Trichloroethylene

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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]
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 External MSDS
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
Supplementary data page
Structure and
properties		 n, εr, etc.
Thermodynamic
data		 Phase behaviour
Solid, liquid, gas
Spectral data UV, IR, NMR, MS
Except where noted otherwise, data are given for
materials in their standard state
(at 25 °C, 100 kPa)
Infobox disclaimer and 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 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, before its toxic properties were realized.

Contents

[edit] 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.

[edit] 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.

[edit] 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 trichloroethylene 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. It retained use in other locations well into the 1990s. It was known for its favorable analgesic properties. Induction of general anesthesia was accomplished by administering up to 1%(v/v) vapor. Equilibration would often result in patient levels of 0.1 to 0.5% vapor. Many patients were given Trilene inhalers to self administer analgesia, especially in obstetrical labor. The number of patients exposed to these high levels of trichloroethylene is difficult to know, but is certainly well into the millions.

[edit] 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.

[edit] Physiological effects

When inhaled, trichloroethylene, as with any anesthetic gas, depresses the central nervous system. Its symptoms are similar to those of alcohol intoxication, beginning with headache, dizziness, and confusion and progressing with increasing exposure to unconsciousness [1]. 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.[citation needed]

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 [2]. 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.[citation needed]

The carcinogenicity of trichloroethylene was first evaluated in laboratory animals in the 1970s.[citation needed] 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 [3][4]. 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.[citation needed] 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.[citation needed] Other studies using physiologically-based pharmacokinetic (PBPK) modeling, have examined the similarities and differences in metabolism between humans and laboratory animals,[citation needed] to better understand the relationship between carcinogenicity observed in laboratory animals and human cancer risks. 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.[citation needed]

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.[citation needed]

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.[4] 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.[citation needed] 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.[citation needed] 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.[citation needed] 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.[5]

[edit] Human exposure

Human exposure to trichloroethylene is potentially widespread.[citation needed] It is a common contaminant in soil and groundwater at hundreds of waste sites across the United States.[citation needed] Some are exposed to trichloroethylene through contaminated drinking water [5](P. 17). Others are potentially exposed through inhalation of vapor from contaminated soil or groundwater entering nearby buildings.[citation needed] Tens of thousands of workers are potentially exposed to trichloroethylene used as a degreasing and cleaning chemical.[citation needed] Other exposures have occurred through the long-term use of trichloroethylene as a surgical anesthetic.[citation needed]

TCE was first detected in groundwater in 1977, and is one of the most frequently detected contaminants in groundwater in the U.S.[citation needed] Up to 34 percent 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 ug/L.[citation needed] 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.[citation needed] Trichloroethylene has been detected in 852 Superfund sites across the United States,[6] according to the Agency for Toxic Substances and Disease Registry (ATSDR).

[edit] 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.[7] 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.

[edit] 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 polluted with trichloroethylene. The chemical has contaminated 23 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.

High-level political appointees in the EPA — notably research director Paul Gilman — sided with the Pentagon and agreed to pull back the risk assessment. In 2004, the National Academy of Sciences was given a a $680,000 contract to study the matter, releasing its report in the summer of 2006. The report has raised greater concern about the adverse health effects of TCE, opening up the debate for better regulation.

[edit] 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.

[edit] Cases of TCE contaminated water

[edit] References

  1. ^ http://ntp.niehs.nih.gov/index.cfm?objectid=72016262-BDB7-CEBA-FA60E922B18C2540/
  2. ^ Elsevier
  3. ^ Assessing the Human Health Risks of Trichloroethylene: Key Scientific Issues
  4. ^ EHP Supplement: Volume 108 (Supplement 2) May 2000
  5. ^ Assessing the Human Health Risks of Trichloroethylene: Key Scientific Issues
  6. ^ ATSDR - ToxFAQs™: Trichloroethylene (TCE)
  7. ^ IARC monograph. "TRICHLOROETHYLENE" Vol. 63, p. 75. Last Updated May 20, 1997. Last retrieved Jun 22, 2007.

[edit] 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., R.E. Tarone and J.K. McLaughlin. 2006. The epidemiology of renal cell carcinoma. Journal of Urology. 176(6): 2353-2358. 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 www.ensolv-europe.com

[edit] External links


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