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Methylene chloride (dichloromethane, DCM) is a volatile, colorless liquid with a chloroform-like odor. It has a wide variety of industrial uses, many of which are based on its solvent properties, including paint stripping, pharmaceutical manufacturing, metal cleaning and degreasing, film base production, agricultural fumigation, and plastics manufacturing. It is not known to occur naturally. Methylene chloride is metabolized to carbon monoxide in vivo and may produce phosgene, chlorine, or hydrogen chloride upon combustion.

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  1. Mechanism of toxicity

    1. Solvent effects. Like other hydrocarbons, DCM is an irritant to mucous membranes, defats the skin epithelium, and may sensitize the myocardium to the dysrhythmogenic effects of catecholamines.

    2. Anesthetic effects. Like other halogenated hydrocarbons, DCM can cause CNS depression and general anesthesia.

    3. Carbon monoxide (CO) is generated in vivo during metabolism by mixed-function oxidases (CYP2E1) in the liver. Elevated carboxyhemoglobin (CO-Hgb) levels may be delayed and prolonged, with CO-Hgb levels as high as 50% reported (see also “Carbon Monoxide”).

    4. Methylene chloride is a suspected human carcinogen (IARC Group 2B [See IARC Group 2]).

  2. Toxic dose. Toxicity may occur after inhalation or ingestion.

    1. Inhalation. The permissible exposure limit (PEL) is 25 ppm as an 8-hour time-weighted average. The ACGIH workplace threshold limit value (TLV-TWA) is 50 ppm (174 mg/m3) for an 8-hour shift, which may result in a CO-Hgb level of 3–4%. The air level considered immediately dangerous to life or health (IDLH) is 2300 ppm. The odor threshold is about 100–200 ppm.

    2. Ingestion. The acute oral toxic dose is approximately 0.5–5 mL/kg.

  3. Clinical presentation

    1. Inhalation is the most common route of exposure and may cause mucous membrane and skin irritation, nausea, vomiting, and headache. Ocular exposure can cause conjunctival irritation. Severe exposure may lead to pulmonary edema or hemorrhage, cardiac dysrhythmias, and CNS depression with respiratory arrest.

    2. Ingestion can cause corrosive injury to the GI tract and systemic intoxication. Renal and hepatic injury and pancreatitis have been reported.

    3. Dermal exposure can cause dermatitis or chemical burns, and systemic symptoms can result from skin absorption.

    4. Chronic exposure can cause bone marrow, hepatic, and renal toxicity. Methylene chloride is a known animal and a suspected human carcinogen (IARC Group 2B).

  4. Diagnosis is based on a history of exposure and clinical presentation.

    1. Specific levels

      1. Carboxyhemoglobin levels should be obtained serially as peak CO-Hgb levels may be delayed.

      2. Expired air and blood or urine levels of methylene chloride may be obtained to assess workplace exposure but are not useful in clinical management.

    2. Other useful laboratory studies include CBC, electrolytes, glucose, BUN, creatinine, liver aminotransferases, and ECG monitoring.

  5. Treatment

    1. Emergency and supportive measures

      1. Maintain an open airway and assist ventilation if necessary (See Airway and Breathing).

      2. Administer supplemental oxygen and treat coma (See Coma and stupor) and pulmonary edema (See Hypoxia) if they occur.

      3. Monitor the ECG for at least 4–6 hours and treat dysrhythmias (See QRS interval prolongation, Tachycardia, and Ventricular dysrhythmias) if they occur. Avoid the use of catecholamines (eg, epinephrine, ...

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