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BIS(CHLOROMETHYL)KETONE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Bis(chloromethyl)ketone occurs as plate or needle-like crystals and is soluble in water.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C3-H4-Cl2-O

Available Forms Sources

    A) FORMS
    1) Bis(chloromethyl)ketone occurs as plate or needle-like crystals and is soluble in water (Budavari, 1996; Lewis, 1996; EPA, 1985).
    B) USES
    1) Bis (chloromethyl)ketone is a solid material used in polyurethane foams, backcoating for textiles, and in adhesives. It was formerly used in textiles such as polyester fabrics (EPA, 1985).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Bis(chloromethyl)ketone is a plate- or needle-like, water soluble, crystalline solid material. It is a lacrimator and vesicant agent, and may be absorbed systemically following ingestion, inhalation, or through intact skin.
    1) Bis(chloromethyl)ketone is used in polyurethane foams, backcoating for textiles, and in adhesives; it was formerly used in textiles such as polyester fabrics.
    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, generally low flammability, 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 lipoid 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) Bis(chloromethyl)ketone releases toxic and irritating fumes of chlorides when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
    0.2.3) VITAL SIGNS
    A) Hypothermia and tachycardia may be noted.
    0.2.4) HEENT
    A) Eye exposure may result in ocular pain and corneal damage. Lacrimation and ocular irritation may be noted following exposure to high vapor concentrations. The ketones are generally irritants of mucous membranes, especially of the mouth, and can cause sore throat, coughing, and salivation.
    0.2.5) CARDIOVASCULAR
    A) Tachycardia may be noted. Cardiac dysrhythmias have been noted with exposure to some hydrocarbon-based solvents. 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.
    B) Exposure can produce an anesthetic type of respiratory depression.
    C) Bis(chloromethyl)ketone releases toxic and irritating fumes of chlorides when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
    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.
    B) Because of the irritant nature of bis(chloromethyl)ketone, ingestion may be predicted to result in irritation or burns of the esophagus or gastrointestinal tract.
    0.2.9) HEPATIC
    A) Ketones have been shown to potentiate the hepatotoxic effects of halogenated hydrocarbons (eg, chloroform and carbon tetrachloride). Bis(chloromethyl)ketone was NOT hepatotoxic in mice.
    0.2.14) DERMATOLOGIC
    A) Skin exposure to vapor or liquid may result in dermatoses and paresthesia of affected area. Skin irritation may occur with direct contact. Vesiculation may occur. Many ketones are absorbed through the skin.
    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) URINALYSIS: 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 severe lipoid pneumonitis, INDUCED EMESIS is CONTRAINDICATED and ACTIVATED CHARCOAL is often NOT RECOMMENDED because of the potential for induction of vomiting.
    1) If the involved ketone- or hydrocarbon-based is of LOW VISCOSITY, GASTRIC LAVAGE is also NOT RECOMMENDED because of the potential for the solvent to "wick" up along the lavage tube and be regurgitated into the trachea.
    C) ADMINISTRATION - of olive or mineral OIL in an attempt to increase viscosity and provide cathartic action SHOULD NOT BE DONE.
    D) Correct acidosis with kilogram intravenous sodium bicarbonate. About 1 to 2 mEq/kg is a useful starting dose. Monitor blood gases to guide bicarbonate therapy.
    E) Ingestions of ketone solvents should be managed as with HYDROCARBONS (TOMES Plus system users may refer to the HYDROCARBONS MEDITEXT Medical Management for more information.)
    F) Monitoring the chest x-ray and arterial blood gases (when indicated) should be done if pulmonary aspiration or pulmonary edema are suspected. Monitor EKG.
    G) If CNS or respiratory depression are present, ensure adequacy of respirations and oxygenation. Endotracheal intubation and assisted ventilation with supplemental oxygenation may be required.
    H) 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 lipoid pneumonitis.
    I) 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.
    J) 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 EKG.
    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 lipoid 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) Bis(chloromethyl)ketone is a plate- or needle-like, water soluble, crystalline solid material. It is a lacrimator and vesicant agent, and may be absorbed systemically following ingestion, inhalation, or through intact skin.
    1) Bis(chloromethyl)ketone is used in polyurethane foams, backcoating for textiles, and in adhesives; it was formerly used in textiles such as polyester fabrics.
    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, generally low flammability, 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 lipoid 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) Bis(chloromethyl)ketone releases toxic and irritating fumes of chlorides when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.

Vital Signs

    3.3.1) SUMMARY
    A) Hypothermia and tachycardia may be noted.
    3.3.3) TEMPERATURE
    A) Hypothermia may be noted (Clayton & Clayton, 1982).
    3.3.5) PULSE
    A) Tachycardia may be noted.

Heent

    3.4.1) SUMMARY
    A) Eye exposure may result in ocular pain and corneal damage. Lacrimation and ocular irritation may be noted following exposure to high vapor concentrations. The ketones are generally irritants of mucous membranes, especially of the 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). Direct contact of the liquid with eyes may cause corneal damage.
    B) IRRITATION - Lacrimation and ocular irritation may be noted following exposure to high vapor concentrations (Parmeggiani, 1983; Finkel, 1983; Clayton & Clayton, 1982; EPA, 1985; Sax & Lewis, 1989; Budavari, 1996).
    3.4.5) NOSE
    A) IRRITATION - Ketones are generally irritants of mucous membranes, especially of the nose (Ellenhorn & Barceloux, 1988; Finkel, 1983; Clayton & Clayton, 1994). Sneezing may occur.
    3.4.6) THROAT
    A) IRRITATION - The ketones are generally irritants of mucous membranes (Ellenhorn & Barceloux, 1988; Finkel, 1983; Clayton & Clayton, 1994), especially of the mouth, and can cause sore throat, coughing, and salivation.

Cardiovascular

    3.5.1) SUMMARY
    A) Tachycardia may be noted. Cardiac dysrhythmias have been noted with exposure to some hydrocarbon-based solvents. 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) CARDIAC ARREST
    1) In severe ketone poisoning cases, death may be due to cardiorespiratory failure (Clayton & Clayton, 1994).

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.
    B) Exposure can produce an anesthetic type of respiratory depression.
    C) Bis(chloromethyl)ketone releases toxic and irritating fumes of chlorides when heated to decomposition. Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) PNEUMONIA
    1) Direct aspiration of liquid ketones into the lungs can result in chemical pneumonia (Ervin & Manske, 1990).
    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 severe lipoid 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) RESPIRATORY CONDITION DUE TO CHEMICAL FUMES AND/OR VAPORS
    1) Bis(chloromethyl)ketone releases toxic and irritating fumes of chlorides when heated to decomposition (Lewis, 1996; EPA, 1985). Inhalation exposure to such fumes would be predicted to result in respiratory tract irritation with bronchospasm, chemical pneumonitis, or noncardiogenic pulmonary edema.

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, 1994). Effects include headache, dizziness, fainting, tremor, incoordination, lowered body temperature, depressed respirations and heart rate, dyspnea, gasping, coma, and death (Clayton & Clayton, 1982; Clayton & Clayton, 1994).
    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.
    B) Because of the irritant nature of bis(chloromethyl)ketone, ingestion may be predicted to result in irritation or burns of the esophagus or gastrointestinal tract.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Inhalation may cause nausea and vomiting (Browning, 1965; Parmeggiani, 1983). 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) Because of the irritant nature of bis(chloromethyl)ketone, ingestion may be predicted to result in irritation or burns of the esophagus or gastrointestinal tract.

Hepatic

    3.9.1) SUMMARY
    A) Ketones have been shown to potentiate the hepatotoxic effects of halogenated hydrocarbons (eg, chloroform and carbon tetrachloride). Bis(chloromethyl)ketone was NOT hepatotoxic in mice.
    3.9.2) CLINICAL EFFECTS
    A) DRUG INTERACTION
    1) Ketones have been shown to potentiate the hepatotoxic effects of halogenated hydrocarbons (eg, chloroform and carbon tetrachloride) (Plaa & Vezina, 1987).
    B) LACK OF EFFECT
    1) Bis(chloromethyl)ketone was NOT hepatotoxic in mice (Laurie et al, 1986).

Dermatologic

    3.14.1) SUMMARY
    A) Skin exposure to vapor or liquid may result in dermatoses and paresthesia of affected area. Skin irritation may occur with direct contact. Vesiculation may occur. Many ketones are absorbed through the skin.
    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    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, 1994). Vesiculation may occur (Budavari, 1996; EPA, 1985) Sax & Lewis; 1989)
    B) SKIN ABSORPTION
    1) Many ketones are absorbed through the skin (Clayton & Clayton, 1994).

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 CAS534-07-6 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) 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.
    3.21.4) ANIMAL STUDIES
    A) CARCINOMA
    1) Repeated topical application of Bis(chloromethyl)ketone to SENCAR mice at 100, 200, and 400 mg/kg/dose with 6 applications over 2 weeks produced evidence of tumor initiation (Robinson et al, 1989).

Genotoxicity

    A) Bis(chloromethyl)ketone induced mutations in S. typhimurium (Ames Test) and S. cerevisiae. Sister chromatid exchange has been observed in hamster lung cells and S. cerevisiae. Sex chromosome loss/nondisjunction has been observed in D. melanogaster.
    B) Bis(chloromethyl)ketone also induced chromosome aberrations in S. cerevisiae during gene conversion and mitotic recombination. Bis(chloromethyl)ketone was cytotoxic to suspensions of male rat hepatocytes in vitro.
    C) EPA GENETOX PROGRAM 1988 -
    1) Positive: Histidine reversion-Ames test
    2) Inconclusive: D melanogaster Sex-linked lethal

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) URINALYSIS: 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) URINALYSIS: 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) DILUTION
    1) 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 (Caravati, 2004).
    B) GASTRIC EMPTYING
    1) As the major problem following ingestion of ketone- or hydrocarbon-based solvents is usually pulmonary aspiration with resultant severe lipoid pneumonitis, INDUCED EMESIS is CONTRAINDICATED and ACTIVATED CHARCOAL is often NOT RECOMMENDED because of the potential for induction of vomiting (Shannon, 1991).
    2) If the involved ketone- or hydrocarbon-based is of LOW VISCOSITY, GASTRIC LAVAGE is also NOT RECOMMENDED because of the potential for the solvent to "wick" up along the lavage tube and be regurgitated into the trachea (Ervin & Manske, 1990).
    C) CONTRAINDICATION
    1) ADMINISTRATION - of olive or mineral OIL in an attempt to increase viscosity and provide cathartic action SHOULD NOT BE DONE (Ervin & Manske, 1990).
    6.5.3) TREATMENT
    A) DILUTION
    1) 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 (Caravati, 2004).
    B) 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.
    C) GENERAL TREATMENT
    1) KETONE SOLVENTS - Ingestion of ketone solvents should be managed as with HYDROCARBONS (Refer to the HYDROCARBONS MEDITEXT(R) Medical Management for more information.)
    D) 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 EKG.
    E) 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 lipoid pneumonitis (Ervin & Manske, 1990).
    F) 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).
    G) 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) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    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 EKG.
    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 lipoid 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) OPHTHALMIC EXAMINATION AND EVALUATION
    1) CONSULTATION - Severe eye irritation might occur with direct splash injury. Prolonged early flushing and early ophthalmologic consultation may be 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) Bis(chloromethyl)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) 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.
    B) ANIMAL DATA
    1) Chronic administration in drinking water to Sprague-Dawley rats at 0, 5, 65, and 125 ppm for 90 days resulted in decreased water consumption and decreased Blood Urea Nitrogen (BUN). 5 ppm was considered to be a No Effect level (Daniel et al, 1993).

Workplace Standards

    A) ACGIH TLV Values for CAS534-07-6 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS534-07-6 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS534-07-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    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 CAS534-07-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2000
    1) LD50- (ORAL)MOUSE:
    a) 18900 mcg/kg

Physicochemical

Physical Characteristics

    A) Bis(chloromethyl)ketone is a crystalline solid that forms plates or needles on distillation (Budavari, 1996); no odor characteristics were reported in available data.

Ph

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

Molecular Weight

    A) 126.97 (Lewis, 1996)

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