Exposure<unk>  is known to form as a by-product of water<unk> orination along with a range of other disinfection by-products and as such is commonly present in municipal tap water and swimming pools. Reported ranges vary considerably but are generally below the current health standard for total trihalomethanes of 100μg/L. Nonetheless, the presence of<unk>  in drinking water at any concentration is considered controversial by some. Historically<unk>  exposure may well have been higher due to its common use as an anesthetic, as an ingredient in cough syrups, and as a constituent of tobacco smoke where DDT had previously been used as a fumigant. Pharmacology It is well absorbed, metabolized, and eliminated rapidly by mammals after oral, inhalation, or dermal exposure. Accidental splashing into the eyes has caused irritation. Prolonged dermal exposure can result in the development of sores as a result of defatting. Elimination is primarily from lungs in the form of<unk>  and carbon dioxide; less than 1% is excreted in urine.<unk>  is metabolized in the liver by the cytochrome P-450 enzymes, by oxidation to<unk> oromethanol and by reduction to the dichloromethyl free radical. Other metabolites of<unk>  include hydrochloric acid and digluathionyl dithiocarbonate, with carbon dioxide as the predominant end product of metabolism. Like most other general anesthetics and sedative-hypnotic drugs,<unk>  is a positive allosteric modulator for the GABAA receptor.<unk>  causes depression of the central nervous system (CNS), ultimately producing deep coma and respiratory center depression. When ingested,<unk>  caused symptoms similar to those seen following inhalation. Serious illness has followed ingestion of . The mean lethal oral dose for an adult is estimated at . The anesthetic use of<unk>  has been discontinued because it caused deaths due to respiratory failure and cardiac arrhythmias. Following<unk> -induced anesthesia, some patients suffered nausea, vomiting, hyperthermia, jaundice, and coma due to hepatic dysfunction. At autopsy, liver necrosis and degeneration have been observed.<unk>  has induced liver tumors in mice and kidney tumors in mice and rats. The hepatotoxicity and nephrotoxicity of<unk>  is thought to be due largely to phosgene. Conversion to phosgene<unk>  converts slowly in air to the extremely poisonous phosgene (COCl2), releasing HCl in the process. :2 CHCl3 + O2 → 2 COCl2 + 2 HCl To prevent accidents, commercial<unk>  is stabilized with ethanol or amylene, but samples that have been recovered or dried no longer contain any stabilizer. Amylene has been found ineffective, and the phosgene can affect analytes in samples, lipids, and nucleic acids dissolved in or extracted with<unk> . Phosgene and HCl can be removed from<unk>  by washing with saturated aqueous carbonate solutions, such as sodium bicarbonate. This procedure is simple and results in harmless products. Phosgene reacts with water to form carbon dioxide and HCl, and the carbonate salt neutralizes the resulting acid. Suspected samples can be tested for phosgene using filter paper (treated with 5% diphenylamine, 5% dimethylaminobenzaldehyde in ethanol, and then dried), which turns yellow in phosgene vapor. There are several colorimetric and fluorometric reagents for phosgene, and it can also be quantified with mass spectrometry. Regulation<unk>  is suspected of causing cancer (i.e., possibly carcinogenic, IARC Group 2B) as per the International Agency for Research on Cancer (IARC) Monographs. It is classified as an extremely hazardous substance in the United States as defined in Section 302 of the U.S. Emergency Planning and Community Right-to-Know Act (42 U.S.C. 11002), and is subject to strict reporting requirements by facilities that produce, store, or use it in significant quantities.
Chloroform
Triphenylchloroethylene
Chloroethane
Benzene
Diethyl ether
Methanol
Vinyl chloride
Triphenylbromoethylene