MOBILE VIEW  | 

METHYL ACETATE

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Methyl acetate is the ester of methanol and acetic acid. It is commonly available with at least 96% purity, with the major contaminant of methanol. It is used in nail polish removers, in synthetic flavoring food additives, and as a solvent in lacquers and paint removers.

Specific Substances

    1) Acetic acid, methyl ester
    2) Devoton
    3) Methyl ester acetic acid
    4) Methyl acetic ester
    5) Methyl ethanoate
    6) Tereton
    7) CAS 79-20-9
    1.2.1) MOLECULAR FORMULA
    1) C3-H6-O2

Available Forms Sources

    A) FORMS
    1) Methyl acetate is commonly available with at least 96% purity, with the major contaminants of methanol (less than or equal to 2.5%) and water (less than or equal to 1.5%) (Heldreth et al, 2012). It can also be available as a mixture of 80/20 methyl acetate/methanol (Hazardous Substances Data Bank (HSDB), 2005).
    2) Methyl acetate may contain up to 0.1% of acetic acid as impurity (Hazardous Substances Data Bank (HSDB), 2005).
    B) SOURCES
    1) Methyl acetate is the ester of methanol and acetic acid (Heldreth et al, 2012). It is manufactured via the esterification of acetamide with methanol catalyzed by an acid and via the refinement of wood spirits (derived from distilled pyroligneous acid derived from wood) (Bingham et al, 2001).
    2) Methyl acetate can also be produced by reaction of methanol and carbon monoxide (Hazardous Substances Data Bank (HSDB), 2005).
    3) Methyl acetate is also a naturally occurring compound and may be released to the environment. Natural sources include mint, fungus, grapes, bananas, coffee, and nectarines (Bingham et al, 2001).
    C) USES
    1) Methyl acetate is used in nail polish removers, in synthetic flavoring food additives, as a solvent in lacquers and paint removers, and as a major component of methyl acetone (a mixed solvent derived from the distillation of wood and widely used at one time). It is also mixed with acetone and methanol and used in the plastic and artificial leather industries and in the production of perfumes, coloring agents, and lacquers (Minns et al, 2013; Heldreth et al, 2012; Grant & Schuman, 1993; HSDB, 2002; Lewis, 1998; ACGIH, 1991a; ILO, 1998).
    2) FOOD FLAVORING: Methyl acetate is permitted for direct addition to food for human consumption for flavoring purposes and is recognized as safe (GRAS) by the US Food and Drug Administration (Heldreth et al, 2012).
    3) NAIL POLISH REMOVERS: Many non-acetone nail polish removers contain methyl acetate (concentration range, 10% to 60%) (Heldreth et al, 2012; Minns et al, 2013).

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Methyl acetate is the ester of methanol and acetic acid. It is commonly available with at least 96% purity, with the major contaminant of methanol. It is used in nail polish removers, in synthetic flavoring food additives, as a solvent in lacquers and paint removers, and as a major component of methyl acetone (a mixed solvent derived from the distillation of wood and widely used at one time). It is also mixed with acetone and methanol and used in the plastic and artificial leather industries and in the production of perfumes, coloring agents, and lacquers. FOOD FLAVORING: Methyl acetate is permitted for direct addition to food for human consumption for flavoring purposes and is recognized as safe (GRAS) by the US Food and Drug Administration.
    B) TOXICOLOGY: Following ingestion and inhalation of methyl acetate, it is hydrolyzed rapidly to methanol and acetic acid. Methyl acetate has the potential to cause methanol poisoning, however there are no well documented cases of methanol poisoning resulting from methyl acetate exposure. Methanol is metabolized to formaldehyde and formic acid via alcohol dehydrogenase and aldehyde dehydrogenase, respectively. Formic acid causes a metabolic acidosis and blindness. Refer to "METHANOL" management for more information.
    C) EPIDEMIOLOGY: Exposure (dermal, inhalational and ingestion) from nail polish remover and other cosmetics is common and has not resulted in significant toxicity. Occupational exposure can cause irritant effects. Extremely large ingestion has the potential to cause significant methanol poisoning but this has not been reported.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Methyl acetate is irritating to eyes, skin, and mucous membranes. Inhalational exposure of methyl acetate may cause throat irritation, cough, dyspnea, chest tightness, palpitations, headache, fatigue, dizziness, lightheadedness, and drowsiness. Ingestion of methyl acetate may cause headache, drowsiness, ataxia, asthenia, fatigue, nausea, vomiting, and abdominal pain. Eye burns, blurred vision, lacrimation may also occur. Dry, red, rough skin, and rash may occur following contact with methyl acetate liquid.
    2) SEVERE TOXICITY: Extremely large exposure has the potential to cause significant methanol poisoning but this has not been reported. Expected effects would include anion gap metabolic acidosis, visual disturbances, blindness, CNS depression, and coma.

Laboratory Monitoring

    A) Asymptomatic patients with taste or a single swallow exposure do not require laboratory studies unless otherwise clinically indicated.
    B) In patients with large ingestions or exposures, and symptomatic patients, monitor blood methanol concentration and serum electrolytes. If serum methanol cannot be obtained in a timely fashion, measure serum osmolality and calculate osmolal gap.
    C) Monitor vital signs and mental status.
    D) Obtain a baseline ECG; continuous cardiac monitoring is indicated in patients following a significant exposure.
    E) In patients with significant CNS depression or metabolic acidosis, obtain arterial or venous blood gases.
    F) Refer to "METHANOL" management for more information.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment of mild to moderate exposure is symptomatic and supportive. Exploratory ingestions of products such as nail polish removers, are not likely to cause methanol poisoning; however, large, deliberate ingestions or industrial exposures to high concentration products may cause methanol poisoning. Removal from inhalational exposure to high concentrations is the primary treatment. Supportive care with oxygen or bronchodilators can be administered. Patients with oral ingestions of high concentrations should be observed for evidence of metabolic acidosis.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Following exposures to high concentrations of methyl acetate, obtain a methanol concentration, serum chemistry, and a serum pH. Patients presenting with severe metabolic acidosis, signs or symptoms of visual changes, elevated methanol concentration, or depressed level of consciousness should be started immediately on an ADH inhibitor (fomepizole or ethanol) and intravenous folate. Hemodialysis should be initiated and should be continued until the methanol concentration is undetectable and the serum pH is normal. Treat seizures with benzodiazepines. A thorough visual exam should be performed, including visual acuity. Treatment for severe inhalational exposures is primarily supportive. Supplemental oxygen should be administered as needed. Mechanical ventilation may be needed. Administer bronchodilators for bronchospasm.
    C) DECONTAMINATION
    1) Toxicity after an acute ingestion of a small amount of methyl acetate-containing nail polish remover is unlikely. After large ingestions, methyl acetate is rapidly absorbed and may cause CNS depression. Gastrointestinal decontamination is generally not recommended in either case. Remove contaminated clothing. Contaminated skin and eyes should be irrigated with water.
    D) AIRWAY MANAGEMENT
    1) Following exposure to high concentrations of methyl acetate, endotracheal intubation may be necessary in patients with significant CNS or respiratory depression. Extreme care must be taken to increase minute ventilation sufficiently to prevent severe acidemia in intubated patients.
    E) ANTIDOTE
    1) Treat patients with signs of methanol poisoning with either fomepizole or ethanol to prevent the production of formate. Indications include documented plasma methanol concentration greater than 20 mg/dL (greater than 200 mg/L) OR documented recent history of ingesting toxic amounts of methanol and osmolal gap greater than 10 mOsm/L OR history or strong clinical suspicion of methanol poisoning with at least 2 of the following criterion: arterial pH less than 7.3; serum bicarbonate less than 20 mEq/L; osmolol gap greater than 10 mOsm/L.
    F) ENHANCED ELIMINATION
    1) Methanol and its metabolites (formaldehyde and formic acid) are readily removed by hemodialysis. Emergent hemodialysis is indicated in any methanol-intoxicated patient with an anion gap metabolic acidosis (pH less than 7.3), visual disturbances, or CNS depression. Because methanol is cleared very slowly once ADH inhibitors are administered, hemodialysis should also be considered in patients with methanol concentrations greater than 50 mEq/L, even in the absence of acidosis or severe symptoms.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients who are asymptomatic or with minimal symptoms after inadvertent exposure to small amounts of methyl acetate-containing products (eg, nail polish removers) and are otherwise improving may be managed at home. Patients with mild eye, skin, or respiratory irritation can be managed at home with decontamination.
    2) OBSERVATION CRITERIA: Intentional or large ingestions should be evaluated in a healthcare facility. Patients with significant eye irritation, or more than mild pulmonary or skin irritation should be sent to a healthcare facility for evaluation.
    3) ADMISSION CRITERIA: Patients who are acidotic, have CNS depression or visual symptoms, or have serum methanol concentrations above 25 mg/dL should be admitted.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist in cases of severe poisonings, in cases where a methanol concentration is not readily available, or in cases where the ingestion is uncertain. Consult a nephrologist for any patient who may require hemodialysis.
    H) PITFALLS
    1) While methanol poisoning is theoretically possible after methyl acetate exposure, there are no well documented cases; do not overtreat.
    I) PHARMACOKINETICS
    1) Methyl acetate is hydrolyzed rapidly to methanol and acetic acid. In vitro, approximately 60% of methyl acetate added to blood was converted to methanol in 2 hours and almost all of it disappeared in 8 hours. Methanol is rapidly absorbed after ingestion and can be absorbed with inhalation of high concentrations. The apparent half-life of methanol is approximately 8 to 28 hours. The volume of distribution is approximately 0.6 L/kg. It is not protein bound.
    J) TOXICOKINETICS
    1) When alcohol dehydrogenase inhibitors are being used, the apparent half-life of methanol is increased to approximately 50 hours.
    K) DIFFERENTIAL DIAGNOSIS
    1) Exposure to other chemicals, such as hydrocarbons, ethanol, ethylene glycol, isopropyl alcohol, and other glycol ethers.
    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) TOXICITY: Human exposure to 10,000 ppm for a short period of time resulted in eye, nose, and throat irritation, which persisted after cessation of exposure. Industrial exposures at or below 200 ppm did not cause any irritation or systemic injury. At a level of 3100 ppm, methyl acetate is considered to be immediately dangerous to life or health (IDLH). ACGIH Threshold Limit Value (TLV): 200 ppm (606 mg/m(3)) TWA; 250 ppm (757 mg/m(3)).
    B) NAIL POLISH REMOVERS: In a retrospective study of exposures to methyl acetate-containing nail polish removers (n=83), 75% of patients did not develop any toxic effects. Minor effects developed in 25% of cases. In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers and remained asymptomatic.

Summary Of Exposure

    A) USES: Methyl acetate is the ester of methanol and acetic acid. It is commonly available with at least 96% purity, with the major contaminant of methanol. It is used in nail polish removers, in synthetic flavoring food additives, as a solvent in lacquers and paint removers, and as a major component of methyl acetone (a mixed solvent derived from the distillation of wood and widely used at one time). It is also mixed with acetone and methanol and used in the plastic and artificial leather industries and in the production of perfumes, coloring agents, and lacquers. FOOD FLAVORING: Methyl acetate is permitted for direct addition to food for human consumption for flavoring purposes and is recognized as safe (GRAS) by the US Food and Drug Administration.
    B) TOXICOLOGY: Following ingestion and inhalation of methyl acetate, it is hydrolyzed rapidly to methanol and acetic acid. Methyl acetate has the potential to cause methanol poisoning, however there are no well documented cases of methanol poisoning resulting from methyl acetate exposure. Methanol is metabolized to formaldehyde and formic acid via alcohol dehydrogenase and aldehyde dehydrogenase, respectively. Formic acid causes a metabolic acidosis and blindness. Refer to "METHANOL" management for more information.
    C) EPIDEMIOLOGY: Exposure (dermal, inhalational and ingestion) from nail polish remover and other cosmetics is common and has not resulted in significant toxicity. Occupational exposure can cause irritant effects. Extremely large ingestion has the potential to cause significant methanol poisoning but this has not been reported.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Methyl acetate is irritating to eyes, skin, and mucous membranes. Inhalational exposure of methyl acetate may cause throat irritation, cough, dyspnea, chest tightness, palpitations, headache, fatigue, dizziness, lightheadedness, and drowsiness. Ingestion of methyl acetate may cause headache, drowsiness, ataxia, asthenia, fatigue, nausea, vomiting, and abdominal pain. Eye burns, blurred vision, lacrimation may also occur. Dry, red, rough skin, and rash may occur following contact with methyl acetate liquid.
    2) SEVERE TOXICITY: Extremely large exposure has the potential to cause significant methanol poisoning but this has not been reported. Expected effects would include anion gap metabolic acidosis, visual disturbances, blindness, CNS depression, and coma.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Eye burns, blurred vision, and lacrimation have been reported after vapor exposure. One patient developed blindness after occupational methyl acetate exposure (Hazardous Substances Data Bank (HSDB), 2005; Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011).
    2) OPTIC NERVE ATROPHY: Optic nerve atrophy may occur with occupational methyl acetate exposure (Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011).
    3) Methanol formed by the hydrolysis of methyl acetate might be responsible for its toxicity, resulting in headache, dizziness, coma, and optic nerve damage (visual disturbances, blindness) (Occupational Safety & Health Administration (OSHA), 2012).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) NOSE IRRITATION: Nose irritation may occur with methyl acetate vapor exposure (Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) THROAT IRRITATION: Throat irritation and sore throat may occur with methyl acetate vapor exposure (Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011).
    2) NAIL POLISH REMOVERS: One retrospective study evaluated 83 cases (75 patients were 5 years and younger; 4 patients were 6 years and older; 4 adult patients) of exposure to methyl acetate-containing nail polish removers. Throat/oral irritation developed in 5 patients (6%). In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers (Minns et al, 2013).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TIGHT CHEST
    1) WITH POISONING/EXPOSURE
    a) Chest tightness may occur with methyl acetate vapor exposure (Hazardous Substances Data Bank (HSDB), 2005; Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011).
    B) PALPITATIONS
    1) WITH POISONING/EXPOSURE
    a) Palpitation has been reported following methyl acetate exposure (Hazardous Substances Data Bank (HSDB), 2005).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) High concentrations of methyl acetate can be irritating to respiratory tract (Hazardous Substances Data Bank (HSDB), 2005).
    B) COUGH
    1) WITH POISONING/EXPOSURE
    a) Cough may occur with methyl acetate vapor exposure (Hazardous Substances Data Bank (HSDB), 2005; Occupational Safety & Health Administration (OSHA), 2012).
    C) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Dyspnea may occur with methyl acetate vapor exposure (Occupational Safety & Health Administration (OSHA), 2012).
    D) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Acute lung injury may occur with inhalational exposure to high concentrations of methyl acetate (New Jersey Department of Health and Senior Services, 2003).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) DROWSY
    1) WITH POISONING/EXPOSURE
    a) Drowsiness may occur with methyl acetate exposure (Hazardous Substances Data Bank (HSDB), 2005; Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011).
    b) NAIL POLISH REMOVERS: One retrospective study evaluated 83 cases (75 patients were 5 years and younger; 4 patients were 6 years and older; 4 adult patients) of exposure to methyl acetate-containing nail polish removers. Drowsiness developed in only 1 patient (1.2%). In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers (Minns et al, 2013).
    B) ATAXIA
    1) WITH POISONING/EXPOSURE
    a) NAIL POLISH REMOVERS: One retrospective study evaluated 83 cases (75 patients were 5 years and younger; 4 patients were 6 years and older; 4 adult patients) of exposure to methyl acetate-containing nail polish removers. Ataxia developed in only 1 patient (1.2%). In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers (Minns et al, 2013).
    C) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache may occur with methyl acetate vapor exposure (Hazardous Substances Data Bank (HSDB), 2005; Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011; New Jersey Department of Health and Senior Services, 2003).
    D) ASTHENIA
    1) WITH POISONING/EXPOSURE
    a) Ingestion of methyl acetate liquid may cause weakness (Occupational Safety & Health Administration (OSHA), 2012).
    E) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Ingestion of methyl acetate can cause dizziness (Hazardous Substances Data Bank (HSDB), 2005; New Jersey Department of Health and Senior Services, 2003).
    F) LOSS OF CONSCIOUSNESS
    1) WITH POISONING/EXPOSURE
    a) Lightheadedness and loss of consciousness may occur with methyl acetate exposure (Hazardous Substances Data Bank (HSDB), 2005; New Jersey Department of Health and Senior Services, 2003).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Ingestion of methyl acetate liquid may cause nausea and vomiting (Occupational Safety & Health Administration (OSHA), 2012; New Jersey Department of Health and Senior Services, 2003).
    b) NAIL POLISH REMOVERS: One retrospective study evaluated 83 cases (75 patients were 5 years and younger; 4 patients were 6 years and older; 4 adult patients) of exposure to methyl acetate-containing nail polish removers. Vomiting developed in 12 patients (14%). In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers (Minns et al, 2013).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) Ingestion of methyl acetate liquid may cause abdominal pain (Occupational Safety & Health Administration (OSHA), 2012).
    b) NAIL POLISH REMOVERS: One retrospective study evaluated 83 cases (75 patients were 5 years and younger; 4 patients were 6 years and older; 4 adult patients) of exposure to methyl acetate-containing nail polish removers. Abdominal pain developed in only 1 patient (1.2%). In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers (Minns et al, 2013).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) METABOLIC ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Methanol formed by the hydrolysis of methyl acetate may be responsible for its toxicity (Occupational Safety & Health Administration (OSHA), 2012). Anion gap metabolic acidosis may occur following exposure to high concentrations, depending on the concentration of methanol produced.
    b) NAIL POLISH REMOVERS: One retrospective study evaluated 83 cases (75 patients were 5 years and younger; 4 patients were 6 years and older; 4 adult patients) of exposure to methyl acetate-containing nail polish removers. In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. A 2-year-old boy developed mild metabolic acidosis (serum bicarbonate 17 mmol/L and anion gap 16) after ingesting about 12 mL of Fung-off No Lift fungal liquid for nails. Metabolic acidosis resolved spontaneously and no other effects were reported (Minns et al, 2013).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN FINDING
    1) WITH POISONING/EXPOSURE
    a) Dry, red, rough skin, and rash may occur following contact with methyl acetate liquid (Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS79-20-9 (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

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Asymptomatic patients with taste or a single swallow exposure do not require laboratory studies unless otherwise clinically indicated.
    B) In patients with large ingestions or exposures, and symptomatic patients, monitor blood methanol concentration and serum electrolytes. If serum methanol cannot be obtained in a timely fashion, measure serum osmolality and calculate osmolal gap.
    C) Monitor vital signs and mental status.
    D) Obtain a baseline ECG; continuous cardiac monitoring is indicated in patients following a significant exposure.
    E) In patients with significant CNS depression or metabolic acidosis, obtain arterial or venous blood gases.
    F) Refer to "METHANOL" management for more information.

Methods

    A) In one study, methyl acetate 15 mL was applied to the skin of the forearm of 4 volunteers and blood samples were obtained prior to and immediately after application. Gas chromatography was used to determine the concentrations of methyl acetate in blood. Methyl acetate blood concentrations ranged from 0.9 mcg/mL 1 hour after application to as high as 3.8 mcg/mL 2 hours after application (Heldreth et al, 2012).
    B) Head-space gas chromatography was used to determine methanol formation following methyl acetate hydrolysis (Mizunuma et al, 1992).

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients who are acidotic, have CNS depression or visual symptoms, or have serum methanol concentrations above 25 mg/dL should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients who are asymptomatic or with minimal symptoms after inadvertent exposure to small amounts of methyl acetate-containing products (eg, nail polish removers) and are otherwise improving may be managed at home. Patients with mild eye, skin, or respiratory irritation can be managed at home with decontamination.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist in cases of severe poisonings, in cases where a methanol concentration is not readily available, or in cases where the ingestion is uncertain. Consult a nephrologist for any patient who may require hemodialysis.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Intentional or large ingestions should be evaluated in a healthcare facility. Patients with significant eye irritation, or more than mild pulmonary or skin irritation should be sent to a healthcare facility for evaluation.

Monitoring

    A) Asymptomatic patients with taste or a single swallow exposure do not require laboratory studies unless otherwise clinically indicated.
    B) In patients with large ingestions or exposures, and symptomatic patients, monitor blood methanol concentration and serum electrolytes. If serum methanol cannot be obtained in a timely fashion, measure serum osmolality and calculate osmolal gap.
    C) Monitor vital signs and mental status.
    D) Obtain a baseline ECG; continuous cardiac monitoring is indicated in patients following a significant exposure.
    E) In patients with significant CNS depression or metabolic acidosis, obtain arterial or venous blood gases.
    F) Refer to "METHANOL" management for more information.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY: Toxicity after an acute ingestion of a small amount of methyl acetate-containing nail polish remover is unlikely. After large ingestions, methyl acetate is rapidly absorbed and may cause CNS depression. GI decontamination is generally not recommended in either case.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment of mild to moderate exposure is symptomatic and supportive. Exploratory ingestions of products such as nail polish removers, are not likely to cause methanol poisoning; however, large, deliberate ingestions or industrial exposures to high concentration products may cause methanol poisoning. Removal from inhalational exposure to high concentrations is the primary treatment. Supportive care with oxygen or bronchodilators can be administered. Patients with oral ingestions of high concentrations should be observed for evidence of metabolic acidosis.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Following exposures to high concentrations of methyl acetate, obtain a methanol concentration, serum chemistry, and a serum pH. Patients presenting with severe metabolic acidosis, signs or symptoms of visual changes, elevated methanol concentration, or depressed level of consciousness should be started immediately on an ADH inhibitor (fomepizole or ethanol) and intravenous folate. Hemodialysis should be initiated and should be continued until the methanol concentration is undetectable and the serum pH is normal. Treat seizures with benzodiazepines. A thorough visual exam should be performed, including visual acuity. Treatment for severe inhalational exposures is primarily supportive. Supplemental oxygen should be administered as needed. Mechanical ventilation may be needed. Administer bronchodilators for bronchospasm.
    B) MONITORING OF PATIENT
    1) Asymptomatic patients with taste or a single swallow exposure do not require laboratory studies unless otherwise clinically indicated.
    2) In patients with large ingestions or exposures, and symptomatic patients, monitor blood methanol concentration and serum electrolytes. If serum methanol cannot be obtained in a timely fashion, measure serum osmolality and calculate osmolal gap.
    3) Monitor vital signs and mental status.
    4) Obtain a baseline ECG; continuous cardiac monitoring is indicated in patients following a significant exposure.
    5) In patients with significant CNS depression or metabolic acidosis, obtain arterial or venous blood gases.
    6) Refer to "METHANOL" management for more information.
    C) ACIDOSIS
    1) METABOLIC ACIDOSIS: Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate, 1 to 2 mEq/kg is a reasonable starting dose(Kraut & Madias, 2010). Monitor serum electrolytes and arterial or venous blood gases to guide further therapy.
    2) Significant metabolic acidosis is an indication for treatment with and ADH inhibitor (fomepizole or ethanol) and emergent hemodialysis. Monitor methanol concentrations. Fomepizole and emergent dialysis is recommended for patients with significant metabolic acidosis or elevated methanol concentrations.
    D) ANTIDOTE
    1) Administer fomepizole or ethanol and perform dialysis in patients with significant methanol poisoning secondary to methyl acetate ingestion. See METHANOL document for further details.
    2) Treat patients with signs of methanol poisoning with either fomepizole or ethanol to prevent the production of formate. Indications include documented plasma methanol concentration greater than 20 mg/dL (greater than 200 mg/L) OR documented recent history of ingesting toxic amounts of methanol and osmolal gap greater than 10 mOsm/L OR history or strong clinical suspicion of methanol poisoning with at least 2 of the following criterion: arterial pH less than 7.3; serum bicarbonate less than 20 mEq/L; osmolol gap greater than 10 mOsm/L (Barceloux et al, 2002).
    a) ETHANOL VS FOMEPIZOLE: Fomepizole is easier to use clinically, requires less monitoring, does not cause CNS depression or hypoglycemia, and may obviate the need for dialysis in some patients. Ethanol requires continuous administration and frequent monitoring of serum ethanol and glucose levels and may cause CNS depression and hypoglycemia (especially in children). The drug cost associated with ethanol use is generally much lower than with fomepizole; however, other costs associated with ethanol use (eg, continuous intravenous infusion, hourly blood draws, nursing costs, and ethanol levels, possibly greater use of hemodialysis) may make the costs more comparable.
    b) FOMEPIZOLE: Fomepizole is administered as a 15 mg/kg loading dose, followed by 4 bolus doses of 10 mg/kg every 12 hours. If therapy is needed beyond this 48-hour period, the dose is then increased to 15 mg/kg every 12 hours for as long as necessary. Fomepizole is also effectively removed by hemodialysis; therefore, doses should be repeated following each round of hemodialysis (Prod Info ANTIZOL(R) IV injection, 2006).
    c) ETHANOL: Ethanol is given to maintain a serum ethanol concentration of 100 to 150 mg/dL. This can be accomplished by using a 5% or 10% ethanol solution administered intravenously through a central line. Intravenous therapy dosing, which is preferred, is 0.8 g/kg as a loading dose (8 mL/kg of 10% ethanol) administered over 20 to 60 minutes as tolerated, followed by an infusion rate of 80 to 150 mg/kg/hr (for 10% ethanol, 0.8 to 1.3 mL/kg/hr for a nondrinker; 1.5 mL/kg/hr for a chronic alcoholic). During hemodialysis, either add ethanol to the dialysate to achieve 100 mg/dL concentration or increase the rate of infusion during dialysis (10% ethanol, 2.5 to 3.5 mL/kg/hr). Oral ethanol may be used as a temporizing measure until intravenous ethanol or fomepizole can be obtained, but it is more difficult to achieve the desired stable ethanol concentration. The loading dose is 0.8 g/kg (4 mL/kg) of 20% {40 proof}) ethanol diluted in juice administered orally or via nasogastric tube. Maintenance dose is 80 to 150 mg/kg/hr (20% {40 proof}) ethanol; 0.4 to 0.7 mL/kg/hr for a nondrinker; 0.8 mL/kg/hr for a chronic alcoholic). Concentrations greater than 30% (60 proof) ethanol should be diluted. For both modalities, blood ethanol levels must be monitored hourly and adjusted accordingly, and both require patient monitoring in an ICU setting (Howland, 2006).
    d) FOLATE: Leucovorin and folic acid enhance the metabolism of formic acid (formate) to carbon dioxide and water (Noker et al, 1980; Anon, 1979; Makar & Tephly, 1976). Either folic acid or leucovorin (folinic acid) may be used in patients with methanol toxicity (Howland, 2011). Leucovorin (folinic acid) is the active form of folic acid and does not require reduction by the enzyme dihydrofolate reductase in order to participate in reactions using folate as a source of one-carbon moieties. It may be used for the initial dose in symptomatic patients, but it is more expensive than folic acid and there is no data that it improves outcome compared with folic acid. In symptomatic patients (anion gap acidosis, visual disturbances) and asymptomatic patients with known or suspected methanol intoxication, administer intravenous folic acid.
    1) DOSE: 1 to 2 mg/kg every 4 to 6 hours for the first 24 hours. It should be continued until methanol is cleared and acidosis resolved. Folate is removed by hemodialysis so in patients undergoing hemodialysis, administer one dose prior to and another at the completion of hemodialysis. In studies, the use of folic acid 50 to 70 mg IV every 4 hours for the first 24 hours did not produce any complications (Howland, 2011).
    3) One study recommended that the critically ill patients with severe metabolic acidosis (base deficit greater than 15 mmol/L) or visual disturbances should receive sodium bicarbonate, fomepizole, and hemodialysis as soon as possible. Stable patients, with little to moderate metabolic acidosis (base deficit less than 15 mmol/L) and no visual disturbances should receive sodium bicarbonate and fomepizole. In these patients, the use of hemodialysis should be discussed with an experienced nephrologist or clinical toxicologist (Hovda & Jacobsen, 2008).
    E) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

Enhanced Elimination

    A) HEMODIALYSIS
    1) Methanol and its metabolites (formaldehyde and formic acid) are readily removed by hemodialysis. Emergent hemodialysis is indicated in any methanol-intoxicated patient with an anion gap metabolic acidosis (pH less than 7.3), visual disturbances, or CNS depression. Because methanol is cleared very slowly once ADH inhibitors are administered, hemodialysis should also be considered in patients with methanol concentrations greater than 50 mEq/L, even in the absence of acidosis or severe symptoms. See METHANOL document for further details.
    2) INDICATIONS: Peak blood methanol concentration greater than 50 mg/dL (15 mmol/L), severe acidosis regardless of the blood methanol level, severe acid-base and or fluid-electrolyte disturbances despite conventional therapy, renal failure, and visual symptoms are indications for dialysis (Prod Info Antizol(R), fomepizole injection, 2000; Vogt et al, 1993).
    3) EFFICACY: Hemodialysis is highly effective at removing methanol (McCoy et al, 1979; Girault et al, 1999) but fomepizole or ethanol therapy should be continued during dialysis.

Summary

    A) TOXICITY: Human exposure to 10,000 ppm for a short period of time resulted in eye, nose, and throat irritation, which persisted after cessation of exposure. Industrial exposures at or below 200 ppm did not cause any irritation or systemic injury. At a level of 3100 ppm, methyl acetate is considered to be immediately dangerous to life or health (IDLH). ACGIH Threshold Limit Value (TLV): 200 ppm (606 mg/m(3)) TWA; 250 ppm (757 mg/m(3)).
    B) NAIL POLISH REMOVERS: In a retrospective study of exposures to methyl acetate-containing nail polish removers (n=83), 75% of patients did not develop any toxic effects. Minor effects developed in 25% of cases. In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers and remained asymptomatic.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) CAT: Inhalation exposure to about 54,000 ppm (163 mg/L) was lethal to cats within 1 to 9 minutes (ACGIH, 1991).
    2) MOUSE: After 10 to 20 minutes of inhalation exposure at 55,440 ppm, immediate irritation, dyspnea, narcosis, and death (from pulmonary edema) were reported (Bingham et al, 2001).
    3) RAT: A concentration of 35,000 ppm in air is lethal to rats (OHM/TADS , 2002).

Maximum Tolerated Exposure

    A) Human exposure to 10,000 ppm (or 30 mg/L) for a short period of time resulted in eye, nose, and throat irritation, which persisted after cessation of exposure (Hazardous Substances Data Bank (HSDB), 2005; Hathaway et al, 1996). Industrial exposures at or below 200 ppm did not cause any irritation or systemic injury (Hazardous Substances Data Bank (HSDB), 2005).
    B) At a level of 3100 ppm, methyl acetate is considered to be immediately dangerous to life or health (IDLH), based on 10% of the lower explosion limit for safety considerations. However, other sources indicated the irreversible health effects of impairment of escape existed only at higher concentrations (Hazardous Substances Data Bank (HSDB), 2005; National Institute for Occupational Safety and Health, 2007).
    C) ACGIH Threshold Limit Value (TLV): 200 ppm (606 mg/m(3)) TWA; 250 ppm (757 mg/m(3)) (Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011). The recommended airborne exposure limit averaged over an 8-hour workshift: 200 ppm. The short-term exposure limits: 250 ppm (New Jersey Department of Health and Senior Services, 2003).
    D) NIOSH Recommended Exposure Limit (REL): 200 ppm (610 mg/m(3)) TWA; 250 ppm (760 mg/m(3)) (Occupational Safety & Health Administration (OSHA), 2012; National Institute for Occupational Safety and Health (NIOSH), 2011). The recommended airborne exposure limit averaged over an 10-hour workshift: 200 ppm. The short-term exposure limits, not to exceed during any 15 minute work period: 250 ppm (New Jersey Department of Health and Senior Services, 2003).
    E) After short inhalation exposure at 4950 ppm, ocular and respiratory irritation were reported in humans (Bingham et al, 2001).
    F) NAIL POLISH REMOVERS
    1) In the United States, methyl acetate containing nail polish removers are available in 2 to 16-ounce (59 to 473 mL) containers.
    2) CALCULATION: Calculations based on the theoretical conversion of methyl acetate to methanol appear to overestimate the likelihood of toxicity. In the International Programme on Chemical Safety (IPCS) report on methanol, the lowest lethal dose of methanol in humans was 0.3 to 1 g/kg body weight. Based on this, the lowest lethal dose in a 10-kg child would be 3 g (or 0.09 mol) methanol, produced from the metabolism of 0.09 mole or 6.9 g of methyl acetate. Therefore, the lethal dose for a 10 kg child could be as low as be 14 g (equivalent to 14 mL) of nail polish remover containing 50% w/w methyl acetate. The Danish EPA reported that methanol poisoning may theoretically occur in children following an ingestion of methyl acetate-containing nail polish remover (European Commission, 2003). However, methanol toxicity has not been reported in children with inadvertent/exploratory ingestions of methyl acetate containing nail polish removers, or in the few adult cases of deliberate ingestion that have been published (Minns et al, 2013).
    a) One retrospective study evaluated 83 cases of exposure to these methyl acetate-containing nail polish removers; 75 patients were 5 years and younger; 4 children were 6 years and older; 4 patients were adults. In most cases, the amount of nail polish remover ingested was unknown, and only 11 (13%) patients ingested more than a mouthful. Four adults ingested "a mouthful" to 150 mL of non-acetone nail polish removers. Overall, 75% (n=62) of patients were referred to a healthcare facility; 75% did not develop any effects. Minor effects developed in 25% of cases and these effects included vomiting (n=12; 14%), throat/oral irritation (n=5; 6%), drowsiness (n=1; 1.2%), abdominal pain (n=1; 1.2%), and ataxia (n=1; 1.2%). A 2-year-old boy developed mild metabolic acidosis (serum bicarbonate 17 mmol/L and anion gap 16) after ingesting about 12 mL of Fung-off No Lift fungal liquid for nails. Acidosis resolved spontaneously and no other effects were reported. Two adults and an adolescent ingested 150 mL, half a bottle, and 80 mL, respectively, one developed only minor throat irritation and the other two remained asymptomatic(Minns et al, 2013).
    G) ANIMAL DATA
    1) CAT: Cats exposed to 5000 ppm methyl acetate experienced ocular irritation and salivation within 20 minutes; after inhaling 18,500 ppm, the cats developed dyspnea, convulsions, and narcosis with slow recovery (ACGIH, 1991).
    2) CAT: Repeated inhalation exposures of cats to methyl acetate at 6600 ppm for 8 days resulted in weight loss, weakness, hematologic changes, and pulmonary irritation. Some deaths were also reported (ACGIH, 1991).
    3) CAT: After 20 minutes of inhalation exposure at 5000 ppm, eye irritation and salivation were reported in cats (Bingham et al, 2001).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) In one study, methyl acetate 15 mL was applied to the skin of the forearm of 4 volunteers and blood samples were obtained prior to and immediately after application. Gas chromatography was used to determine the concentrations of methyl acetate in blood. Methyl acetate blood concentrations ranged from 0.9 mcg/mL 1 hour after application to as high as 3.8 mcg/mL 2 hours after application (Heldreth et al, 2012).

Workplace Standards

    A) ACGIH TLV Values for CAS79-20-9 (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) Methyl acetate
    a) TLV:
    1) TLV-TWA: 200 ppm
    2) TLV-STEL: 250 ppm
    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): Headache; eye and URT irr; ocular nerve dam
    d) Molecular Weight: 74.08
    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) Under Study
    1) Methyl acetate
    a) TLV:
    1) TLV-TWA:
    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):
    d) Molecular Weight:
    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 CAS79-20-9 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Methyl acetate
    2) REL:
    a) TWA: 200 ppm (610 mg/m(3))
    b) STEL: 250 ppm (760 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 3100 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 CAS79-20-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methyl acetate
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methyl acetate
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Methyl acetate
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS79-20-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Methyl acetate
    2) Table Z-1 for Methyl acetate:
    a) 8-hour TWA:
    1) ppm: 200
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 610
    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) LD50- (ORAL)RAT:
    1) >5 g/kg (RTECS , 2002; OHM/TADS , 2002; ITI, 1995a)
    2) 6970 mg/kg for 14D (OHM/TADS , 2002)
    B) TCLo- (INHALATION)HUMAN:
    1) 15,000 mg/m(3) -- caused lacrimation; affected respiratory system (RTECS , 2002; OHM/TADS , 2002; ITI, 1995a)

Toxicologic Mechanism

    A) Following ingestion and inhalation of methyl acetate, it is hydrolyzed rapidly to methanol and acetic acid (Hazardous Substances Data Bank (HSDB), 2005). In vitro, methyl acetate was stoichiometrically rapidly hydrolyzed to methanol. Approximately 60% of methyl acetate added to blood was converted to methanol in 2 hours and almost all of it disappeared in 8 hours (Mizunuma et al, 1992). Methanol is an alcohol that is metabolized to formaldehyde and formic acid via alcohol dehydrogenase and aldehyde dehydrogenase, respectively. Formic acid causes a metabolic acidosis and causes blindness through direct retinal toxicity. Toxicity is most common after ingestion but has been reported with inhalation and dermal exposures. The risk of methanol poisoning from an ingestion of nail polish remover is low (Liesivuori & Savolainen, 1991; Hantson et al, 2005; Osterloh et al, 1996).

Physical Characteristics

    A) Methyl acetate is a colorless volatile liquid that is lighter than water (AAR, 2000; (Lewis, 2000). It has a mild sweet, fragrant, fruity , and pleasing odor and a fleeting, fruity taste (HSDB , 2002; Lewis, 1998).

Molecular Weight

    A) 74.08

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