Trichloroethylene Explained

Trichloroethylene (TCE) is a halocarbon with the formula C2HCl3, commonly used as an industrial degreasing solvent. It is a clear, colourless, non-flammable, volatile liquid with a chloroform-like pleasant mild smell and sweet taste.[1] Its IUPAC name is trichloroethene. Trichloroethylene has been sold under a variety of trade names. Industrial abbreviations include TCE, trichlor, Trike, Tricky and tri. Under the trade names Trimar and Trilene, it was used as a volatile anesthetic and as an inhaled obstetrical analgesic. It should not be confused with the similar 1,1,1-trichloroethane, which is commonly known as chlorothene.

TCE is classified as a volatile organic compound.[1]

History

The earliest record of trichloroethylene synthesis dates back to 1836. It was obtained from the action of potassium hydroxide on 1,1,2,2-tetrachloroethane and 1,1,1,2-tetrachloroethane by Auguste Laurent and notated as (then the atomic weight of carbon was thought to be the half of it really was). Laurent did not investigate the compound further.[2] [3]

Trichloroethylene's discovery is widely attributed to E. Fischer who made it in 1864 via the reduction of hexachloroethane with hydrogen. Fischer investigated TCE and noted its boiling point as between 87 and 90 degrees Celsius.[4] [5] [6] Commercial production began in Germany, in 1920 and in the US in 1925.[7]

Pioneered by Imperial Chemical Industries in Britain, under the trade name "Trilene" (from trichloroethylene), its development was hailed as an anesthetic revolution. It was mostly known as "Trimar" in the United States. The –mar suffix indicates study and development at the University of Maryland, e.g., "Fluoromar" for fluroxene and "Vinamar" for ethyl vinyl ether".[8] 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, low volatility and high solubility preventing 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 about the carcinogenic potential of TCE led to its abandonment in developed countries by the 1980s.

The use of trichloroethylene in the food and pharmaceutical industries has been banned in much of the world since the 1970s due to concerns about its toxicity. Legislation has forced the replacement of trichloroethylene in many processes in Europe as the chemical was classified as a carcinogen carrying an R45 risk phrase, May cause cancer. 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 of May impair fertility, and would not be a legally acceptable substitute.

Production

Today, 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.

Prior to the early 1970s, however, 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 be accomplished either 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

Common impurities in reagent and technical grade TCE are methyl chloroform, carbon tetrachloride, ethylene dichloride, tetrachloroethanes, benzene and phenol. However, these compounds are present in very small amounts and do not possess any risk.

Uses

Trichloroethylene is an effective solvent for a variety of organic materials. It is mainly used for cleaning. Trichloroethylene is an ingredient in various printing ink, varnishes and industrial paint formulations, as an active ingredient.[9] Other uses include dyeing and finishing operations, adhesive formulations, the rubber industry, adhesives, lacquers, and paint strippers. It is applied before plating, anodizing, and painting.[10]

When trichloroethylene 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 (removal of caffeine) and the preparation of flavoring extracts from hops and spices. TCE was used a freezing point depressant in carbon tetrachloride fire extinguishers.

Dehydrochlorination of trichloroethylene with potassium hydride gives dichloroacetylene.[11] Trichloroethylene is also a chain terminator for polyvinyl chloride. Chlorination gives pentachloroethane.

Anaesthesia

Trichloroethylene is a good analgesic at 0.35 to 0.5% concentrations.[12] Trichloroethylene was used in the treatment of trigeminal neuralgia beginning in 1916.[13]

From the 1940s through the 1980s, both in Europe and North America, trichloroethylene was used as a volatile anesthetic almost invariably administered with nitrous oxide. Marketed in the UK by Imperial Chemical Industries under the trade name Trilene it was coloured blue (with a dye called waxoline blue in 1:200,000 concentration)[14] to avoid confusion with the similar-smelling chloroform. Trilene was stabilised with 0.01% thymol.[14]

TCE replaced earlier anesthetics chloroform and ether in the 1940s due to its lower toxicity than chloroform and being relatively non-flammable (unlike ether which is extremely flammable), but was itself replaced in the 1960s in developed countries with the introduction of halothane, which allowed much faster induction and recovery times and was considerably easier to administer. Trilene was also used as an inhaled analgesic, mainly during childbirth, often self-applied by the patient. Trichloroethylene was introduced for obstetrical anaesthesia in 1943, and used until the 1980s.[12] Its anaesthetic use was banned in the United States in 1977 but the anaesthetic use in the United Kingdom remained until the late 1980s.[13]

TCE was used with halothane in the tri-service field anaesthetic apparatus used by the UK armed forces under field conditions. As of 2000, TCE was still in use as an anesthetic in Africa.[15]

Trichloroethylene has been used in the production of halothane.

Cleaning solvent

TCE has also been used as a dry cleaning solvent, although mostly replaced by tetrachloroethylene (also known as perchloroethylene), except for spot cleaning where it is still used under the trade name Picrin.

Perhaps the greatest use of TCE is as a degreaser for metal parts. It has been widely used in degreasing and cleaning since the 1920s because of its low cost, low flammability, low toxicity and high effectivity as a solvent. 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 due to its effect of ozone depletion. As a result, trichloroethylene has experienced some resurgence in use as a degreaser.[13]

Trichloroethylene is used to remove grease and lanolin from wool before weaving.[13]

TCE has also been used in the United States to clean kerosene-fueled rocket engines (TCE was not used to clean hydrogen-fueled engines such as the Space Shuttle Main Engine). During static firing, the RP-1 fuel would leave hydrocarbon deposits and vapors in the engine. These deposits had to be flushed from the engine to avoid the possibility of explosion during engine handling and future firing. TCE was used to flush the engine's fuel system immediately before and after each test firing. The flushing procedure involved pumping TCE through the engine's fuel system and letting the solvent overflow for a period ranging from several seconds to 30–35 minutes, depending upon the engine. For some engines, the engine's gas generator and liquid oxygen (LOX) dome were also flushed with TCE before test firing.[16] [17] The F-1 rocket engine had its LOX dome, gas generator, and thrust chamber fuel jacket flushed with TCE during launch preparations.[17]

Refrigerants

TCE is also used in the manufacture of a range of fluorocarbon refrigerants[18] such as 1,1,1,2-tetrafluoroethane more commonly known as HFC 134a. TCE was also used in industrial refrigeration applications due to its high heat transfer capabilities and its low-temperature specification.

Safety

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 to 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 under a reflux condenser and observing decomposition. Definitive documentation of 1,4-dioxane as a stabilizing agent for TCE is scant due to the lack of specificity in early patent literature describing TCE formulations.[19] [20] Epichlorohydrin, butylene oxide, N-methylpyrrole and ethyl acetate are common stabilisers for TCE, with epichlorohydrin being the most persistent and effective.[21] Other chemical stabilizers include ketones such as methyl ethyl ketone.

Physiological effects

When inhaled, trichloroethylene produces central nervous system depression resulting in general anesthesia. These effects may be mediated by trichloroethylene acting as a positive allosteric modulator of inhibitory GABAA and glycine receptors.[22] [23] Its high blood 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 by dehydrochlorination and phosgene.[24] Cranial nerve dysfunction (especially the fifth cranial nerve) was common when TCE anesthesia was given using CO2 absorbing systems. 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 anesthetics such as halothane by the 1960s.[25]

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.[26] Much of what is known about the chronic human health effects of trichloroethylene is based on occupational exposures. Besides the effects to the central nervous system, workplace exposure to trichloroethylene has been associated with toxic effects in the liver and kidney.[26] A history of long-term exposure to high concentrations of trichloroethylene is a suspected environmental risk of Parkinson's disease.[27]

Metabolism

Trichloroethylene is metabolised to trichloroepoxyethane (TCE oxide) which rapidly isomerises to trichloroacetaldehyde (chloral).[28] Chloral hydrates to chloral hydrate in the body. Chloral hydrate is either reduced to 2,2,2-trichloroethanol or oxidised to trichloroacetic acid. Monochloroacetic acid, dichloroacetic acid[29] and trichloromethane[30] [31] [32] were also detected as minor metabolites of TCE.

Exposure and regulations

See main article: List of trichloroethylene-related incidents. With a specific gravity greater than 1 (denser than water), trichloroethylene can be present as a dense non-aqueous phase liquid (DNAPL) if sufficient quantities are spilt in the environment.

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.[33] Based on available federal and state surveys, between 9% and 34% of the drinking water supply sources tested in the US may have some TCE contamination, though EPA has reported that most water supplies comply with the maximum contaminant level (MCL) of 5 ppb.[34]

Generally, atmospheric levels of TCE are highest in areas of concentrated industry and population. Atmospheric levels tend to be lowest in rural and remote regions. Average TCE concentrations measured in air across the United States are generally between 0.01 ppb and 0.3 ppb, although mean levels as high as 3.4 ppb have been reported.[35] TCE levels in the low parts per billion range have been measured in food; however, levels as high as 140 ppb were measured in a few samples of food. TCE levels above background have been found in homes undergoing renovation.[36]

Existing regulations in the United States and European Union

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.

State, federal, and international agencies classify trichloroethylene as a known or probable carcinogen for humans. In 2014, the International Agency for Research on Cancer updated its classification of trichloroethylene to Group 1, indicating that sufficient evidence exists that it can cause cancer of the kidney in humans as well as some evidence of cancer of the liver and non-Hodgkin's lymphoma.[37]

In the European Union, the Scientific Committee on Occupational Exposure Limit Values (SCOEL) recommends an exposure limit for workers exposed to trichloroethylene of 10 ppm (54.7 mg/m3) for 8-hour TWA and of 30 ppm (164.1 mg/m3) for STEL (15 minutes).[38]

Existing EU legislation aimed at protection of workers against risks to their health (including Chemical Agents Directive 98/24/EC[39] and Carcinogens Directive 2004/37/EC[40]) currently do not impose binding minimum requirements for controlling risks to workers' health during the use phase or throughout the life cycle of trichloroethylene.

In 2023, the United States EPA determined that trichloroethylene presents a risk of injury to human health in various uses, including during manufacturing, processing, mixing, recycling, vapor degreasing, as a lubricant, adhesive, sealant, cleaning product, and spray. It is dangerous from both inhalation and dermal exposure and was most strongly associated with immunosuppressive effects for acute exposure, as well as autoimmune effects for chronic exposures.[41] As of June 1, 2023, two U.S. states (Minnesota and New York) have acted on the EPA's findings and banned trichloroethylene in all cases but research and development.[42] [43] According to the US EPA, in October 2023 it "proposed to ban the manufacture (including import), processing, and distribution in commerce of TCE for all uses, with longer compliance time frames and workplace controls (including an exposure limit) for some processing and industrial and commercial uses until the prohibitions come into effect" to "protect everyone including bystanders from the harmful health effects of TCE".[44]

Remediation

Recent research has focused on the in-place remediation of trichloroethylene in soil and groundwater using potassium permanganate instead of removal for off-site treatment and disposal. Naturally occurring bacteria have been identified with the ability to degrade TCE. Dehalococcoides sp. degrade trichloroethylene by reductive dechlorination under anaerobic conditions. Under aerobic conditions, Pseudomonas fluorescens can co-metabolize TCE. Soil and groundwater contamination by TCE has also been successfully remediated by chemical treatment and extraction. The bacteria Nitrosomonas europaea can degrade a variety of halogenated compounds including trichloroethylene.[45] Toluene dioxygenase has been reported to be involved in TCE degradation by Pseudomonas putida.[46] In some cases, Xanthobacter autotrophicus can convert up to 51% of TCE to CO and .[46]

Society and culture

Groundwater and drinking water contamination from industrial discharge including trichloroethylene is a major concern for human health and has precipitated numerous incidents and lawsuits in the United States.

The 1995 non-fiction book A Civil Action was written about a lawsuit (Anderson v. Cryovac) against following the increase in cancer cases after trichloroethylene pollution incidents and it was adapted to cinema in 1998.

TCE has been used as a recreational drug.[47] Common methods of taking trichloroethylene recreationally include inhalation from a rag (similar to taking an inhalational anaesthetic) and drinking.[48] Most TCE abusers were young people and workers who use the chemical in their workplace. The main reason for abuse is TCE's euphoriant and slight hallucinogenic effect.[48] Some workers had become addicted to TCE.[49]

Further reading

External links

Notes and References

  1. https://wwwn.cdc.gov/tsp/substances/toxsubstance.aspx?toxid=30 Trichloroethylene (TCE)
  2. Essai sur l'Action du Chlore sur la Liqueur des Hollandais et sur quelques Ethers in Annal. de Chimie, LXIII. (1836) page 379
  3. The so-called Perchloride of Formyl, Gmelin, L. (translated in 1855). Hand-book of Chemistry: Organic chemistry. UK: Cavendish Society. pages 200–201
  4. Ueber die Einwirkung von Wasserstoff auf Einfach-Chlorkohlenstoff, Fischer, E. (1864) in Zeitschrift für Chemie. page 268
  5. Waters EM, Gerstner HB, Huff JE. Trichloroethylene. I. An overview. J Toxicol Environ Health. 1977 Jan;2(3):671-707. doi: 10.1080/15287397709529469. PMID 403297.
  6. Hardie DWF (1964). Chlorocarbons and chlorohydrocarbons. 1,1,2,2-Tetrachloroethane. In: Encyclopedia of Chemical Technology. Kirk RE, Othmer DF, editors. New York: John Wiley & Sons, pp. 159–164
  7. Mertens JA (1993). Chlorocarbons and chlorohydrocarbons. In: Kirk-Othmer Encyclopedia of Chemical Technology, 4th Ed. Kroschwitz JI, Howe-Grant M, editors. New York: John Wiley & Sons, pp. 40–50.
  8. A Portrait of Medical History and Current Medical Problem (1962), p. 130
  9. Web site: Subramanian . Indu . Is Most Parkinson's Disease Man-Made? . Medscape . 20 Nov 2023 . 29 Nov 2023.
  10. Caudle . W. Michael . Guillot . Thomas S. . Lazo . Carlos R. . Miller . Gary W. . Industrial toxicants and Parkinson's disease . NeuroToxicology . Elsevier BV . 33 . 2 . 2012 . 0161-813X . 10.1016/j.neuro.2012.01.010 . 178–188. 22309908 . 3299826 .
  11. 10.1021/jo00391a059. Practical synthesis of dichloroacetylene. 1987. Denis. Jean Noel. Moyano. Albert. Greene. Andrew E.. The Journal of Organic Chemistry. 52. 15. 3461–3462.
  12. Textbook of Obstetric Anaesthesia. (2002). UK: Greenwich Medical Media. Pages 64-65
  13. Chapter 4: Trichloroethylene, Morrison, R. D., Murphy, B. L. (2015). Chlorinated Solvents: A Forensic Evaluation: Royal Society of Chemistry.
  14. Current Researches in Anesthesia & Analgesia. (1951). USA: International Anesthesia Research Society. p.278
  15. Web site: Volatile Anaesthetic Agents . P. Fenton . 2000 . 2012-02-11 . dead . https://web.archive.org/web/20120107011331/http://www.nda.ox.ac.uk/wfsa/html/u11/u1115_02.htm . 2012-01-07 .
  16. Web site: Santa Susana Field Laboratory : The Use of Trichloroethylene at NASA's SSFL Sites . Ssfl.msfc.nasa.gov . 22 February 2015 . dead . https://web.archive.org/web/20131114001621/http://ssfl.msfc.nasa.gov/public-involvement/docs/SSFL_TCE_Final_Fact_Sheet.pdf . 14 November 2013 .
  17. Web site: F-1 Rocket Engine Operating Instructions. Ntrs.nasa.gov. 20 October 2014.
  18. Web site: Production of R-134a . Nd.edu. 21 February 2015 . dead . https://web.archive.org/web/20090711235310/http://www.nd.edu/~enviro/design/r134a.pdf . 11 July 2009 .
  19. Book: Murphy. Brian L. Morrison. Robert D.. 2015. 9. Source Identification and Age Dating of Chlorinated Solvents. Introduction to environmental forensics. Academic Press. 978-0124047075. 3rd. sec. 9.2.2.1 1,4-Dioxane.
  20. Book: Mohr, Thomas K. G.. Environmental investigation and remediation: 1,4-dioxane and other solvent stabilizers. 2010. CRC Press. 978-1566706629. Historical Use of Chlorinated Solvents and Their Stabilizing Compounds. p. 53 "Was 1,4-Dioxane a Stabilizer for Trichloroethylene?".
  21. Morrison, R. D., Murphy, B. L. (2013). Chlorinated Solvents: A Forensic Evaluation. UK Royal Society of Chemistry.
  22. M. J. Beckstead, J. L. Weiner, E. I. 2nd Eger, D. H. Gong & S. J. Mihic . Glycine and gamma-aminobutyric acid(A) receptor function is enhanced by inhaled drugs of abuse . . 57 . 6 . 1199–1205 . 2000 . 10825391.
  23. M. D. Krasowski & N. L. Harrison . The actions of ether, alcohol and alkane general anaesthetics on GABAA and glycine receptors and the effects of TM2 and TM3 mutations . . 129 . 4 . 731–743 . 2000 . 10.1038/sj.bjp.0703087 . 10683198. 1571881 .
  24. Orkin, F. K. (1986) Anesthesia Systems (Chapter 5). In R. D. Miller (Ed.), Anesthesia (second edition). New York, NY: Churchill Livingstone.
  25. 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.
  26. Web site: Trichloroethylene | Technology Transfer Network Air Toxics Web site | US EPA . Epa.gov . 2013-10-05.
  27. Dorsey ER, Zafar M, Lettenberger SE, et al . Trichloroethylene: An Invisible Cause of Parkinson's Disease? . J Parkinsons Dis . 13 . 2 . 203–218 . 2023 . 36938742 . 10.3233/JPD-225047 . 10041423 .
  28. Fishbein, L. (1977). Potential Industrial Carcinogens and Mutagens. Environmental Protection Agency, Office of Toxic Substances
  29. Biologically Based Methods for Cancer Risk Assessment. (2013). Springer US.
  30. 21.4.25: Trichloroethylene in Biological Monitoring: An Introduction. (1993). UK: Wiley.
  31. Toxicological Profile for Trichloroethylene: Draft. (1995). U.S. Department of Health and Human Services.
  32. Mutagenesis. (1978). page 268
  33. Lyne FA, McLachlan T (1949). "Contamination of water by trichloroethylene" p. 513 in 10.1039/AN9497400510 . Notes . 1949 . Lilliman . B. . Houlihan . J. E. . Lyne . F. A. . McLachlan . T. . The Analyst . 74 . 882 . 510–513. 1949Ana....74..510L .
  34. Web site: Consumer Factsheet on: Trichloroethylene . Epa.gov . 22 February 2015.
  35. Web site: 2022-09-09 . Trichloroethylene Toxicity: Where is Trichloroethylene Found? Environmental Medicine ATSDR . 2023-03-02 . www.atsdr.cdc.gov . en-us.
  36. Web site: Trichloroethylene (tce) TEACH Chemical Summary - epa nepis.
  37. Book: Trichloroethylene (IARC Summary & Evaluation, Volume 106, 2014) . iarc.fr . 2016-03-08.
  38. Web site: Recommendation from the Scientific Committee on Occupational Exposure Limits for Trichloroethylene (SCOEL/SUM/142) . PDF . April 2009.
  39. Web site: Council Directive 98/24/EC . PDF . Eur-lex.europa.eu . 21 February 2015.
  40. Web site: Directive 2004/37/EC . PDF . Eur-lex.europa.eu . 21 February 2015.
  41. Web site: US EPA . OCSPP . 2020-02-12 . Final Risk Evaluation for Trichloroethylene . 2023-06-03 . www.epa.gov . en . PDF.
  42. Web site: How Minnesota passed the country's first ban on trichloroethylene . 28 August 2023 . www.pca.state.mn.us/news-and-stories . Minnesota Pollution Control Agency . 6 September 2023 . live . https://web.archive.org/web/20230906174016/https://www.pca.state.mn.us/news-and-stories/tce-ban-in-effect . 6 September 2023 . en.
  43. act . 116.38 (also known as "White Bear Area Neighborhood Concerned Citizens Group Ban TCE Act") . 2022 . Chapter 116, Section 116.385 . Environmental Protection, . Minnesota Statutes . Minnesota Legislature . live . https://web.archive.org/web/20230906174558/https://www.revisor.mn.gov/statutes/2022/cite/116.385 . 6 September 2023 . en.
  44. Web site: Risk Management for Trichloroethylene (TCE) . US EPA . 21 Nov 2023 . 23 Nov 2023.
  45. Web site: Nitrosomonas europaea . Genome.jgi-psf.org . 2015-02-05 . 2015-02-21 . https://web.archive.org/web/20090703071550/http://genome.jgi-psf.org/finished_microbes/niteu/niteu.home.html . 2009-07-03 . dead .
  46. Book: Bioremediation Technologies: Principles and Practice. Robert L. Irvine. Subhas K. Sikdar. 21 February 2015. 978-1566765619. 1998. 142, 144. CRC Press .
  47. https://books.google.com/books?id=mpnaPQd_fZsC&pg=PT6077&dq=%22Trichloroethylene%22+%22recreational%22&hl=tr&newbks=1&newbks_redir=0&source=gb_mobile_search&sa=X&ved=2ahUKEwiEus_-oe2CAxVTtKQKHSxbC7I4HhDoAXoECAMQAw#v=onepage&q&f=false Trichloroethylene
  48. https://books.google.com/books?id=OWFiVaDZnkQC&pg=PA743&dq=%22Trichloroethylene%22+%22abuse%22&hl=ro&newbks=1&newbks_redir=0&source=gb_mobile_search&sa=X&ved=2ahUKEwjr_dTa5-2CAxXHSfEDHVTkAfIQ6AF6BAgIEAM#v=onepage&q&f=false Chapter 50: Trichloroethylene
  49. Trichlorethylene Addiction and its Effects (1972) Boleslaw Alapin M.D., M.R.C. Psych. British Journal of Addiction to Alcohol & Other DrugsVolume 68, Issue 4 p. 331-335 DOI