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Introduction

Methylene chloride (dichloromethane, DCM) is a volatile, colorless liquid with a chloroform-like odor. Even though DCM is thought to be one of the least toxic chlorinated hydrocarbons, it can cause substantial toxic effects and mortality when used improperly. It has a wide variety of industrial uses, many of which are based on its solvent properties, including paint stripping, bathtub refinishing, pharmaceutical manufacturing, metal cleaning and degreasing, adhesives, film base production, agricultural fumigation, and plastics manufacturing. Methylene chloride is metabolized to carbon monoxide in vivo and upon combustion may produce phosgene, chlorine, or hydrogen chloride.

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 ranging from mild sedation to coma.
  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. CO-Hgb levels associated with DCM are usually lower than severe exogenous exposures to CO, but a level as high as 50% has been reported (see also “Carbon Monoxide,”).
  4. Methylene chloride is a suspected human carcinogen (IARC Group 2A).

Toxic Dose

Toxicity may occur after inhalation or ingestion.

  1. Inhalation. Inhalational toxicity typically occurs when DCM is used in poorly ventilated, enclosed areas. 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 short-term exposure limit (STEL) is 125 ppm. The air level considered immediately dangerous to life or health (IDLH) is 2,300 ppm. The odor threshold is about 100-200 ppm.
  2. Ingestion. The acute oral toxic dose is approximately 0.5-5 mL/kg.

Clinical Presentation

  1. Inhalation is the most common route of exposure and may cause irritation of mucous membranes, upper airway and skin, nausea, vomiting, tachypnea, sweating, and headache. Ocular exposure may cause conjunctival irritation. Severe exposure may lead to pulmonary edema or hemorrhage, CNS and respiratory depression, and cardiac dysrhythmias.
  2. Ingestion can cause corrosive injury to the GI tract and systemic intoxication. Renal injury, hepatic injury, and pancreatitis have been reported.
  3. Dermal exposure can cause dermatitis or chemical burns. Systemic symptoms may result from prolonged skin absorption.
  4. Chronic exposure may cause bone marrow, hepatic, and renal toxicity. Methylene chloride is a known animal and a probable human carcinogen (IARC Group 2A).

Diagnosis

Is based on a history of exposure and clinical presentation.

  1. Specific levels
    1. Carboxyhemoglobin levels via co-oximetry should be obtained serially as CO-Hgb levels may have a delayed peak and prolonged elimination.
    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, cardiac troponin, and ECG monitoring.

Treatment

  1. Emergency and supportive measures
    1. Maintain an open airway and assist ventilation if necessary.
    2. Administer supplemental oxygen. Manage coma and pulmonary edema if they occur.
    3. Monitor the ECG for at least 4-6 hours and treat dysrhythmias if they occur. Avoid the use of catecholamines (eg, epinephrine, dopamine), which may precipitate cardiac dysrhythmias. Tachydysrhythmias caused by myocardial sensitization may be treated with esmolol, 0.025-0.1 mg/kg/min IV, or propranolol, 1-2 mg IV.
    4. If corrosive injury is suspected after ingestion, consult a gastroenterologist regarding possible endoscopic evaluation.
  2. Specific drugs and antidotes. Administer 100% oxygen by tight-fitting mask or endotracheal tube if the CO-Hgb level is elevated. Consider hyperbaric oxygen if the CO-Hgb level is elevated and the patient has findings of CNS toxicity.
  3. Decontamination
    1. Inhalation. Remove the victim from exposure and give supplemental oxygen, if available.
    2. Skin and eyes. Remove contaminated clothing and wash exposed skin with soap and water. Irrigate exposed eye(s) with copious saline or water.
    3. Ingestion. Activated charcoal is of limited value and may make endoscopic evaluation difficult if corrosive injury is suspected. Perform nasogastric suction (if there has been a large, recent ingestion).
  4. Enhanced elimination. There is no documented efficacy for repeat-dose activated charcoal, hemodialysis, or hemoperfusion. Although treatment with hyperbaric oxygen may enhance elimination of carbon monoxide, its efficacy for patients with acute methylene chloride poisoning remains unproven.