Trichloroethylene

Trichloroethylene
IUPAC name	trichloroethene
Other names	1,1,2-Trichloroethene, 1,1-Dichloro-2-Chloroethylene, 1-Chloro-2,2-Dichloroethylene, Acetylene Trichloride, TCE, Trethylene, Triclene, Tri, Trimar, Trilene
Identifiers
Abbreviations	TCE
CAS number	79-01-6
PubChem	6575
EINECS number	201-61-04
RTECS number	KX4550000
SMILES	ClC=C(Cl)Cl
InChI	1/C2HCl3/c3-1-2(4)5/h1H
Properties
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 °C)
Solubility in water	0.1 g/100 cm³ at 25 °C
Solubility	ether, ethanol, chloroform
Refractive index (nD)	1.4777 at 19.8 °C
Hazards
MSDS	Mallinckrodt Baker
Main hazards	Harmful if swallowed or inhaled.
NFPA 704	1 2 0
Autoignition temperature	420 °C
Related compounds
Related vinyl halide	vinyl chloride
Related compounds	chloroform 1,1,1-Trichloroethane 1,1,2-Trichloroethane
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.

Its IUPAC name is trichloroethene. In industry, it is informally referred to by the abbreviations TCE, Trike, Tricky and tri, and it is sold under a variety of trade names. In addition to its industrial uses, trichloroethylene was used from about 1930 as a volatile anesthetic and analgesic in millions of patients.

History

Pioneered by Imperial Chemical Industries in Britain, its development was hailed as a revolution: lacking the great hepatotoxic liability of chloroform and the unpleasant pungency and flammability of ether, it nonetheless had several pitfalls, including the sensitization of the myocardium to epinephrine, potentially acting in an arrhythmogenic manner. Its low volatility demanded the employment of carefully regulated heat in its vaporization. Research demonstrating its transient elevation of serum hepatic enzymes raised concerns regarding its hepatotoxic potential. Several deaths occurred as a result, though the incidence was comparable to that of halothane hepatitis. Incompatibility with soda lime (the CO₂ adsorbent utilized in closed-circuit, low-flow rebreathing systems) was also a concern. TCE was readily decomposed into 1,2-dichloroacetylene, a neurotoxic compound potentially responsible for its hepatotoxic potential, though its metabolite trichloroacetic acid is more probably the etiological source of the latter. Halothane usurped a great portion of its market in 1956, with its total abandonment not achieved until the 1980s, when its use as an analgesic in obstetrics was implicated in fetal death. Concerns of its carcinogenic potential were raised simultaneously.

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 process in Europe as the chemical was classified as a carcinogen carrying an R45 risk phrase. Many alternatives are being promoted such as Ensolv and Leksol, however each of these is based on nPropyl Bromide which carries an R60 risk phrase and they would not be a legally acceptable substitute.

Production

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 Cl₂ → Cl₂CHCHCl₂

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 + Cl₂ → ClCH₂CH₂Cl

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.

Uses

Trichloroethylene is an effective solvent for a variety of organic materials. When it was first widely produced in the 1920s, its 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 was also used as a dry cleaning solvent, although tetrachloroethylene (also known as perchloroethylene) surpassed it in this role in the 1950s.

Trichloroethylene has been widely used as a degreaser for metal parts. In the late 1950s, the demand for TCE as a degreaser began to decline in favor of the less toxic 1,1,1-trichloroethane. Another problem with trichloroethylene is that it's just too good a solvent in many mechanical applications, as it easily will strip many paints almost instantly and dissolves some plastics. 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 a resurgence in use. It has also been used for drying out the last bit of water for production of 100% ethanol.

Trichloroethylene (Trimar and Trilene) was used as a volatile gas anesthetic from the 1930s through the 1960s in Europe and North America. Supplanting chloroform and ether for a significant period of time, trichloroethylene demonstrated superior efficacy in induction times and cost-effectiveness.

Chemical instability

Although it has proven useful as a metal degreaser, trichloroethylene itself is unstable in the presence of metal over prolonged exposure. As early as 1961, this phenomenon was clearly recognized by the manufacturing industry, since an additive was instilled in the commercial formulation of trichloroethylene. The reactive instability is accentuated by higher temperatures, so that the search for stabilizing additives is 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 trichlorethylene. The principal family of chemicals that showed promise was the ketone family, such as methyl ethyl ketone. Considerable research was conducted at Frontier Chemical Company, Wichita, Kansas on this class of ketones using reflux condensation experiments.

Physiological effects

When inhaled, trichloroethylene, as with any anesthetic gas, depresses the central nervous system. In the 1950s and 60's anesthesiologists used various gases no longer in use for such purposes like ether and chloroform. When the neurotoxic and neurological side effects of acute exposure were recognized, the use of TCE in anesthesia was discontinued.(1) The effect of inhaling TCE vapors may have long lasting implications for those with chronic exposure. A study done at the University of Kentucky and released in 2007 suggested an association of Parksonism and occupational TCE exposure. (original article reference needed).

The symptoms of acute exposure are similar to those of alcohol intoxication, beginning with headache, dizziness, and confusion and progressing with increasing exposure to unconsciousness [2]. Respiratory and circulatory depression from any anesthetic can result in death if administration is not carefully controlled. As mentioned above, cardiac sensitization to catecholamines such as epinephrine can result in dangerous cardiac arrhythmias. Caution should be exercised anywhere a high concentration of trichloroethylene vapors may be present; the drug can desensitize the nose to its scent, and it is possible to unknowingly inhale harmful or lethal amounts of the vapor.

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 [3]. Over time, occupational exposure limits on trichloroethylene have tightened, resulting in more stringent ventilation controls and personal protective equipment use by workers. The tightening of occupational exposure limits and increased need for worker protection in part contributed to the substitution of other lower toxicity chemicals for trichloroethylene in solvent cleaning and degreasing.

The carcinogenicity of trichloroethylene was first evaluated in laboratory animals in the 1970s. Newly published 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 [4][5]. Numerous epidemiological studies have been conducted on trichloroethylene exposure in the workplace, with differing opinions regarding the strength of evidence between trichloroethylene and human cancer. Recent studies on the mechanisms of carcinogenicity have shown that metabolism of trichloroethylene in the liver produces metabolites (such as trichloroacetic acid and dichloroacetic acid, which are responsible for liver tumors in mice) that are the ultimate carcinogens in laboratory animals. Other studies using physiologically-based pharmacokinetic (PBPK) modeling, have examined the similarities and differences in metabolism between humans and laboratory animals, to better understand the relationship between carcinogenicity observed in laboratory animals and human cancer risks. Research published in 1994 examined the incidence of leukemia and non-Hodgkins lymphoma in populations exposed to TCE in their drinking water. New Jersey Department of Health, Environmental Health Services, Trenton, NJ 08625 USA.

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.^[1]

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.^[2] 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".^[3] 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. However, the NAS also concluded that higher levels of exposure, such as workplace exposure, or locations with significant environmental contamination, might be associated with a liver cancer risk in humans.

Recent studies in laboratory animals and observations in human populations suggest that exposure to trichloroethylene might be associated with congenital heart defects (J Am Coll Cardiol. 1990 Jul;16(1):155-64.; J Am Coll Cardiol. 1993 May;21(6):1466-72; Toxicol Sci. 2000 Jan;53(1):109-17; Birth Defects Res A Clin Mol Teratol. 2003 Jul;67(7):488-95; Environ Health Perspect. 2006 Jun;114(6):842-7). While it is not clear what levels of exposure are associated with cardiac defects in humans, there is consistency between the cadiac defects observed in studies of communities exposed to trichloroethylene contamination in groundwater, and the effects observed in laboratory animals. Trichloroethylene can also affect the fertility of males and females in laboratory animals, but the relevance of these findings to humans is not clear. A study published in August 2008, has demonstrated effects of TCE on human mitochondria. The article questions whether this might impact female reproductive function. ^[4]

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.^[5] Based on this review, the EPA published a risk assessment that concluded trichloroethylene posed a more significant human health risk than previous studies had indicated. EPA's report provoked considerable debate about the quality of evidence describing the health risks of trichloroethylene, and the methods used to assess that evidence. In 2004, an interagency group composed of the EPA, Department of Defense, Department of Energy, and the National Aeronautics and Space Administration requested the National Academy of Sciences (NAS) to provide independent guidance on the scientific issues related regarding trichloroethylene health risks. The NAS report 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.^[3]

Human exposure

Human exposure to trichloroethylene is potentially widespread. It is a common contaminant in soil and groundwater at hundreds of waste sites across the United States. Some are exposed to TCE through contaminated drinking water [6](P. 17). Others are potentially exposed through inhalation of vapor from contaminated soil or groundwater entering nearby buildings. 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 volatalise more TCE into the air.In a home closed tightly to conserve the cost of heating and cooling, these vapors would then recirculate. Tens of thousands of workers are potentially were exposed to trichloroethylene used as a degreasing and cleaning chemical. Other exposures have occurred through the long-term use of trichloroethylene as a surgical anesthetic.

TCE was first detected in groundwater in 1977, and is one of the most frequently detected contaminants in groundwater in the U.S. 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.^[6] 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. Trichloroethylene has been detected in 852 Superfund sites across the United States,^[7] according to the Agency for Toxic Substances and Disease Registry (ATSDR). and 34% of the drinking water supply sources that have been tested in the United States may have some trichloroethylene contamination. Under the Safe Drinking Water Act of 1974, and as amended http://www.epa.gov/safewater/sdwa/ annual water quality testing is required for all public drinking water distributors. The EPA'S current guidelines for TCE can be found here: http://www.epa.gov/OGWDW/contaminants/dw_contamfs/trichlor.html 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. http://yosemite.epa.gov/r9/sfund/r9sfdocw.nsf/webdisplay/oid-3a4364e2a3ab3c7688256de9006819f2?OpenDocument

As of 2007, 57,000 thousand 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. http://www.epa.gov/region09/waste/sfund/indianbend/index.html 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." http://www.scottsdaleaz.gov/water/superfund.asp

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 Seimens 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 (TCE) ^[8]

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 ^[9],^[10].

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.^[11] 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 www.cpeo.org and include a former ammunition plant in the Twin Cities area. http://www.cpeo.org/milit.html. 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 http://www.thomas.gov/cgi-bin/thomas. 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 aerobic degradation pathways in order to reduce environmental pollution through the use of genetically modified bacteria. Limited success has been attained thus far; the intended application is for treatment and detoxification of industrial wastewater.

Cases of TCE contaminated water

• Wichita, Kansas
• Shannon, Quebec and Val-Belair, Quebec
• Woburn, Massachusetts (the town from the book/movie A Civil Action)
• Camp Lejeune, North Carolina
• Lisle, Illinois
• Scottsdale, Arizona (from the Indian Bend Wash Area Superfund site, 2007 and 2008)
• Cambridge, Ontario: http://news.therecord.com/News/Local/article/271823
• Salem, Ohio Nease Chemical, Supplied U.S. Army with chemicals for Agent Orange: http://cfpub.epa.gov/supercpad/SiteProfiles/index.cfm?fuseaction=second.Contams&id=0504619
• Tuscon, Arizona
• Walkersville, Maryland [7]
• Victor, New York
• Salina, Kansas
• Lancaster, Pennsylvania (from U.S. EPA, Region III) ^[12]#REDIRECT [8]

References

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

• Lipworth L, Tarone RE, McLaughlin JK (December 2006). "The epidemiology of renal cell carcinoma". J. Urol. 176 (6 Pt 1): 2353–8. doi:10.1016/j.juro.2006.07.130. PMID 17085101. http://www.jurology.com/article/PIIS0022534706019537. 

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 [9]

External links

• Q&A on trichloroethylene from Euro Chlor - ECSA (European Chlorinated Solvent Association)
• ATSDR - Case Studies in Environmental Medicine: Trichloroethylene Toxicity U.S. Department of Health and Human Services (public domain)
• Assessing Human Health Risks of Trichloroethylene - Key Scientific Issues, National Academy of Sciences
• EPA's Trichloroethylene web site
• Eleventh Report on Carcinogens: Trichloroethylene Monograph
• NIOSH Safety and Health Topic: Trichloroethylene
• The TCE Blog