X10-5 atm-cu m/mole(SRC) derived from its experimental values for vapor pressure, 0.18 mm Hg(4), and water solubility, 3.1X10+3 mg/l(5). Biodegradation of benzyl acetate in soil may be important(SRC), based upon its biodegradation in water(5).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 280(SRC), determined from a log Kow of 1.96(2) and a regression-derived equation(3), indicates some adsorption of benzyl acetate to suspended solids and sediment in the water column is expected(SRC). Benzyl acetate is expected to volatilize from water surfaces(3,SRC) based on an estimated Henry's Law constant of 1.1X10-5 atm-cu m/mole(SRC) from its experimental values for vapor pressure, 0.18 mm Hg(4), and water solubility, 3.1X10+3 mg/l(5). Estimated volatilization half-lives for a model river and model lake are 4.1 and 34 days, respectively(3,SRC). According to a classification scheme(6), an estimated BCF of 18(3,SRC), from a log Kow(2), suggests that bioconcentration in aquatic organisms is low(SRC). Benzyl acetate is expected to biodegrade in aquatic systems(SRC); benzyl acetate reached 92 to 96% of its theoretical BOD over a period of 4 weeks(5). An estimated hydrolysis half-life of 38 days at pH 7(7), indicates hydrolysis may be an important process(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), benzyl acetate, which has a vapor pressure of 0.18 mm Hg at 25 °C(2,SRC), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase benzyl acetate is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be about 2.5 days(3,SRC).

The substance can be absorbed into the body by inhalation and by ingestion.

Oral (L1223) ; inhalation (L1223) ; dermal (L1223) ; eye contact (L1223)

IDENTIFICATION: Benzyl acetate is a solvent used in perfumery and in chemical synthesis. HUMAN EXPOSURE: Benzyl acetate is absorbed from the gastrointestinal tract, through the lungs and through intact skin. It is hydrolyzed in man to benzyl alcohol and acetate; the benzyl radical is oxidized to benzoic acid and excreted as hippuric acid. ANIMAL/BACTERIAL STUDIES: This compound is hydrolyzed in vitro with a pancreatin preparation. Benzylmercapturic acid and hippuric acid were isolated from the urine of rats that had been injected sc with benzyl acetate. Mice and rats were dosed either iv or po with (14)C labeled benzyl acetate. Elimination of benzyl acetate as carbon dioxide or volatiles was minimal. The elimination of the (14)C label occurred mainly in urine with less than 1% excreted in the feces. More than 90% of the (14)C in urine was present as hippuric acid with minor amounts present as benzyl alcohol. Neither route of administration or dose had any significant effect on the pattern of elimination. Groups of 5 B6C3F1 mice of each sex were dosed with benzyl acetate in corn oil by gavage daily for 14 days. All male mice at the highest dose level had died by day 3 of the study. Weight changes were not dose related. At autopsy the only effect reported was a thickening of the mucosa of the stomach and in the cardiac region in two males and all females in the highest dose group and one female in the medium dose group. Groups of 50 male and female B6C3F1 mice were administered benzyl acetate in corn oil by gavage for 5 days/wk for 103 weeks. Vehicle control groups of 50 animals per sex were administered corn oil by gavage. The high mortality rate in female mice was associated with infection, resulting in inflammation or abcesses of the ovaries, uterus, mesentery, peritoneum or multiple organs. There was no association of treatment with the reported incidences of hepatocellular and forestomach tumors after the administration of benz yl acetate. Groups of 50 male and female F344/N rats of each sex were administered benzyl acetate in corn oil 5 days/wk for 103 weeks. Vehicle control groups consisted of 50 animals per sex were administered corn oil by gavage. The incidence of all malignant epithelial tumors in the preputial gland of male rats was elevated in the high dose group. There was increased incidence of retinopathy and cataracts in the high dose males and low dose females. In mutagenicity tests using Salmonella typhimurium TA100, TA1535, TA1537, TA98 with or without rat or hamster-9 activation results were negative. In vitro mammalian cytogenicity chromosomal aberrations in Chinese hamster ovary cells produced a negative response, in presence or absence of induced rat liver S-9 fraction. In the mouse lymphoma cell assay, it was positive for mutagenicity when induced by metabolic activation and negative in the absence of activation. Bacterial gene mutation with Bacillus subtilus and unscheduled DNA synthesis in vitro and in vivo were both negative.[

Benzyl acetate is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

Burning sensation. Confusion. Dizziness. Drowsiness. Laboured breathing. Sore throat.

Dry skin.

Redness.

Burning sensation. Convulsions. Diarrhoea. Drowsiness. Vomiting.

Vomiting, drowiness, diarrhea, convulsions and burning sensation may result from ingestion or inhalation. Moreover, inhalation may cause laboured breathing and sore throat. Redness of the eyes, dry skin, depending of the contact surface (L1225).

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=140-11-4N]

The Koc of benzyl acetate is estimated as approximately 180(SRC), using a log Kow of 1.96(1) and a regression-derived equation(2,SRC). According to a classification scheme(3), this estimated Koc value suggests that benzyl acetate is expected to have moderate mobility in soil(SRC).

PRESENT AS MAIN CONSTITUENT IN SEVERAL OILS & FLOWER ABSOLUTES: YLANG-YLANG, CANANGA, NEROLI, JASMINE, HYACINTH, GARDENIA, TUBEROSE. IT HAS BEEN ISOLATED FROM FLOWERS OF ... /AZALEA/ ... CAN BE ISOLATED FROM NATURAL SOURCES (IN WHICH IT MAY OCCUR AT LEVELS UP TO 65%).

Benzyl acetate occurs in a number of plants, particularly jasmine(1). Benzyl acetate was identified as a volatile component of roasted filberts(2) and in the juice of Japanese Kogyoku apples(3).

Benzyl acetate is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) when intended for use in or on food it is of appropriate food grade and is prepared and handled as a food ingredient. Synthetic flavoring substances and adjuvants incl benzyl acetate may be safely used in foods.

... BENZYL ACETATE IS RAPIDLY HYDROLYZED TO ACETIC ACID AND BENZYL ALCOHOL, AND THE LATTER OXIDIZED TO BENZOIC ACID & ... EXCRETED AS HIPPURIC ACID.

In rats, benzyl acetate is hydrolyzed to benzyl alcohol, which is oxidized to benzoic acid and excreted as hippuric acid and benzyl mercapturic acid.

In a chemical disposition study conducted by the NTP, male Fischer 344 rats and male B6C3F1 mice were shown to efficiently absorb and rapidly metabolize and excrete orally administered benzyl acetate. The doses used in this study were 5, 50, or 500 mg/kg for rats and 10, 100, or 1000 mg/kg for mice in single dose corn oil gavage administrations and 500 mg/kg for rats and 1000 mg/kg for mice daily five times per week for two weeks, also administered by gavage in corn oil. Most (90%) of the benzyl acetate-derived radioactivity was recovered in the urine and none was detected in the liver, blood, muscle, adipose tissue skin, lung, kidney, or stomach of treated rats or mice. The major metabolite isolated in the urine was hippuric acid (94%-99% of the dose). Other metabolites found were mercapturic acid and benzyl alcohol. Benzyl acetate was not detected in the urine of treated animals. Neither the size of the dose nor the frequency of dosing had any effect on the absorption, metabolism, or excretion of this compound. There was no evidence to indicate any saturation of this metabolizing capacity in either species over the range of doses studied.

Effects of gavage versus dosed feed administration on the toxicokinetics of benzyl acetate were studied in male F344 rats and B6C3F1 mice. Benzyl acetate was rapidly hydrolyzed to benzyl alcohol and then oxidized to benzoic acid. After gavage administration of benzyl acetate in corn oil at 500 mg/kg (rats) and 1000 mg/kg(mice), high benzoic acid plasma concentrations were observed. In contrast, much lower benzoic acid plasma concentrations were found after dosed feed administration at about 615 mg/kg/day for rats and about 850 mg/kg/day for mice. Results show that although the daily doses of benzyl acetate are comparable, bolus gavage administration effectively saturated the benzoic acid elimination pathway whereas dosed feed administration did not. In contrast, hippuric acid plasma concentrations were similar after both gavage and dosed feed administration due to the depletion of the glycine supply pool. ...

Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of OP exposure.

Benzyl acetate was absorbed from the gastrointestinal tract of rats and mice, with approximately 90% of the administered dose recovered as various metabolites in the urine within 24 hr. ... This capacity for absorption, metabolism, and disposition was unaffected by the amount or number of doses administered.

The effect of vehicle and occlusion on the in vitro percutaneous absorption of [methylene-14C]-benzyl acetate (1.7-16.6 mg/sq cm) has been studied in diffusion cells using full thickness skin from male Fischer 344 rats. Absorption of neat benzyl acetate through rat skin occluded with parafilm was 49.3 +/- 2.0% (mean +/- SD, n=4) after 48 hr. When benzyl acetate in ethanol was applied to the skin and the skin was occluded with parafilm, the extent of absorption at 48 hr was not significantly different from that after neat application. However at 6 hr, as the ethanol content of the application mixture was increased, the absorption of benzyl acetate through occluded skin was enhanced proportionally. When phenylethanol was used as a vehicle, the extent of the benzyl acetate absorption through occluded skin at 48 hr was enhanced (P less than 0.05) compared with that after application neat; with 50% (v/v) phenyl-ethanol, absorption at 48 hr was 56.3 +/- 4.9%. However, this enhanced absorption did not correlate with the proportion of phenylethanol in the application mixture. When dimethylsulphoxide was used as a vehicle, the extent of absorption of benzyl acetate through occluded skin at 48 hr was enhanced (P less than 0.05) compared with that after application neat (absorption was 59.3 +/- 3.7% of the applied dose when 50% (v/v) dimethylsulphoxide was used). As the dimethylsulphoxide content of the application mixture was increased, the absorption of benzyl acetate was enhanced proportionally. Occlusion of the skin surface with parafilm often significantly enhanced absorption (P less than 0.05), although the effect varied with time and vehicle. In general, the degree of any enhanced absorption caused by the use of a vehicle or occlusion of the skin was small, and, in most cases, would be unlikely to be toxicologically significant.

The comparative absorption of ... benzyl acetate has been studied in rat and human skin, using shaved, full-thickness dorsal skin of male Fischer 344 rats and full-thickness human skin obtained from patients undergoing surgical resection. Penetration of the compound through rat and human skin was evaluated in vitro in flow-through diffusion cells following topical application of neat [methylene-14C] benzyl acetate (33.1 mg/sq cm) to the epidermal surface and occlusion with a teflon cap, 2.9 cm above the skin surface. The absorption of benzyl acetate across rat skin was rapid and extensive, reaching 34.3 +/- 3.9% of the applied dose (11.3 +/- 1.3 mg/sq cm) (mean +/-SD, n=12) at 24 hr and 55.8 +/- 5.0% of the applied dose (18.5 +/- 1.7 mg/sq cm)at 72 hr. The penetration of benzyl acetate was significantly (P<0.05) less rapid and extensive through human skin, reaching 5.5 +/- 0.1% of the applied dose (1.8 +/- 0.0 mg/sq cm) (mean +/- SD, n=12) at 24 hr and 17.8 +/- 3.3% of the applied dose (5.9 +/-1.1 mg sq cm) at 72 hr. The rate of penetration of benzyl acetate was greater through rat skin than through human tissue at all time points studied up to 72 hr. The maximum rate of skin penetration was 0.6 +/- mg/sq cm/hr and 0.1 +/_- 0.0 mg/sq cm/hr through rat and human skin, respectively. These data indicate that systemic exposure to benzyl acetate may occur after skin contact in humans. They also support the evidence from the literature that human skin is generally less permeable to xenobiotics than rat skin.

Used as a fragrance, flavoring agent, and solvent; Also used in inks, varnish removers, oils, lacquers, and polishes; [CHEMINFO] Found in many plants, especially jasmine; [Merck Index] Used as a flavoring agent; [FDA]

Painting (Solvents) [Category: Paint]

In perfumery, solvent for cellulose acetate and nitrate.

Artificial jasmine and other perfumes; soap perfume; flavoring; solvent and high boiler for cellulose acetate and nitrate, natural and synthetic resins; oils; lacquers; polishes; printing inks; varnish removers.

It is used widely in perfumery and cosmetics for its aroma and in flavorings to impart apple and pear flavors (L1222).

(1972) 6.61X10+6 GRAMS (PRINCPL CUSTMS DISTS)

(1975) 1.60X10+6 GRAMS (PRINCPL CUSTMS DISTS)

(1984) 4.83X10+9 g

2023: 10,000,000 - <25,000,000 lb

(1972) 6.42X10+8 GRAMS

(1975) 5.87X10+8 GRAMS

BY INTERACTION OF BENZYL CHLORIDE & SODIUM ACETATE; BY ACETYLATION OF BENZYL ALCOHOL; OR FROM BENZALDEHYDE & ACETIC ACID WITH ZINC DUST.

METHOD OF PURIFICATION: DISTILLATION.

Prepared from benzyl chloride, acetic acid or sodium acetate and triethylamine: Merker, Scott, J Org Chem 26, 5180 (1961); Hennis et al, Ind Eng Chem Prod Res Develop 6, 193 (1967).

FREE FROM CHLORINE GRADE WHICH SHOULD HAVE ESTER CONTENT OF 97% BUT FOR WHICH LOWER GRADE MATERIAL IS SOMETIMES SUBSTITUTED; TECHNICAL GRADE WHICH IS NOT FREE FROM CHLORINE & FOR WHICH ESTER CONTENT VARIES CONSIDERABLY; "FOOD CHEMICALS CODEX".

Information on 5 consumer products that contain Benzyl acetate in the following categories is provided:

Information on 477 consumer products that contain Benzyl acetate in the following categories is provided:

Fragrance Ingredients

Flavouring Agent -> FLAVOURING_AGENT -> JECFA Functional Classes

Flavoring Agents -> JECFA Flavorings Index

Flavouring Agent -> FLAVOURING_AGENT -> JECFA Functional Classes

Flavouring Agent -> FLAVOURING_AGENT -> JECFA Functional Classes

Cosmetics -> Solvent

Wholesale and Retail Trade

Acetic acid, phenylmethyl ester: ACTIVE

FEMA NUMBER 2135. NON-ALCOHOLIC BEVERAGES, 7.8 PPM; ICE CREAM, ICES ... 14 PPM; CANDY, 34 PPM; BAKED GOODS, 22 PPM; GELATINS & PUDDINGS, 23 PPM; CHEWING GUM, 760 PPM.