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CHLOROMETHYL METHYL ETHER

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Chloromethyl methyl ether is a chlorinated methylated methyl ether.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C2-H5-Cl-O CH3OCH2Cl ClCH2OCH3 H3CO-CH2Cl

Available Forms Sources

    A) FORMS
    1) The commercial product usually contains 1% to 7% bis(chloromethyl)ether, a highly carcinogenic compound (Budavari, 1996; Sittig, 1991).
    B) SOURCES
    1) Chloromethyl methyl ether is prepared by passing hydrogen chloride through a formaldehyde and methanol mixture (Ashford, 1994; Budavari, 1996).
    C) USES
    1) Chloromethyl methyl ether is primarily used as a chemical intermediate. Specifically, it is used in the preparation of ion-exchange resins, the synthesis of chloromethylated compounds, and the manufacture of water repellants and industrial polymers. It is also used as an alkylating agent and a solvent (ACGIH, 1991; Budavari, 1996) Hathaway, 1996; (HSDB , 1998; NFPA, 1997).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Chloromethyl methyl ether is irritating to the eyes, skin, and mucous membranes. Signs and symptoms following exposure may include sore throat, cough, wheezing, pulmonary congestion, bronchial secretions, blood stained sputum, weight loss, fever, and chills. Pulmonary edema, pneumonia, and skin burns and necrosis may occur. Pulmonary edema and hemorrhage and necrotizing bronchitis have occurred in experimental animals.
    B) Inhalation may cause death from noncardiogenic pulmonary edema or chemical pneumonitis. Chronic bronchitis, lung cancer, and possibly laryngeal cancer are associated with chronic inhalation exposure to chloromethyl ethers.
    C) Chloromethyl methyl ether is a suspected human carcinogen; oat cell lung cancer has been associated with chronic exposure. Its contaminant, bis-chloromethyl ether, is also a known human carcinogen.
    0.2.3) VITAL SIGNS
    A) Dyspnea and fever may occur from vapor inhalation.
    0.2.4) HEENT
    A) Severe burns of the eyes may occur upon direct contact. Chloromethyl methyl ether is a lacrimator. The vapor is irritating to the nose and throat.
    0.2.6) RESPIRATORY
    A) Noncardiogenic pulmonary edema or chemical pneumonitis may be the cause of death in acute inhalation exposure.
    0.2.14) DERMATOLOGIC
    A) Burns and necrosis of the skin may occur from direct contact with the liquid.
    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.
    0.2.21) CARCINOGENICITY
    A) SUSPECTED HUMAN CARCINOGEN - Oat cell cancer has been linked with exposure to chloromethyl methyl ether. Its contaminant, bis(chloromethyl) ether, is also a known human carcinogen.
    B) LUNG CANCER - Chloromethyl ether chronic inhalation exposure has been associated with an increased incidence of lung cancer (predominantly small or oat cell carcinomas) in humans.
    C) LARYNGEAL CANCER - Two workers with chronic inhalation exposure developed laryngeal cancer.
    D) NASAL TUMORS - Exposed experimental animals have a high incidence of nasal tumors.
    E) The impurity bis(chloromethyl) ether is a more potent carcinogen than chloromethyl ether.
    0.2.22) OTHER
    A) Chloromethyl methyl ether may be hazardous by the inhalation, dermal, or oral exposure routes.

Laboratory Monitoring

    A) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.
    B) If respiratory tract irritation is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Specific medical surveillance is required by OSHA for employees working in regulated areas where bis(chloromethyl) ether is present.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) 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.
    C) Significant esophageal or gastrointestinal tract irritation or burns may occur following ingestion. The possible benefit of early removal of some ingested material by cautious gastric lavage must be weighed against potential complications of bleeding or perforation.
    D) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    E) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    F) 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) CHRONIC EXPOSURE - A regular screening program including chest x-rays should be established for potentially exposed workers. Engineering controls and personal protective equipment should be used to decrease the risks of exposure.
    D) Chronic bronchitis should respond to standard therapy.
    E) The development of cancer requires immediate surgical and oncologic referral and evaluation.
    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).
    2) 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) The minimum lethal and maximum tolerated exposures are not well defined.

Clinical Effects

Summary Of Exposure

    A) Chloromethyl methyl ether is irritating to the eyes, skin, and mucous membranes. Signs and symptoms following exposure may include sore throat, cough, wheezing, pulmonary congestion, bronchial secretions, blood stained sputum, weight loss, fever, and chills. Pulmonary edema, pneumonia, and skin burns and necrosis may occur. Pulmonary edema and hemorrhage and necrotizing bronchitis have occurred in experimental animals.
    B) Inhalation may cause death from noncardiogenic pulmonary edema or chemical pneumonitis. Chronic bronchitis, lung cancer, and possibly laryngeal cancer are associated with chronic inhalation exposure to chloromethyl ethers.
    C) Chloromethyl methyl ether is a suspected human carcinogen; oat cell lung cancer has been associated with chronic exposure. Its contaminant, bis-chloromethyl ether, is also a known human carcinogen.

Vital Signs

    3.3.1) SUMMARY
    A) Dyspnea and fever may occur from vapor inhalation.
    3.3.2) RESPIRATIONS
    A) DYSPNEA occurs upon inhalation of the vapors (CHRIS , 1996).
    3.3.3) TEMPERATURE
    A) FEVER and chills may occur from inhalation of the vapor (CHRIS , 1996).

Heent

    3.4.1) SUMMARY
    A) Severe burns of the eyes may occur upon direct contact. Chloromethyl methyl ether is a lacrimator. The vapor is irritating to the nose and throat.
    3.4.3) EYES
    A) BURNS - Chloromethyl methyl ether may cause severe burns and necrosis of the eyes (ACGIH, 1991).
    B) LACRIMATION - The vapor is a powerful tear gas (CHRIS , 1996).
    3.4.5) NOSE
    A) IRRITATION - The vapor is irritating to the nose (CHRIS , 1996).
    3.4.6) THROAT
    A) IRRITATION - The vapor is irritating to the throat (CHRIS , 1996).

Respiratory

    3.6.1) SUMMARY
    A) Noncardiogenic pulmonary edema or chemical pneumonitis may be the cause of death in acute inhalation exposure.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Inhalation of the vapors produces dyspnea (CHRIS , 1996).
    B) ACUTE LUNG INJURY
    1) Noncardiogenic pulmonary edema with frothy exudate may be the cause of death in acute inhalation exposure (EPA, 1985).
    2) Pulmonary edema with hemorrhage and necrotizing bronchitis were produced in rats and hamsters exposed to chloromethyl methyl ether (Hathaway et al, 1991).
    C) PNEUMONITIS
    1) Chemical pneumonitis may also develop (EPA, 1985).

Dermatologic

    3.14.1) SUMMARY
    A) Burns and necrosis of the skin may occur from direct contact with the liquid.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Chloromethyl methyl ether may cause severe burns and necrosis of the skin (ACGIH, 1991). Pain and second-degree burns may occur after a few minutes of direct contact (CHRIS , 1996).

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.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) LACK OF INFORMATION
    a) 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) LACK OF INFORMATION
    a) 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 CAS107-30-2 (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) SUSPECTED HUMAN CARCINOGEN - Oat cell cancer has been linked with exposure to chloromethyl methyl ether. Its contaminant, bis(chloromethyl) ether, is also a known human carcinogen.
    B) LUNG CANCER - Chloromethyl ether chronic inhalation exposure has been associated with an increased incidence of lung cancer (predominantly small or oat cell carcinomas) in humans.
    C) LARYNGEAL CANCER - Two workers with chronic inhalation exposure developed laryngeal cancer.
    D) NASAL TUMORS - Exposed experimental animals have a high incidence of nasal tumors.
    E) The impurity bis(chloromethyl) ether is a more potent carcinogen than chloromethyl ether.
    3.21.3) HUMAN STUDIES
    A) NEOPLASM
    1) In the NTP Fifth Annual Report on Carcinogens, 1989, chloromethyl methyl ether was designated as known to be carcinogenic (RTECS , 1996).
    B) CARCINOMA
    1) SUSPECTED HUMAN CARCINOGEN - Oat cell cancer has been linked with exposure to chloromethyl methyl ether (Gower et al, 1993). Its contaminant, bis(chloromethyl) ether, is also a known human carcinogen.
    2) Fourteen cases of lung cancer were found in a group of 111 chloromethyl methyl ether workers exposed to high levels (Figueroa et al, 1973).
    3) Mortality from respiratory cancer was increased in chloromethyl ether workers (32 observed versus 11.5 expected), with a latent period of 10 to 19 years (Maher & DeFonso, 1987).
    4) In an industry-wide study of 2460 workers exposed to chloromethyl methyl ether, excess mortality from respiratory cancer was seen at two companies (Collingwood et al, 1987).
    5) The relative risk for developing lung cancer in one factory in the UK was 10.97 in persons exposed when using an older and discontinued process (McCallum et al, 1983).
    6) By 1975 a total of 47 cases of lung cancer had been found in chloromethyl methyl ether workers (Nelson, 1975).
    7) By 1989 87 deaths from respiratory cancer had been reported among 3024 persons exposed to chloromethyl methyl ether (Van Duuren, 1989).
    8) At a factory in France which used chloromethyl methyl ether to make anion exchange resins since 1958, an excess of lung cancers was found; most were oat-cell (Gowers et al, 1993).
    C) RELATED COMPOUNDS
    1) BIS(CHLOROMETHYL) ETHER - In a prospective cohort of 125 male workers with chronic industrial inhalation exposure to chloromethyl ether contaminated with small amounts of bis(chloromethyl) ether, 18 cases of lung cancer were found; 13 of these were small (oat) cell carcinomas (Weiss, 1982).
    2) The risk of developing lung cancer in this cohort was greater in nonsmokers than in cigarette smokers (Weiss, 1980).
    3) The latent period (interval from onset of exposure to time of disease) in these 14 lung cancer victims ranged from 10 to 25 years (mean 15.5 to 17 years) (Weiss, 1982).
    4) A retrospective cohort mortality study of 1827 chloromethyl ether exposed workers from 6 firms for the period 1948-1972 found an excess respiratory cancer rate only in workers at one firm where exposure was felt to be greater than in the other 5 firms studied (Pasternak et al, 1977).
    5) Three workers exposed to bis(chloromethyl) ether not from degradation of chloromethyl ether but from a reaction of gaseous formaldehyde and hydrogen chloride in a chloromethylating process developed lung tumors (2 oat cell and 1 anaplastic squamous cell carcinoma) (Roe, 1985).
    6) LARYNGEAL CANCER - Two of the 125 workers described above (Weiss, 1982) developed laryngeal cancer, with a latent period of 16 to 17 years.
    7) The carcinogenic potency of bis(chloromethyl) ether is greater than that of chloromethyl ether (ACGIH, 1991).
    3.21.4) ANIMAL STUDIES
    A) ANIMAL STUDIES
    1) In rat, mouse and hamster studies, chloromethyl methyl ether was found to be an equivocal tumorigenic agent by RTECS criteria with lung, thorax, or respiration tumors. Endocrine tumors were also observed in the rat studies. In mouse studies, chloromethyl methyl ether was also found to be neoplastic by RTECS criteria with tumors at the site of application (RTECS , 1996).
    2) NASAL TUMORS - Rats exposed to 100 ppb of bis(chloromethyl) ether developed nasal tumors (estesioneuroepitheliomas) (Leong et al, 1981).

Genotoxicity

    A) Chloromethyl methyl ether has been genotoxic at the level of DNA inhibition and damage, chromosome aberrations, and oncogenic transformation.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.
    B) If respiratory tract irritation is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Specific medical surveillance is required by OSHA for employees working in regulated areas where bis(chloromethyl) ether is present.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) OSHA MEDICAL SURVEILLANCE METHODS (OSHA, 1990) - At no cost to the employee, a program of medical surveillance shall be established and implemented for employees considered for assignment to enter regulated areas, and for authorized employees.
    b) EXAMINATIONS -
    1) Before an employee is assigned to enter a regulated area, a preassignment physical examination by a physician shall be provided. The examination shall include the personal history of the employee, family and occupational background, including genetic and environmental factors.
    2) Authorized employees shall be provided periodic physical examinations, not less often than annually, following the preassignment examination.
    3) In all physical examinations, the examining physician shall consider whether there exist conditions of increased risk, including reduced immunological competence, those undergoing treatment with steroids or cytotoxic agents, pregnancy and cigarette smoking.
    c) RECORDS -
    1) Employers of employees examined pursuant to this paragraph shall cause to be maintained complete and accurate records of all such medical examinations. Records shall be maintained for the duration of the employee's employment. Upon termination of the employee's employment, including retirement or death, or in the event that the employer ceases business without a successor, records, or notarized true copies thereof, shall be forwarded by registered mail to the Director.
    2) Records required by this paragraph shall be provided upon request to employees, designated representatives, and the Assistant Secretary in accordance with 29 CFR 1910.20 (a)-(e) and (g)-(i). These records shall also be provided upon request to the Director.
    3) Any physician who conducts a medical examination required by this paragraph shall furnish to the employer a statement of the employee's suitability for employment in the specific exposure.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) The possible development of lung cancer with chronic inhalation exposure suggests that regular screening chest x-rays might be valuable for early detection.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No specific lab work (CBC, electrolytes, urinalysis) is needed unless otherwise clinically indicated.
    B) If respiratory tract irritation is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) Specific medical surveillance is required by OSHA for employees working in regulated areas where bis(chloromethyl) ether is present.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis.
    B) GASTRIC LAVAGE
    1) Significant esophageal or gastrointestinal tract irritation or burns may occur following ingestion. The possible benefit of early removal of some ingested material by cautious gastric lavage must be weighed against potential complications of bleeding or perforation.
    2) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    3) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    4) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    5) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    6) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    C) ACTIVATED CHARCOAL/CATHARTIC
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) 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) CHRONIC POISONING
    1) The development of chronic bronchitis after long-term exposure and the relationship of lung and perhaps laryngeal cancer to chronic exposure mandate a regular screening program including chest x-rays and careful exposure prevention by engineering controls and personal protective equipment.
    2) Prevention of exposure is the primary concern.
    3) A regular screening program including chest x-rays should be undertaken for workers with potential exposure. Because of the 10-25 year latent period for tumor development (Weiss, 1982), follow-up screening should probably be continued for extended periods after termination of exposure.
    4) Chronic bronchitis would likely respond to standard therapy.
    5) CANCER - Patients developing lung or laryngeal cancer should have immediate surgical and oncologic referral and evaluation.
    C) 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 - Because of the corrosive properties of chloromethyl methyl ether, prolonged initial flushing and early ophthalmological consultation should be considered.
    B) SUPPORT
    1) Observe patients with significant eye exposure for possible development of systemic signs and symptoms and treat symptomatically.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL EXPOSURE
    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) 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.
    B) SKIN ABSORPTION
    1) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) The minimum lethal and maximum tolerated exposures are not well defined.

Minimum Lethal Exposure

    A) Chronic occupational exposure to chloromethyl methyl ether has caused fatal lung cancer in several cases (Hathaway et al, 1996; HSDB , 1998).
    1) Commercial grade chloromethyl methyl ether (CMME) contains bis(chloromethyl)ether (BCME), which is highly carcinogenic. Differentiation between the carcinogenic effects of the two compounds is difficult. However, since commercial CMME contains BCME and the hydrolysis products, formaldehyde and hydrogen chloride, may recombine to form BCME, chloromethyl methyl ether is also considered a carcinogen (Hathaway et al, 1996).

Maximum Tolerated Exposure

    A) The maximum tolerated human exposure to this agent has not been delineated.

Workplace Standards

    A) ACGIH TLV Values for CAS107-30-2 (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) Chloromethyl methyl ether
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A2
    2) Codes: L
    3) Definitions:
    a) A2: Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
    b) L: Exposure by all routes should be carefully controlled to levels as low as possible.
    c) TLV Basis - Critical Effect(s): Lung cancer
    d) Molecular Weight: 80.5
    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 CAS107-30-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Chloromethyl methyl ether
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Ca) NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    e) Skin Designation: Not Listed
    f) Note(s): See Appendix A
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS107-30-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A2 ; Listed as: Chloromethyl methyl ether
    a) A2 :Suspected Human Carcinogen: Human data are accepted as adequate in quality but are conflicting or insufficient to classify the agent as a confirmed human carcinogen; OR, the agent is carcinogenic in experimental animals at dose(s), by route(s) of exposure, at site(s), of histologic type(s), or by mechanism(s) considered relevant to worker exposure. The A2 is used primarily when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals with relevance to humans.
    2) EPA (U.S. Environmental Protection Agency, 2011): A ; Listed as: Chloromethyl methyl ether (CMME)
    a) A : Human Carcinogen.
    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): Ca ; Listed as: Chloromethyl methyl ether
    a) Ca : NIOSH considers this substance to be a potential occupational carcinogen (See Appendix A in the NIOSH Pocket Guide to Chemical Hazards).
    5) MAK (DFG, 2002): Category 1 ; Listed as: Monochlorodimethyl ether
    a) Category 1 : Substances that cause cancer in man and can be assumed to make a significant contribution to cancer risk. Epidemiological studies provide adequate evidence of a positive correlation between the exposure of humans and the occurence of cancer. Limited epidemiological data can be substantiated by evidence that the substance causes cancer by a mode of action that is relevant to man.
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): K ; Listed as: Chloromethyl Methyl Ether
    a) K : KNOWN = Known to be a human carcinogen

    D) OSHA PEL Values for CAS107-30-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Chloromethyl methyl ether; see 29 CFR 1910.1006
    2) Table Z-1 for Chloromethyl methyl ether; see 29 CFR 1910.1006:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3:
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Lewis, 1996 RTECS, 1998
    1) TCLo- (INHALATION)MOUSE:
    a) 2 ppm for 82D-I -- ETA
    2) TCLo- (INHALATION)RAT:
    a) 1 ppm for 6H/72W -- ETA

Physicochemical

Physical Characteristics

    A) Chloromethyl methyl ether is a colorless liquid that emits an irritating odor (Budavari, 1996) Hathaway, 1996; (NFPA, 1997; NIOSH , 1998).

Molecular Weight

    A) 80.51

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