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IUPAC name
Other names 1,1,2-Trichloroethene, 1,1-Dichloro-2-Chloroethylene, 1-Chloro-2,2-Dichloroethylene, Acetylene Trichloride, TCE, Trethylene, Triclene, Tri, Trimar, Trilene
Abbreviations TCE
CAS number 79-01-6 Yes check.svgY
PubChem 6575
EC number 201-61-04
RTECS number KX4550000
Molecular formula C2HCl3
Molar mass 131.39 g mol−1
Appearance Colorless liquid
Density 1.46 g/cm³ (liquid) at 20 °C
Melting point

200 K (−73 °C)

Boiling point

360 K (87.2 °C)[1]

Solubility in water 1.280 g/L (25°C)[1]
Solubility ether, ethanol, chloroform
Refractive index (nD) 1.4777 at 19.8 °C
MSDS External MSDS
Main hazards Harmful if swallowed or inhaled.
NFPA 704
NFPA 704.svg
420 °C
Related compounds
Related vinyl halide vinyl chloride
Related compounds chloroform
Supplementary data page
Structure and
n, εr, etc.
Phase behaviour
Solid, liquid, gas
Spectral data UV, IR, NMR, MS
 Yes check.svgY (what is this?)  (verify)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

The chemical compound trichloroethylene is a chlorinated hydrocarbon commonly used as an industrial solvent. It is a clear non-flammable liquid with a sweet smell.

The IUPAC name is trichloroethene. Industrial abbreviations include TCE, trichlor, Trike, Tricky and tri. It has been sold under a variety of trade names. Under the trade names Trimar and Trilene, trichloroethylene was used as a volatile anesthetic and as an inhaled obstetrical analgesic in millions of patients.



Pioneered by Imperial Chemical Industries in Britain, its development was hailed as an anesthetic revolution. Originally thought to possess less hepatotoxicity than chloroform, and without the unpleasant pungency and flammability of ether, TCE use was nonetheless soon found to have several pitfalls. These included promotion of cardiac arrhythmias, too low a volatility for quick anesthetic induction, reactions with soda lime used in carbon dioxide absorbing systems, prolonged neurologic dysfunction when used with soda lime, and evidence of hepatotoxicity as had been found with chloroform.

The introduction of halothane in 1956 greatly diminished the use of TCE as a general anesthetic. TCE was still used as an inhalation analgesic in childbirth given by self-administration. Fetal toxicity and concerns for carcinogenic potential of TCE led to its abandonment in the 1980s.

Due to concerns about its toxicity, the use of trichloroethylene in the food and pharmaceutical industries has been banned in much of the world since the 1970s. Legislation has forced the substitution of trichloroethylene in many processes in Europe as the chemical was classified as a carcinogen carrying an R45 risk phrase. Many degreasing chemical alternatives are being promoted such as Ensolv and Leksol, however each of these is based on n-propyl bromide which carries an R60 risk phrase and they would not be a legally acceptable substitute.

Groundwater contamination by TCE has become an important environmental concern. Seepage of the compound into groundwater has raised health concerns in many locations.


Prior to the early 1970s, most trichloroethylene was produced in a two-step process from acetylene. First, acetylene was treated with chlorine using a ferric chloride catalyst at 90 °C to produce 1,1,2,2-tetrachloroethane according to the chemical equation

HC≡CH + 2 Cl2Cl2CHCHCl2

The 1,1,2,2-tetrachloroethane is then dehydrochlorinated to give trichloroethylene. This can either be accomplished with an aqueous solution of calcium hydroxide

2 Cl2CHCHCl2 + Ca(OH)2 → 2 ClCH=CCl2 + CaCl2 + 2 H2O

or in the vapor phase by heating it to 300-500°C on a barium chloride or calcium chloride catalyst

Cl2CHCHCl2 → ClCH=CCl2 + HCl

Today, however, most trichloroethylene is produced from ethylene. First, ethylene is chlorinated over a ferric chloride catalyst to produce 1,2-dichloroethane.

CH2=CH2 + Cl2ClCH2CH2Cl

When heated to around 400 °C with additional chlorine, 1,2-dichloroethane is converted to trichloroethylene

ClCH2CH2Cl + 2 Cl2 → ClCH=CCl2 + 3 HCl

This reaction can be catalyzed by a variety of substances. The most commonly used catalyst is a mixture of potassium chloride and aluminum chloride. However, various forms of porous carbon can also be used. This reaction produces tetrachloroethylene as a byproduct, and depending on the amount of chlorine fed to the reaction, tetrachloroethylene can even be the major product. Typically, trichloroethylene and tetrachloroethylene are collected together and then separated by distillation.


Trichloroethylene is an effective solvent for a variety of organic materials.

When it was first widely produced in the 1920s, trichloroethylene's major use was to extract vegetable oils from plant materials such as soy, coconut, and palm. Other uses in the food industry included coffee decaffeination and the preparation of flavoring extracts from hops and spices. It has also been used for drying out the last bit of water for production of 100% ethanol.

From the 1930s through the 1970s, both in Europe and North America, trichloroethylene was used as a volatile gas anesthetic. TCE was used in place of earlier the anesthetics chloroform and ether in the 1940s, but was itself replaced in the 1950s by the newer halothane, which allowed much faster induction and recovery times. Marketed in the UK by ICI under the trade name Trilene it was coloured blue (with a dye called waxolene blue) to avoid confusion with the similar smelling chloroform.

It has also been used as a dry cleaning solvent, although replaced in the 1950s by tetrachloroethylene (also known as perchloroethylene).

Perhaps the greatest use of TCE has been as a degreaser for metal parts. The demand for TCE as a degreaser began to decline in the 1950s in favor of the less toxic 1,1,1-trichloroethane. However, 1,1,1-trichloroethane production has been phased out in most of the world under the terms of the Montreal Protocol, and as a result trichloroethylene has experienced some resurgence in use as a degreaser.

Chemical instability

Despite its widespread use as a metal degreaser, trichloroethylene itself is unstable in the presence of metal over prolonged exposure. As early as 1961 this phenomenon was recognized by the manufacturing industry, when stabilizing additives were added in the commercial formulation. Since the reactive instability is accentuated by higher temperatures, the search for stabilizing additives was conducted by heating trichloroethylene to its boiling point in a reflux condenser and observing decomposition. The first widely used stabilizing additive was dioxane; however, its use was patented by Dow Chemical Company and could not be used by other manufacturers. Considerable research took place in the 1960s to develop alternative stabilizers for trichloroethylene. Other chemical stabilizers include ketones such as methyl ethyl ketone.

Physiological effects

When inhaled, trichloroethylene produces central nervous system depression resulting in general anesthesia. Its high lipid solubility results in a less desirable slower induction of anesthesia. At low concentrations it is relatively non-irritating to the respiratory tract. Higher concentrations result in tachypnea. Many types of cardiac arrhythmias can occur and are exacerbated by epinephrine (adrenaline). It was noted in the 1940s that TCE reacted with carbon dioxide (CO2) absorbing systems (soda lime) to produce dichloroacetylene and phosgene.[2] Cranial nerve dysfunction (especially the fifth cranial nerve) was not uncommon when TCE anesthesia was given using CO2 absorbing systems. These nerve deficits could last for months. Occasionally facial numbness was permanent. Muscle relaxation with TCE anesthesia sufficient for surgery was poor. For these reasons as well as problems with hepatotoxicity, TCE lost popularity in North America and Europe to more potent anesthestics such as halothane by the 1960s.[3]

The symptoms of acute non-medical exposure are similar to those of alcohol intoxication, beginning with headache, dizziness, and confusion and progressing with increasing exposure to unconsciousness.[4] Respiratory and circulatory depression can result in death.

Much of what is known about the human health effects of trichloroethylene is based on occupational exposures. Beyond the effects to the central nervous system, workplace exposure to trichloroethylene has been associated with toxic effects in the liver and kidney [5]. Over time, occupational exposure limits on trichloroethylene have tightened, resulting in more stringent ventilation controls and personal protective equipment use by workers.

Research from Cancer bioassays performed by the National Cancer Institute (later the National Toxicology Program) showed that exposure to trichloroethylene is carcinogenic in animals, producing liver cancer in mice, and kidney cancer in rats.[6][7] Research published in 1994 examined the incidence of leukemia and non-Hodgkin lymphoma in populations exposed to TCE in their drinking water.[8]

The National Toxicology Program’s 11th Report on Carcinogens categorizes trichloroethylene as “reasonably anticipated to be a human carcinogen”, based on limited evidence of carcinogenicity from studies in humans and sufficient evidence of carcinogenicity from studies in experimental animals.[9]

One recent review of the epidemiology of kidney cancer rated cigarette smoking and obesity as more important risk factors for kidney cancer than exposure to solvents such as trichloroethylene.[10] In contrast, the most recent overall assessment of human health risks associated with trichloroethylene states, "[t]here is concordance between animal and human studies, which supports the conclusion that trichloroethylene is a potential kidney carcinogen".[11] The evidence appears to be less certain at this time regarding the relationship between humans and liver cancer observed in mice, with the NAS suggesting that low-level exposure might not represent a significant liver cancer risk in the general population.

Recent studies in laboratory animals and observations in human populations suggest that exposure to trichloroethylene might be associated with congenital heart defects [12][13][14][15][16] While it is not clear what levels of exposure are associated with cardiac defects in humans, there is consistency between the cardiac defects observed in studies of communities exposed to trichloroethylene contamination in groundwater, and the effects observed in laboratory animals. A study published in August 2008, has demonstrated effects of TCE on human mitochondria. The article questions whether this might impact female reproductive function. [17]

The health risks of trichloroethylene have been studied extensively. The U.S. Environmental Protection Agency (EPA) sponsored a "state of the science" review of the health effects associated with exposure to trichloroethylene.[18] The National Academy of Sciences concluded that evidence on the carcinogenic risk and other potential health hazards from exposure to TCE has strengthened since EPA released their toxicological assessment of TCE, and encourages federal agencies to finalize the risk assessment for TCE using currently available information, so that risk management decisions for this chemical can be expedited.[11]

Human exposure

Some are exposed to TCE through contaminated drinking water.[19] Another significant source of vapor exposure in Superfund sites that had contaminated groundwater, such as the Twin Cities Army Ammunition Plant, was by showering. TCE readily volatilizes out of hot water and into the air. Long, hot showers would then volatilize more TCE into the air. In a home closed tightly to conserve the cost of heating and cooling, these vapors would then recirculate.

The first known report of TCE in groundwater was given in 1949 by two English public chemists who described two separate instances of well contamination by industrial releases of TCE.[20] Based on available federal and state surveys, between 9% to 34% of the drinking water supply sources tested in the U.S. may have some TCE contamination, though EPA has reported that most water supplies are in compliance with the Maximum Contaminant Level (MCL) of 5 ppb.[21] In addition, a growing concern in recent years at sites with TCE contamination in soil or groundwater has been vapor intrusion in buildings, which has resulted in indoor air exposures, such is in a recent case in the McCook Field Neighborhood of Dayton, Ohio.[22] Trichloroethylene has been detected in 852 Superfund sites across the United States,[23] according to the Agency for Toxic Substances and Disease Registry (ATSDR). Under the Safe Drinking Water Act of 1974, and as amended [24] annual water quality testing is required for all public drinking water distributors. The EPA'S current guidelines for TCE can be found here. It should be noted that the EPA's table of "TCE Releases to Ground" is dated 1987 to 1993, thereby omitting one of the largest Superfund Cleanup sites in the nation, the NIBW in Scottsdale, Arizona. The TCE "released" here occurred prior to its appearance in the municipal drinking wells in 1982.[25]

In 1998, the View-Master factory supply well in Beaverton, Oregon was found to have been contaminated with high levels of TCE. It was estimated that 25,000 factory workers had been exposed to it from 1950–2001.[26]

As of 2007, 57,000 pounds, or roughly 19 tons of TCE have been removed from the system of wells that once supplied drinking water to the residents of Scottsdale. [27] One of the three drinking water wells previously owned by the City of Phoenix and ultimately sold to the City of Scottsdale, tested at 390 ppb TCE when it was closed in 1982. (see East Valley Tribune, April 6, 2007, "Feds to Examine Superfund Site" by John Yantis) Some Scottsdale residents who received their water bills from the City of Phoenix throughout the 1960s and 70's were understandably confused as to whether they indeed had been consuming contaminated water when information about the Superfund site was first disseminated. The City of Scottsdale recently updated their website to clarify that the contaminated wells were "in the Scottsdale area" and to delete all references to the levels of TCE discovered when the wells were closed as "trace".[28]

A spot was then ultimately chosen to receive and treat the contaminated drinking water known as the Central Groundwater Treatment Facility. Then 1989, as now, this treatment facility (CGTF) is situated on land adjacent to Pima Park and the Siemens facility documented as one of the Potentially Responsible Parties at the corner of Thomas and Pima roads. Close proximity to this park did not appear to enter into Motorola's calculations when asserting that it would save money to remove the carbon air filters in 2007. (See East Valley Tribune, October 5, 2007, "Motorola wants to axe filters at Superfund site" by Ari Cohn)

Camp Lejeune in North Carolina may be the largest TCE contamination site in the country. Legislation could force the EPA to establish a health advisory and a national public drinking water regulation to limit trichloroethylene.[29]

For over twenty years of operation, the US-based multinational Radio Company of America (RCA) had been pouring toxic wastewater into a well in its Taoyuan, Taiwan facility. The pollution from the plant was not revealed until 1994, when former workers brought it to light. Investigation by the Taiwan Environmental Protection Administration confirmed that RCA had been dumping chlorinated organic solvents into a secret well and caused contamination to the soil and groundwater surrounding the plant site. High levels of TCE tetrachloroethylene (PCE) can be found in groundwater drawn as far as two kilometers from the site. An organization of former RCA employees reports 1375 cancer cases, 216 cancer deaths, and 102 cases of various tumors among its members.[30][31]

Trichloroethylene is a cleaning solvent that was used to clean military weapons during the Gulf War. There are reports associating exposure to this solvent with amyotrophic lateral sclerosis (Kasarskis EJ et al. Amyotrophic Lateral Sclerosis, 2008 Sep 16:1-7, Clinical aspects of ALS in Gulf War Veterans), and also with a neurologic syndrome resembling Parkinson's disease (Gash DM. et al. Ann Neurol. 2008 Feb;63(2):184-92. Trichloroethylene: Parkinsonism and complex 1 mitochondrial neurotoxicity).

Existing regulation

Until recent years, the US Agency for Toxic Substances and Disease Registry (ATSDR) contended that trichloroethylene had little-to-no carcinogenic potential, and was probably a co-carcinogen—that is, it acted in concert with other substances to promote the formation of tumors.

Half a dozen state, federal, and international agencies now classify trichloroethylene as a probable carcinogen. The International Agency for Research on Cancer considers trichloroethylene a Group 2A carcinogen, indicating that it considers it is probably carcinogenic to humans.[32] California EPA regulators consider it a known carcinogen and issued a risk assessment in 1999 that concluded that it was far more toxic than previous scientific studies had shown.

Proposed U.S. federal regulation

In 2001, a draft report of the Environmental Protection Agency (EPA) laid the groundwork for tough new standards to limit public exposure to trichloroethylene. The assessment set off a fight between the EPA and the Department of Defense (DoD), the Department of Energy, and NASA, who appealed directly to the White House. They argued that the EPA had produced junk science, its assumptions were badly flawed, and that evidence exonerating the chemical was ignored.

The DoD has about 1,400 military properties nationwide that are contaminated with trichloroethylene. Many of these sites are detailed and updated by and include a former ammunition plant in the Twin Cities area.[33] Twenty three sites in the Energy Department's nuclear weapons complex — including Lawrence Livermore National Laboratory in the San Francisco Bay area, and NASA centers, including the Jet Propulsion Laboratory in La Cañada Flintridge are reported to have TCE contamination.

Political appointees in the EPA sided with the Pentagon and agreed to pull back the risk assessment. In 2004, the National Academy of Sciences was given a $680,000 contract to study the matter, releasing its report in the summer of 2006. The report has raised more concerns about the health effects of TCE.

In response to the heightened awareness of environmental toxins such as TCE and the role they may be playing in childhood disease, Sen. Obama proposed S1068, cosponsored by Hillary Clinton and others.[34] This legislation aims to inform and protect communities that are threatened with environmental contamination. Sen. Clinton's own bill, S1911, is known as the TCE Reduction Act. This bill was co-sponsored by Sen. Elizabeth Dole (R-North Carolina).

Reduced production and remediation

In recent times, there has been a substantial reduction in the production output of trichloroethylene; alternatives for use in metal degreasing abound, chlorinated aliphatic hydrocarbons being phased out in a large majority of industries due to the potential for irreversible health effects and the legal liability that ensues as a result.

The U.S. military has virtually eliminated its use of the chemical, purchasing only 11 gallons in 2005. About 100 tons of it is used annually in the U.S. as of 2006.

Recent research has focused on the in-place remediation of trichloroethylene in soil and ground water instead of removal for off-site treatment and disposal. Naturally-occuring bacteria have been identifed with the ability to degrade or completely mineralize thrichloroethylene. Dehalococcoide sp. degrade trichloroethylene by reductive dechlorination under anaerobic conditions. Under aerobic conditions, Pseudomonas fluorescence can cometabolize TCE. Soil and ground water contamination by TCE has also been successfully remediated by chemical treatment and extraction.

Cases of TCE contaminated water


In the John Travolta film A Civil Action, the case of a TCE-contaminated tannery and town water supply is covered in detail.


  1. ^ a b Trichloroethylene on ChemIDplus
  2. ^ Orkin, F. K. (1986) Anesthesia Systems (Chapter 5). In R. D. Miller (Ed.), Anesthesia (second edition). New York, NY: Churchill Livingstone.
  3. ^ Stevens, W.C. and Kingston H. G. G. (1989) Inhalation Anesthesia (Chapter 11). In P. G. Barash et al. (Eds.) Clinical Anesthesia. Philadelphia, PA: Lippincott.
  4. ^
  5. ^
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  7. ^
  8. ^ New Jersey Department of Health, Environmental Health Services, Trenton, NJ 08625 USA.
  9. ^
  10. ^ Elsevier
  11. ^ a b Assessing the Human Health Risks of Trichloroethylene: Key Scientific Issues
  12. ^ J Am Coll Cardiol. 1990 Jul;16(1):155-64.
  13. ^ J Am Coll Cardiol. 1993 May;21(6):1466-72
  14. ^ Toxicol Sci. 2000 Jan;53(1):109-17
  15. ^ Birth Defects Res A Clin Mol Teratol. 2003 Jul;67(7):488-95
  16. ^ Environ Health Perspect. 2006 Jun;114(6):842-7
  17. ^ Xu F, Papanayotou I, Putt DA, Wang J, Lash LH (August 2008). "Role of mitochondrial dysfunction in cellular responses to S-(1,2-dichlorovinyl)-L-cysteine in primary cultures of human proximal tubular cells". Biochem. Pharmacol. 76 (4): 552–67. doi:10.1016/j.bcp.2008.05.016. PMID 18602084.  
  18. ^ EHP Supplement: Volume 108 (Supplement 2) May 2000
  19. ^ 17)
  20. ^ Lyne, F.A. and T. McLachlan, "Contamination of water by trichloroethylene," The Analyst, 74, p. 513, 1949.
  21. ^ [1] EPA - Consumer Factsheet on: TRICHLOROETHYLENE
  22. ^ EPA Long-Term Study Begins Behr-Dayton Thermal Systems VOC Plume Site
  23. ^ ATSDR - ToxFAQs: Trichloroethylene (TCE)
  24. ^
  25. ^
  26. ^
  27. ^
  28. ^
  29. ^ "Lejeune water contamination bill could force EPA to establish public standard", by Jennifer Hlad in Jacksonville, NC DAILY NEWS , August 10, 2008
  30. ^ Poisoned RCA Workers Demand Justice And Peace,
  31. ^ "Facing Up to a Dirty Secret", Far Eastern Economic Review, Dec. 12, 2002. en&sa=X&oi=book_result&resnum=5&ct=result#PPA68,M1
  32. ^ IARC monograph. "TRICHLOROETHYLENE" Vol. 63, p. 75. Last Updated May 20, 1997. Last retrieved June 22, 2007.
  33. ^
  34. ^
  35. ^
  36. ^
  37. ^ [2] Radio-Canada - documentary on the contamination of Shannon
  38. ^ Shannon class action
  39. ^ [3]
  40. ^
  41. ^
  42. ^
  43. ^
  44. ^
  45. ^ EPA SDWIS Violation Report
  46. ^
  47. ^
  48. ^
  49. ^
  50. ^

Further reading

  • Agency for Toxic Substances and Disease Registry (ATSDR). 1997. Toxicological Profile for Trichloroethylene. link
  • Doherty, R.E. 2000. A History of the Production and Use of Carbon Tetrachloride, Tetrachloroethylene, Trichloroethylene and 1,1,1-Trichloroethane in the United States: Part 2 - Trichloroethylene and 1,1,1-Trichloroethane. Journal of Environmental Forensics (2000) 1, 83-93. link
  • U.S. Environmental Protection Agency (USEPA). 2001. Trichloroethylene Health Risk Assessment: Synthesis and Characterization (External Review Draft) link
  • U.S. National Academy of Sciences (NAS). 2006. Assessing Human Health Risks of Trichloroethylene - Key Scientific Issues. Committee on Human Health Risks of Trichloroethylene, National Research Council. link
  • U.S. National Toxicology Program (NTP). 2005. Trichloroethylene, in the 11th Annual Report of Carcinogens. link
  • Comment on Voluntary Scheme for users of Trichloroethylene at [4]

External links


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