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METHYL VINYL KETONE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Methyl vinyl ketone is used as an alkylating agent, a beginning compound in plastics synthesis (vinyl resins), a component of ionomer resins, and a chemical intermediate in the synthesis of vitamin A and steroids.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C4-H6-O

Available Forms Sources

    A) FORMS
    1) Methyl vinyl ketone occurs as a colorless to light yellow, flammable liquid with a pungent, powerfully irritating odor (HSDB , 1993).
    2) Methyl vinyl ketone is available in a grade of 98.5 percent purity (CHRIS , 1993).
    B) USES
    1) Methyl vinyl ketone is used as an alkylating agent, a beginning compound in plastics synthesis (vinyl resins), a component of ionomer resins, and a chemical intermediate in the synthesis of vitamin A and steroids (Budavari, 1989; Sax & Lewis, 1989; Sax & Lewis, 1987) AAR, 1987; (Grant, 1986; CHRIS , 1993; EPA, 1985; HSDB , 1993).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Methyl vinyl ketone is a colorless to light yellow, flammable liquid with a pungent, powerfully irritating odor which is used as an alkylating agent, a beginning compound in plastics synthesis (vinyl resins), a component of ionomer resins, and a chemical intermediate in the synthesis of vitamin A and steroids.
    1) Methyl vinyl ketone can be readily absorbed through the skin, and is severely irritating to the skin (sometimes with blistering), eyes, and mucous membranes. The vapors are heavier than air, and the liquid is both lighter than water and soluble in water. It may also be absorbed following ingestion or inhalation.
    a) Hazardous polymerization may occur, especially if this material is heated in a container or on standing. Up to 1% hydroquinone may be added as a polymerization inhibitor. Methyl vinyl ketone is available in a grade of 98.5% purity.
    B) Ketones are hydrocarbons with the general structural formula of (R-CO-R) (where "R" represents various functional groups). Because of good solvent properties, low cost factors, and generally low toxicity, ketones are frequently used as chemical intermediates and solvents for lacquers, vinyl polymers, resins, cotton, dyes, and pigments.
    1) The primary toxicity of the ketones is as central nervous system depressants and mild irritants of the eyes, skin, and mucous membranes.
    2) Various ketones are absorbed by ingestion, inhalation, and dermal exposure. Absorption through the skin of toxic amounts of ketones is common and rapid.
    3) Animals exposed to HIGH concentrations of most of the ketones sustained damage to lungs (emphysema), liver, kidneys, and brain (edema), but such has not been found in long term occupational epidemiologic studies in humans.
    C) Exposure to ketone solvents should be generally be managed as HYDROCARBON exposures (Refer to the HYDROCARBONS MEDITEXT Medical Management for more information).
    1) The LOWER the VISCOSITY of the involved solvent, the more readily it can penetrate deeply into the pulmonary tree after aspiration; also the greater the likelihood of serious pneumonitis.
    D) The minimal toxic or lethal dose of various ketones are not well established in the literature. Estimation of the severity of intoxication should be based primarily on clinical findings.
    E) For most ketone compounds, the exposures required for development of such effects as peripheral neuropathies and hepatotoxicity are well above those generally found in the workplace.
    F) Methyl vinyl ketone releases irritating acrid smoke and fumes when heated to decomposition.
    0.2.3) VITAL SIGNS
    A) Hypothermia may be noted.
    0.2.4) HEENT
    A) Eye exposure may result in ocular pain or irritation, lacrimation, and corneal damage. Ketones are generally irritants of mucous membranes, especially of the nose and mouth, and can cause sore throat, coughing, and salivation.
    0.2.5) CARDIOVASCULAR
    A) Tachycardia or cardiac dysrhythmias may be noted. In severe ketone poisoning cases, death may be due to cardiorespiratory failure.
    0.2.6) RESPIRATORY
    A) Direct aspiration of liquid ketones into the lungs can result in chemical pneumonia. Ingestion of hydrocarbon-based solvents is usually associated with nausea and vomiting, which may increase the risk of pulmonary aspiration of gastric contents with resultant severe lipoid pneumonitis and potential chronic subclinical pulmonary function abnormalities.
    1) Exposure can produce an anesthetic type of respiratory depression, dyspnea, and gasping. Methyl vinyl ketone is severely irritating to the mucous membranes of the respiratory tract. Serious lung irritation with pulmonary edema could occur.
    0.2.7) NEUROLOGIC
    A) Inhalation of high concentrations of ketones produce CNS depressant effects, including headache, dizziness, fainting, tremor, incoordination, lowered body temperature, depressed respirations and heart rate, dyspnea, gasping, coma, and death. Skin exposure to vapor or liquid may result in paresthesia of affected areas.
    0.2.8) GASTROINTESTINAL
    A) Inhalation may cause nausea and vomiting. Ingestion of hydrocarbon-based solvents is usually associated with nausea and vomiting, which may increase the risk of pulmonary aspiration of gastric contents. Methyl vinyl ketone is very irritating, and would be predicted to result in esophageal or gastrointestinal tract irritation or burns following ingestion.
    0.2.9) HEPATIC
    A) Ketones have been shown to potentiate the hepatotoxic effects of halogenated hydrocarbons (eg, chloroform and carbon tetrachloride).
    0.2.14) DERMATOLOGIC
    A) Skin exposure to vapor or liquid may result in dermatoses and paresthesia of affected area. Methyl vinyl ketone can be readily absorbed through the skin, and is severely irritating to the skin (sometimes causing blistering).
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    C) No information about possible male reproductive effects was found in available references at the time of this review.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) No biological monitoring parameters for exposed humans were established at the time of this review.
    B) The urine can be tested for an increase in conjugated glucuronic acid.
    C) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    B) As the major problem following ingestion of ketone- or hydrocarbon-based solvents is usually pulmonary aspiration with resultant pneumonitis, induced emesis, activated charoal, and gastric lavage are NOT RECOMMENDED.
    C) Correct severe acidosis with intravenous sodium bicarbonate. About 1 to 2 mEq/kg is a useful starting dose. Monitor blood gases to guide bicarbonate therapy.
    D) Ingestions of ketone solvents should be managed as with HYDROCARBONS. Refer to the HYDROCARBONS MEDITEXT(R) Medical Management for more information.
    E) Monitoring the chest x-ray and arterial blood gases (when indicated) should be done if pulmonary aspiration or pulmonary edema are suspected. Monitor ECG.
    F) If CNS or respiratory depression are present, ensure adequacy of respirations and oxygenation. Endotracheal intubation and assisted ventilation with supplemental oxygenation may be required.
    G) Routine administration of antibiotics and steroids when aspiration has occurred has generally been shown NOT to be useful; steroids may increase the risk of superinfection, and antibiotics should be reserved for suspected or proven infectious complications of pneumonitis.
    H) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    I) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    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.
    B) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    C) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    D) Monitoring the chest x-ray and arterial blood gases (when indicated) should be done if pulmonary aspiration or pulmonary edema are suspected. Monitor ECG.
    E) If CNS or respiratory depression are present, ensure adequacy of respirations and oxygenation. Endotracheal intubation and assisted ventilation with supplemental oxygenation may be required.
    F) Routine administration of antibiotics and steroids when aspiration has occurred has generally been shown NOT to be useful; steroids may increase the risk of superinfection, and antibiotics should be reserved for suspected or proven infectious complications of pneumonitis.
    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.
    B) Corneal burns or damage may occur. Prolonged initial flushing and early ophthalmologic consultation are advisable.
    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).
    2) Methyl vinyl ketone may be absorbed following dermal contact.
    a) If systemic toxicity should occur following dermal exposure -
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    3) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Minimum lethal human exposure is unknown.

Clinical Effects

Summary Of Exposure

    A) Methyl vinyl ketone is a colorless to light yellow, flammable liquid with a pungent, powerfully irritating odor which is used as an alkylating agent, a beginning compound in plastics synthesis (vinyl resins), a component of ionomer resins, and a chemical intermediate in the synthesis of vitamin A and steroids.
    1) Methyl vinyl ketone can be readily absorbed through the skin, and is severely irritating to the skin (sometimes with blistering), eyes, and mucous membranes. The vapors are heavier than air, and the liquid is both lighter than water and soluble in water. It may also be absorbed following ingestion or inhalation.
    a) Hazardous polymerization may occur, especially if this material is heated in a container or on standing. Up to 1% hydroquinone may be added as a polymerization inhibitor. Methyl vinyl ketone is available in a grade of 98.5% purity.
    B) Ketones are hydrocarbons with the general structural formula of (R-CO-R) (where "R" represents various functional groups). Because of good solvent properties, low cost factors, and generally low toxicity, ketones are frequently used as chemical intermediates and solvents for lacquers, vinyl polymers, resins, cotton, dyes, and pigments.
    1) The primary toxicity of the ketones is as central nervous system depressants and mild irritants of the eyes, skin, and mucous membranes.
    2) Various ketones are absorbed by ingestion, inhalation, and dermal exposure. Absorption through the skin of toxic amounts of ketones is common and rapid.
    3) Animals exposed to HIGH concentrations of most of the ketones sustained damage to lungs (emphysema), liver, kidneys, and brain (edema), but such has not been found in long term occupational epidemiologic studies in humans.
    C) Exposure to ketone solvents should be generally be managed as HYDROCARBON exposures (Refer to the HYDROCARBONS MEDITEXT Medical Management for more information).
    1) The LOWER the VISCOSITY of the involved solvent, the more readily it can penetrate deeply into the pulmonary tree after aspiration; also the greater the likelihood of serious pneumonitis.
    D) The minimal toxic or lethal dose of various ketones are not well established in the literature. Estimation of the severity of intoxication should be based primarily on clinical findings.
    E) For most ketone compounds, the exposures required for development of such effects as peripheral neuropathies and hepatotoxicity are well above those generally found in the workplace.
    F) Methyl vinyl ketone releases irritating acrid smoke and fumes when heated to decomposition.

Vital Signs

    3.3.1) SUMMARY
    A) Hypothermia may be noted.
    3.3.3) TEMPERATURE
    A) Hypothermia may be noted (Sittig, 1991).

Heent

    3.4.1) SUMMARY
    A) Eye exposure may result in ocular pain or irritation, lacrimation, and corneal damage. Ketones are generally irritants of mucous membranes, especially of the nose and mouth, and can cause sore throat, coughing, and salivation.
    3.4.3) EYES
    A) CORNEAL DAMAGE - Eye exposure may result in ocular pain and corneal damage (Finkel, 1983; Clayton & Clayton, 1982; Grant, 1986; EPA, 1985). Direct contact of the liquid with eyes may cause corneal damage (Grant, 1986; EPA, 1985).
    B) IRRITATION - Lacrimation and ocular irritation may be noted following exposure to high vapor concentrations (Parmeggiani, 1983; Finkel, 1983; Clayton & Clayton, 1982; Grant, 1986; EPA, 1985; Lewis, 1996; Sittig, 1991).
    3.4.5) NOSE
    A) IRRITATION - Ketones are generally irritants of mucous membranes, especially of the nose (Ellenhorn & Barceloux, 1988; Finkel, 1983; Clayton & Clayton, 1982). Sneezing may occur (Sittig, 1991).
    1) Methyl vinyl ketone can be readily absorbed through the skin, and is severely irritating to the skin (sometimes with blistering), eyes, and mucous membranes (Budavari, 1996; Lewis, 1996) Grant, 1996; CHRIS, 1996; (EPA, 1985) HSDB, 1996).
    3.4.6) THROAT
    A) IRRITATION - The ketones are generally irritants of mucous membranes (Ellenhorn & Barceloux, 1988; Finkel, 1983; Clayton & Clayton, 1982), especially of the mouth, and can cause sore throat, coughing, and salivation.
    1) Methyl vinyl ketone can be readily absorbed through the skin, and is severely irritating to the skin (sometimes with blistering), eyes, and mucous membranes (Budavari, 1996; Lewis, 1996; Grant, 1986) CHRIS, 1996; (EPA, 1985) HSDB, 1996).

Cardiovascular

    3.5.1) SUMMARY
    A) Tachycardia or cardiac dysrhythmias may be noted. In severe ketone poisoning cases, death may be due to cardiorespiratory failure.
    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) Tachycardia may be noted.
    B) CONDUCTION DISORDER OF THE HEART
    1) Cardiac dysrhythmias have been noted with exposure to some hydrocarbon-based solvents (Ervin & Manske, 1990).
    C) HEART FAILURE
    1) In severe ketone poisoning cases, death may be due to cardiorespiratory failure (Clayton & Clayton, 1982).

Respiratory

    3.6.1) SUMMARY
    A) Direct aspiration of liquid ketones into the lungs can result in chemical pneumonia. Ingestion of hydrocarbon-based solvents is usually associated with nausea and vomiting, which may increase the risk of pulmonary aspiration of gastric contents with resultant severe lipoid pneumonitis and potential chronic subclinical pulmonary function abnormalities.
    1) Exposure can produce an anesthetic type of respiratory depression, dyspnea, and gasping. Methyl vinyl ketone is severely irritating to the mucous membranes of the respiratory tract. Serious lung irritation with pulmonary edema could occur.
    3.6.2) CLINICAL EFFECTS
    A) PNEUMONIA
    1) Direct aspiration of liquid ketones into the lungs can result in chemical pneumonia (Ervin & Manske, 1990; Sittig, 1991).
    2) Ingestion of hydrocarbon-based solvents is usually associated with nausea and vomiting, which may increase the risk of pulmonary aspiration of gastric contents with resultant pneumonitis and potential chronic subclinical pulmonary function abnormalities (Shannon, 1991).
    B) ACUTE RESPIRATORY INSUFFICIENCY
    1) Exposure can produce an anesthetic type of respiratory depression (Ervin & Manske, 1990; Shannon, 1991), dyspnea, and gasping.
    C) IRRITATION SYMPTOM
    1) Methyl vinyl ketone is severely irritating to the mucous membranes of the respiratory tract (Lewis, 1996; Grant, 1986) CHRIS, 1996; (EPA, 1985) HSDB, 1996).
    D) ACUTE LUNG INJURY
    1) Serious lung irritation with pulmonary edema could occur (EPA, 1985).

Neurologic

    3.7.1) SUMMARY
    A) Inhalation of high concentrations of ketones produce CNS depressant effects, including headache, dizziness, fainting, tremor, incoordination, lowered body temperature, depressed respirations and heart rate, dyspnea, gasping, coma, and death. Skin exposure to vapor or liquid may result in paresthesia of affected areas.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Inhalation of high concentrations of ketones produce CNS depressant effects (Ellenhorn & Barceloux, 1988) Ervin & Manske, 1991; (Finkel, 1983; Clayton & Clayton, 1982; EPA, 1985). Effects include headache, dizziness, fainting, tremor, incoordination, lowered body temperature, depressed respirations and heart rate, dyspnea, gasping, coma, and death (Clayton & Clayton, 1982; Sittig, 1991).
    B) PARESTHESIA
    1) Skin exposure to vapor or liquid may result in paresthesia of affected areas.

Gastrointestinal

    3.8.1) SUMMARY
    A) Inhalation may cause nausea and vomiting. Ingestion of hydrocarbon-based solvents is usually associated with nausea and vomiting, which may increase the risk of pulmonary aspiration of gastric contents. Methyl vinyl ketone is very irritating, and would be predicted to result in esophageal or gastrointestinal tract irritation or burns following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Inhalation may cause nausea and vomiting (Browning, 1965; Parmeggiani, 1983; Sittig, 1991). Ingestion of hydrocarbon-based solvents is usually associated with nausea and vomiting, which may increase the risk of pulmonary aspiration of gastric contents (Shannon, 1991).
    B) GASTROINTESTINAL IRRITATION
    1) Methyl vinyl ketone is very irritating, and would be predicted to result in esophageal or gastrointestinal tract irritation or burns following ingestion (EPA, 1985).

Hepatic

    3.9.1) SUMMARY
    A) Ketones have been shown to potentiate the hepatotoxic effects of halogenated hydrocarbons (eg, chloroform and carbon tetrachloride).
    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) Ketones have been shown to potentiate the hepatotoxic effects of halogenated hydrocarbons (eg, chloroform and carbon tetrachloride) (Plaa & Vezina, 1987).

Dermatologic

    3.14.1) SUMMARY
    A) Skin exposure to vapor or liquid may result in dermatoses and paresthesia of affected area. Methyl vinyl ketone can be readily absorbed through the skin, and is severely irritating to the skin (sometimes causing blistering).
    3.14.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) Skin exposure to vapor or liquid may result in dermatoses and paresthesia of affected area. Skin irritation may occur with direct contact (Ellenhorn & Barceloux, 1988; Finkel, 1983; Clayton & Clayton, 1982).
    B) SKIN ABSORPTION
    1) Many ketones are absorbed through the skin (Clayton & Clayton, 1982).
    C) SKIN IRRITATION
    1) Methyl vinyl ketone can be readily absorbed through the skin, and is severely irritating to the skin (sometimes causing blistering) (Budavari, 1996; Lewis, 1996; Grant, 1986) CHRIS, 1996; (EPA, 1985) HSDB, 1996; (Sittig, 1991).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    B) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    C) No information about possible male reproductive effects was found in available references at the time of this review.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS78-94-4 (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) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) Methyl vinyl ketone induced mutations in S. typhimurium (Ames Test). It was a strong inhibitor of cell division in E. coli, possibly by interference with thiol compounds necessary for cell division and gene control.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No biological monitoring parameters for exposed humans were established at the time of this review.
    B) The urine can be tested for an increase in conjugated glucuronic acid.
    C) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No biological monitoring parameters for exposed humans were established at the time of this review.
    B) The urine can be tested for an increase in conjugated glucuronic acid.
    C) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) As the major problem following ingestion of ketone- or hydrocarbon-based solvents is usually pulmonary aspiration with resultant pneumonitis, induced emesis, activated charoal, and gastric lavage are NOT RECOMMENDED(Shannon, 1991).
    6.5.3) TREATMENT
    A) 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.
    B) SOLVENT
    1) Ketone Solvents - Ingestions of ketone solvents should be managed as with HYDROCARBONS.
    C) MONITORING OF PATIENT
    1) Monitoring the chest x-ray and arterial blood gases (when indicated) should be done if pulmonary aspiration or pulmonary edema are suspected.
    2) Monitor ECG.
    D) SUPPORT
    1) If CNS or respiratory depression are present, ensure adequacy of respirations and oxygenation. Endotracheal intubation and assisted ventilation with supplemental oxygenation may be required.
    2) Routine administration of antibiotics and steroids when aspiration has occurred has generally been shown NOT to be useful; steroids may increase the risk of superinfection, and antibiotics should be reserved for suspected or proven infectious complications of pneumonitis (Ervin & Manske, 1990).
    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).
    F) IRRITATION SYMPTOM
    1) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.

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.
    6.7.2) TREATMENT
    A) 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).
    B) BRONCHOSPASM
    1) BRONCHOSPASM SUMMARY
    a) Administer beta2 adrenergic agonists. Consider use of inhaled ipratropium and systemic corticosteroids. Monitor peak expiratory flow rate, monitor for hypoxia and respiratory failure, and administer oxygen as necessary.
    2) ALBUTEROL/ADULT DOSE
    a) 2.5 to 5 milligrams diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response, administer 2.5 to 10 milligrams every 1 to 4 hours as needed OR administer 10 to 15 milligrams every hour by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.5 milligram by nebulizer every 30 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    3) ALBUTEROL/PEDIATRIC DOSE
    a) 0.15 milligram/kilogram (minimum 2.5 milligrams) diluted with 4 milliliters of 0.9% saline by nebulizer every 20 minutes for three doses. If incomplete response administer 0.15 to 0.3 milligram/kilogram (maximum 10 milligrams) every 1 to 4 hours as needed OR administer 0.5 mg/kg/hr by continuous nebulizer as needed. Consider adding ipratropium to the nebulized albuterol; DOSE: 0.25 to 0.5 milligram by nebulizer every 20 minutes for three doses then every 2 to 4 hours as needed, NOT administered as a single agent (National Heart,Lung,and Blood Institute, 2007).
    4) ALBUTEROL/CAUTIONS
    a) The incidence of adverse effects of beta2-agonists may be increased in older patients, particularly those with pre-existing ischemic heart disease (National Asthma Education and Prevention Program, 2007). Monitor for tachycardia, tremors.
    5) CORTICOSTEROIDS
    a) Consider systemic corticosteroids in patients with significant bronchospasm. PREDNISONE: ADULT: 40 to 80 milligrams/day in 1 or 2 divided doses. CHILD: 1 to 2 milligrams/kilogram/day (maximum 60 mg) in 1 or 2 divided doses (National Heart,Lung,and Blood Institute, 2007).
    C) MONITORING OF PATIENT
    1) Monitoring the chest x-ray and arterial blood gases (when indicated) should be done if pulmonary aspiration or pulmonary edema are suspected.
    2) Monitor ECG.
    D) SUPPORT
    1) If CNS or respiratory depression are present, ensure adequacy of respirations and oxygenation. Endotracheal intubation and assisted ventilation with supplemental oxygenation may be required.
    2) Routine administration of antibiotics and steroids when aspiration has occurred has generally been shown NOT to be useful; steroids may increase the risk of superinfection, and antibiotics should be reserved for suspected or proven infectious complications of pneumonitis (Ervin & Manske, 1990).
    E) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) CONSULTATION - Serious corneal injury may follow direct splash exposures. Prolonged initial flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) SKIN ABSORPTION
    1) Methyl vinyl ketone may be absorbed following dermal contact.
    2) If systemic toxicity should occur following dermal exposure -
    a) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    B) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    C) BURN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) Minimum lethal human exposure is unknown.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.

Workplace Standards

    A) ACGIH TLV Values for CAS78-94-4 (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 vinyl ketone
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 0.2 ppm
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: SEN, Skin
    3) Definitions:
    a) SEN: The designation SEN refers to the potential for an agent to produce sensitization, as confirmed by human or animal data. The notation does not imply that this is the critical effect or that this is the sole basis for the TLV. Although, for those TLVs that are based on sensitization, the TLV is meant to protect workers from induction of this effect, but cannot protect workers who have already become sensitized. The notation should be used to assist in identifying sensitization hazards and reducing respiratory, dermal, and conjunctival exposures to sensitizing agents in the workplace. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    b) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): URT and eye irr; CNS impair
    d) Molecular Weight: 70.1
    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 CAS78-94-4 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS78-94-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Methyl vinyl ketone
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    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
    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 CAS78-94-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: (RTECS, 1996; EPA, 1985
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 76 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 23300 mcg/kg
    3) LD50- (ORAL)RAT:
    a) 23100 mcg/kg

Physicochemical

Physical Characteristics

    A) Methyl vinyl ketone is a colorless to light yellow liquid with a strong irritating odor (CHRIS, 1996; (Lewis, 1996).
    B) Pungent odor (Budavari, 1989).

Molecular Weight

    A) 70.09 (Budavari, 1996)

Other

    A) ODOR THRESHOLD
    1) 0.5 mg/m3 (CHRIS , 2002)

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