Trichloroethane and trichloroethylene are organic solvents that have historically been used as ingredients in many products, including typewriter correction fluid, color film cleaners, insecticides, spot removers, fabric-cleaning solutions, and adhesives. They have also been used extensively in industry as degreasers. Trichloroethane is available in two isomeric forms, 1,1,2-trichloroethane and 1,1,1-trichloroethane, with the latter (also known as methyl chloroform) being the more common. Tetrachloroethylene (perchloroethylene) is another related solvent that is widely used in the dry cleaning industry, although some regulatory agencies, such as the California Air Resources Board, have mandated its gradual phase-out for this application. Similarly, recognition of the stratospheric ozone depletion potential of 1,1,1-trichloroethane has resulted in the substitution of other chemicals for most applications.

1. These solvents act as respiratory and CNS depressants and skin and mucous membrane irritants. As a result of their high lipid solubility and CNS penetration, they have rapid anesthetic action, and both trichloroethylene and trichloroethane were used for this purpose medically until the advent of safer agents. Peak blood levels occur within minutes of inhalation exposure or 1-2 hours after ingestion. Their proposed mechanism of action includes neuronal calcium channel blockade and gamma-aminobutyric acid (GABA) stimulation.
2. Trichloroethane, trichloroethylene, their metabolite trichloroethanol, and tetrachloroethylene may sensitize the myocardium to the arrhythmogenic effects of catecholamines.
3. Trichloroethylene or a metabolite may act to inhibit acetaldehyde dehydrogenase, blocking the metabolism of ethanol and causing “degreaser's flush.”
4. Carcinogenicity.
   1. In 2014, the International Agency for Research on Cancer (IARC) upgraded its classification of trichloroethylene to carcinogenic in humans (Group 1), based on sufficient evidence for kidney cancer and suggestive evidence for non-Hodgkin lymphoma and liver cancer. IARC continues to classify tetrachloroethylene as having limited evidence as a human bladder carcinogen, but showing sufficient evidence in animals (Group 2A). The US National Toxicology Program (NTP) classifies both trichloroethylene and tetrachloroethylene as “Reasonably Anticipated to Be Human Carcinogens.”
   2. Both 1,1,1- and 1,1,2-trichloroethane are listed by IARC as “not classifiable as to carcinogenicity in humans” (Group 3), and neither has been systematically evaluated by the NTP.

1. Trichloroethane (TCA). The acute lethal oral dose to humans is reportedly between 0.5 and 5 mL/kg. The recommended workplace limits (ACGIH TLV-TWA) in air for the 1,1,1-trichloroethane and 1,1,2-trichloroethane isomers are 350 and 10 ppm, respectively, and the air levels considered immediately dangerous to life or health (IDLH) are 700 and 100 ppm, respectively. Anesthetic levels are in the range of 10,000-26,000 ppm. The odor is detectable by a majority of people at 500 ppm, but olfactory fatigue commonly occurs.
2. Trichloroethylene (TCE). The acute lethal oral dose is reported to be approximately 3-5 mL/kg. The recommended workplace limit (ACGIH TLV-TWA) is 10 ppm (269 mg/m³), although the US OSHA-enforceable Permissible Exposure Limit is ten times higher (100 ppm), and the air level considered immediately dangerous to life or health (IDLH) is 1,000 ppm.
3. Tetrachloroethylene (“PERC”). The recommended workplace limit (ACGIH TLV-TWA) is 25 ppm (170 mg/m³), although the US OSHA-enforceable Permissible Exposure Limit is four times higher (100 ppm), and the air level considered immediately dangerous to life or health (IDLH) is 150 ppm.

Toxicity may be a result of inhalation, skin contact, or ingestion.

1. Inhalation or ingestion may cause nausea, euphoria, headache, ataxia, dizziness, agitation, confusion, and lethargy and, if intoxication is significant, respiratory arrest, seizures, and coma. Hypotension and cardiac dysrhythmias may occur. Inhalational exposure may result in cough, dyspnea, and bronchospasm. With severe overdose, renal and hepatic injury may be apparent 1-2 days after exposure.
2. Local effects of exposure to liquid or vapors include irritation of the eyes, nose, and throat. Prolonged skin contact can cause a defatting dermatitis and, in the case of trichloroethane and tetrachloroethylene, may result in scleroderma-like skin changes.
3. Ingestion can produce GI irritation associated with nausea, vomiting, diarrhea, and abdominal pain. Aspiration into the tracheobronchial tree may result in hydrocarbon pneumonitis.
4. Degreaser's flush. Workers exposed to trichloroethylene vapors may have a transient flushing and orthostatic hypotension if they ingest alcohol, owing to a disulfiram-like effect (see “Disulfiram,”).
5. Other. Numerous case reports link high-level trichloroethylene exposures with the development of cranial neuropathies. Sporadic cases of optic neuritis have also been reported after trichloroethylene or tetrachloroethylene exposure. Several studies link occupational exposures to tetrachloroethylene (and environmental exposures to trichloroethane) to the occurrence of spontaneous abortion. Based on exposure modeling, tetrachloroethylene is likely to be present in breast milk.

Is based on a history of exposure and typical symptoms.

1. Specific levels
   1. Although all three solvents can be measured in expired air, blood, and urine, levels are not routinely rapidly available and are not needed for emergency evaluation or treatment. Confirmation of exposure to trichloroethane may be possible by detecting the metabolite trichloroethanol in the blood or urine but is not usually available in most laboratories.
   2. Breath analysis is becoming more widely used for workplace exposure control, and serial measurements may allow estimation of the amount absorbed.
2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, liver aminotransferases, arterial blood gases, chest radiography, and ECG monitoring.

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen and treat hydrocarbon aspiration pneumonitis if it occurs.
   2. Treat seizures, coma, and dysrhythmias if they occur. Caution: Avoid the use of epinephrine or other sympathomimetic amines because of the risk for inducing or aggravating cardiac dysrhythmias. Tachyarrhythmias caused by myocardial sensitization may be treated with propranolol, 1-2 mg IV, or esmolol, 0.025-0.1 mg/kg/min IV.
   3. Monitor for a minimum of 4-6 hours after significant exposure.
2. Specific drugs and antidotes. There is no specific antidote.
3. Decontamination
   1. Inhalation. Remove the victim from exposure and administer supplemental oxygen, if available.
   2. Skin and eyes. Remove contaminated clothing and wash exposed skin with soap and water. Irrigate exposed eyes with copious tepid water or saline.
   3. Ingestion. Do not give activated charcoal or induce vomiting because of the danger of rapid absorption and abrupt onset of seizures or coma. Consider removal by nasogastric tube only if the ingestion was very large and recent (<30 minutes). The efficacy of activated charcoal is unknown.
4. Enhanced elimination. These procedures are not effective or necessary.