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ETHYL ACETATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Ethyl acetate is a solvent used in the lacquer industry and is added to various artificial fruit essences.

Specific Substances

    1) Acetic acid ethyl ester
    2) Acetic ether
    3) Vinegar naphtha
    4) Ethyl ethanoate
    5) CAS 141-78-6
    6) Molecular Formula: C4-H8-O2
    1.2.1) MOLECULAR FORMULA
    1) C4H8O2 CH3COOCH2CH3 CH3COOC2H5

Available Forms Sources

    A) FORMS
    1) Commercial Grades (Sax & Lewis, 1987):
    1) 85% to 88%
    2) 95% to 98%
    3) 99%
    4) NF (99%)
    5) FCC
    2) The major constituent other than ethyl acetate in the 85% to 88% grade is ethyl alcohol (HSDB , 2002).
    B) SOURCES
    1) Ethyl acetate occurs naturally in yeast and sugar cane.
    C) USES
    1) Ethyl acetate is used in artificial fruit essences, and as a solvent for nitrocellulose, varnishes, lacquers, food processing, airplane dopes, as well as in the manufacture of smokeless powder, artificial leather, photographic film and plates, artificial silk, perfumes, pharmaceutical preparations, and also for cleaning textiles (S Sweetman , 2002; Budavari, 1996).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Ethyl acetate is low in toxicity. It is a mild mucous membrane irritant, but is not caustic. In high concentrations it may be a CNS depressant. Animal studies have demonstrated pulmonary edema, decreased cardiac contractility, seizures and hepatic damage, but these have NOT been reported in humans.
    0.2.4) HEENT
    A) Ethyl acetate is irritating to the conjunctivae but leaves no residual effects. Nose and throat irritation is seen at levels greater than 400 ppm for 3 to 5 minutes.
    0.2.7) NEUROLOGIC
    A) Chronic exposure to solvent mixtures including ethyl acetate has been associated with poorer performance on neurobehavioral tests. High concentrations orally administered to rabbits caused lack of coordination. High concentrations have intoxicating properties in animals and would be expected to cause narcosis in humans.
    0.2.14) DERMATOLOGIC
    A) Drying as well as skin defatting and cracking may be seen with dermal application. Sensitizations to ethyl acetate have been reported but are rare.
    0.2.20) REPRODUCTIVE
    A) No reproductive studies were found for ethyl acetate in humans. Inhalation of lacquer thinner, which contains ethyl acetate, in male rats produced lower testicular and prostate weights. Ethyl acetate alone produced similar effects and also reduced the number of spermatozoa.
    0.2.21) CARCINOGENICITY
    A) Ethyl acetate exposure was associated with increased risk for lymphatic leukemia in rubber workers however, ethyl acetate is not generally regarded as a human carcinogen at the present time.

Laboratory Monitoring

    A) Various techniques are available, primarily using gas chromatography or spectrometric techniques. Toxic levels have not been established.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Activated charcoal is unlikely to be necessary due to the low toxicity of these compounds.
    B) No specific antidotes or treatments are available. Monitor patients ingesting large amounts for CNS depression, respiratory depression, and decreased cardiac contractility.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) No adverse symptoms were noted in workers exposed to 375 to 1,500 ppm for several months. Humans find concentrations greater than 200 ppm objectionable because of the strong odor. 400 ppm caused nose and throat irritation. The TLV is 400 ppm (1,400 mg/m(3)).

Clinical Effects

Summary Of Exposure

    A) Ethyl acetate is low in toxicity. It is a mild mucous membrane irritant, but is not caustic. In high concentrations it may be a CNS depressant. Animal studies have demonstrated pulmonary edema, decreased cardiac contractility, seizures and hepatic damage, but these have NOT been reported in humans.

Heent

    3.4.1) SUMMARY
    A) Ethyl acetate is irritating to the conjunctivae but leaves no residual effects. Nose and throat irritation is seen at levels greater than 400 ppm for 3 to 5 minutes.
    3.4.3) EYES
    A) CONJUNCTIVITIS - Ethyl acetate is irritating to the conjunctivae but leaves no residual effects (Grant & Schuman, 1993). Rabbits exposed to vapor concentrations which would scarcely be tolerated by workers did not develop corneal damage despite exposures to 8 hours daily, 5 days a week for up to 7 weeks (Anon, 1981).
    B) IRRITATION of the eyes in humans occurred at 400 ppm using the standard Draize test (RTECS , 2002).
    3.4.5) NOSE
    A) Nasal irritation is seen at levels greater than 400 ppm for 3 to 5 minutes (Nelson et al, 1943).
    3.4.6) THROAT
    A) Throat irritation is seen at levels greater than 400 ppm for 3 to 5 minutes (Nelson et al, 1943).

Cardiovascular

    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) CARDIAC FAILURE
    a) When tested on isolated guinea pig ventricular strips, ethyl acetate was noted to depress the myocardium approximately 10 times as much as ethanol (Nakano et al, 1973). Doses of 5 mg/kg/min IV in dogs decreased heart rate, systemic arterial pressure, and, after a transient increase, myocardial contractile force (Nakano & Kessinger, 1972).

Respiratory

    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY EDEMA
    a) Cats fatally poisoned with levels of 43,000 ppm were found on autopsy to have developed pulmonary edema with hemorrhage and hyperemia of the respiratory tract (von Oettingen, 1960). This symptom has NOT been reported in humans.

Neurologic

    3.7.1) SUMMARY
    A) Chronic exposure to solvent mixtures including ethyl acetate has been associated with poorer performance on neurobehavioral tests. High concentrations orally administered to rabbits caused lack of coordination. High concentrations have intoxicating properties in animals and would be expected to cause narcosis in humans.
    3.7.2) CLINICAL EFFECTS
    A) ALTERED MENTAL STATUS
    1) Chronic occupational exposure to mixed solvents (82% toluene, 12% ethyl acetate, 6% methyl ethyl ketone) was associated with poorer performance on tests of short-term memory, visual motor speed and manual dexterity in one study (Foo et al, 1993).
    a) Poorer performance was associated with longer duration of exposure to the mixed solvents, not exposure intensity, suggesting that a component of this effect may be irreversible.
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) COORDINATION ABNORMAL
    a) High concentrations orally administered to rabbits caused lack of coordination, possibly due to hydrolysis into acetic acid and ethanol (Clayton & Clayton, 1982). High concentrations have intoxicating properties in animals and would be expected to cause narcosis in humans (Hathaway et al, 1996).
    2) SEIZURES
    a) Ethyl acetate administered intraperitoneally to mice at doses of 0.75 grams/kilogram and above induced clonic seizures (Silva-Filho et al, 1992).

Hepatic

    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEPATOCELLULAR DAMAGE
    a) Liver damage was reported by von Oettingen (1960) in rabbits exposed to 4450 ppm repeatedly. Liver damage has NOT been reported in humans.

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) In theory, acidosis may occur if large amounts are ingested. This effect has not been reported in humans (Clayton & Clayton, 1982).

Hematologic

    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LEUKOCYTOSIS
    a) Rabbits repeatedly exposed to 4450 ppm developed leukocytosis and secondary anemia (Hathaway et al, 1996). This has NOT been reported in humans.

Dermatologic

    3.14.1) SUMMARY
    A) Drying as well as skin defatting and cracking may be seen with dermal application. Sensitizations to ethyl acetate have been reported but are rare.
    3.14.2) CLINICAL EFFECTS
    A) ECZEMA
    1) Sensitizations to ethyl acetate have resulted in inflammation of mucous membranes and eczematous eruptions (von Oettingen, 1960). This is a rare occurrence. Kligman tested 25 volunteers with 10% ethyl acetate and petrolatum and found no sensitization (Opdyke, 1974).
    B) DRY SKIN
    1) Drying as well as skin defatting and cracking may be seen with dermal application (Finkel, 1983).

Reproductive

    3.20.1) SUMMARY
    A) No reproductive studies were found for ethyl acetate in humans. Inhalation of lacquer thinner, which contains ethyl acetate, in male rats produced lower testicular and prostate weights. Ethyl acetate alone produced similar effects and also reduced the number of spermatozoa.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Ethyl acetate was more toxic than ethanol when injected into chick embryos but was apparently not teratogenic (McLaughlin, 1964). The implications of this study for the human situation are not clear.
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY DISORDER
    1) Ethyl acetate is hydrolyzed to form acetic acid and ETHANOL in the body. Ethanol is a known human reproductive hazard and can cause fetal alcohol syndrome. The no-effect dose of ethanol during pregnancy which would not cause fetal alcohol syndrome is not known.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS141-78-6 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) Ethyl acetate exposure was associated with increased risk for lymphatic leukemia in rubber workers however, ethyl acetate is not generally regarded as a human carcinogen at the present time.
    3.21.3) HUMAN STUDIES
    A) CARCINOGENICITY RISK
    1) Ethyl acetate exposure was associated with increased risk for lymphatic leukemia in rubber workers (Wilcosky, 1984); however, ethyl acetate is not generally regarded as a human carcinogen at the present time.

Genotoxicity

    A) Few genetic studies regarding ethyl acetate were found at the time of this review. Ethyl acetate was not mutagenic in Drosophila.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Various techniques are available, primarily using gas chromatography or spectrometric techniques. Toxic levels have not been established.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) Toxic levels of ethyl acetate have not been established. If large amounts have been ingested, ethanol levels may aid in assessing metabolism and toxicity.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Various techniques are available, primarily using gas chromatography or spectrometric techniques (Bingham et al, 2001).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Various techniques are available, primarily using gas chromatography or spectrometric techniques. Toxic levels have not been established.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Activated charcoal is unlikely to be necessary due to the low toxicity of these compounds.
    B) ACTIVATED CHARCOAL -
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) No specific antidotes or treatments are available. Patients who ingest large amounts should be monitored for CNS depression, respiratory function, and decreased cardiac contractility. For ingestions of large amounts, respiratory and cardiac supportive care should be available.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) This substance is only a mild irritant. Patients exposed dermally should dilute the area copiously with cool water. A physician may need to examine the exposed area if irritation or pain persists after the area is washed.

Range Of Toxicity

Summary

    A) No adverse symptoms were noted in workers exposed to 375 to 1,500 ppm for several months. Humans find concentrations greater than 200 ppm objectionable because of the strong odor. 400 ppm caused nose and throat irritation. The TLV is 400 ppm (1,400 mg/m(3)).

Therapeutic Dose

    7.2.1) ADULT
    A) DISEASE STATE
    1) Ethyl acetate has been used as a carminative and antispasmodic in a dose of 1 to 2 milliliters orally (HSDB , 1990).
    2) When used externally ethyl acetate has counterirritant properties (HSDB , 1990).

Minimum Lethal Exposure

    A) ROUTE OF EXPOSURE
    1) There is a single case report of a death ascribed to inhalation of ethyl acetate in a tank painter (Lehmann & Flury, 1943).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) No adverse symptoms were noted in workers exposed to 375 to 1500 parts per million for several months (Clayton & Clayton, 1982).
    B) ACUTE
    1) TCLo - (INHL) HUMAN: 400 ppm (RTECS , 1998)

Workplace Standards

    A) ACGIH TLV Values for CAS141-78-6 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Ethyl acetate
    a) TLV:
    1) TLV-TWA: 400 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): URT and eye irr
    d) Molecular Weight: 88.1
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS141-78-6 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Ethyl acetate
    2) REL:
    a) TWA: 400 ppm (1400 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 2000 ppm
    b) Note(s): [10%LEL]
    1) [10%LEL]: The 10%LEL designation is provided where the IDLH was based on 10% of the lower explosive limit. This is used for safety purposes in some cases even though toxicity is not indicative of irreversible health effects or impairment of escape exists only at higher concentrations.

    C) Carcinogenicity Ratings for CAS141-78-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Ethyl acetate
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Ethyl acetate
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Ethyl acetate
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS141-78-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Ethyl acetate
    2) Table Z-1 for Ethyl acetate:
    a) 8-hour TWA:
    1) ppm: 400
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 1400
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2002 Budavari, 1996 Sax & Lewis, 1989
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 709 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 4100 mg/kg
    3) LD50- (ORAL)RAT:
    a) 5620 mg/kg
    b) 11.3 mL/kg
    4) TCLo- (INHALATION)HUMAN:
    a) 400 ppm

Pharmacology Toxicology

Toxicologic Mechanism

    A) Toxicity appears to be due to unhydrolyzed esters and not to ethyl alcohol (Gosselin et al, 1984).

Physicochemical

Physical Characteristics

    A) Ethyl acetate is a clear, volatile, flammable liquid with an ether-like, fruity odor and a bittersweet, wine-like burning taste. It has a pleasant taste when diluted (Budavari, 1996) NIOSH, 1990; (HSDB , 1991).
    B) Clear, volatile, fragrant liquid with pleasant taste when diluted (Sax & Lewis, 1987)

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 88.11 (Budavari, 1996)

Other

    A) ODOR THRESHOLD
    1) 1 ppm (CHRIS , 2002).

References

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