Trichloroethylene is a non-flammable liquid chlorinated hydrocarbon used as an industrial solvent. It is often referred to as TCE, Trike, or tri and is sold under numerous brand names.

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Sean Foley
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Just the facts

Physical Information

Name:Trichloroethylene, 1,1,2-Trichloroethene, 1,1-Dichloro-2-Chloroethylene, 1-Chloro-2,2-Dichloroethylene, Acetylene Trichloride, TCE, Trethylene, Triclene, Tri, Trimar, Trilene

Trade Names: Acetylene trichloroethylene, Algylen, Anameth, Benzinol, Chlorilen, CirCosolv, Germalgene, Lethurin, Perm-a-chlor, Petzinol, Philex, TRI-Plus M and Vitran

Use: Solvent

Source: Industrial, environmental

Recommended daily intake: None

Absorption: intestine, inhalation, skin

Sensitive individuals: Unknown

Toxicity/symptoms: Nervous system, cancer

Regulatory facts:

General facts: Long history of use as a solvent. Common occupational hazard in certain industries. Toxicity to humans and wildlife is well documented.

Environmental:Found in indoor and outdoor air, drinking and surface water. An important chemical found in US EPA Superfund sites.

Recommendations: Avoid, proper workplace protection

Chemical Structure

Physical Properties

Molecular formula: C 2 HCl 3

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

Pharmacology and Metabolism

Understanding the absorption, distribution, metabolism, and elimination of trichloroethylene is critical to the qualitative and quantitative assessment of human health risks from environmental exposures. Qualitatively, pharmacokinetics is helpful in identifying the chemical species that might be causally associated with observed toxic responses. This is particularly important for trichloroethylene because many of its toxic effects are thought to be due to metabolites rather than to trichloroethylene. The delineation of interspecies and intraspecies pharmacokinetic differences can provide insights into how laboratory animal and epidemiologic data might reveal overall human health risks and the basis for individual differences in susceptibility. Furthermore, physiologically based pharmacokinetic models can quantify the relationship between external measures of exposure and internal measures of a toxicologically relevant dose. Selecting the appropriate dose metric for use in risk assessment depends on the understanding of the target tissue, active chemical, and mode of action for a particular toxic effect as well as the reliability of physiologically based pharmacokinetic models (#National Research Council, 2006).

Trichloroethylene is rapidly and extensively absorbed by all routes of environmental exposures, including ingestion, inhalation, and dermal contact. Once absorbed, trichloroethylene distributes throughout the body via the circulatory system. Most trichloroethylene taken into the body is metabolized; direct exhalation of the parent compound is the other major route of elimination.

Figure 1

Metabolism of trichloroethylene. Metabolites marked with U are known urinary metabolites. Arrows with broken lines indicate other possible steps in forming dichloroacetic acid. Abbreviations: CYP, cytochrome P-450; DCA, dichloroacetic acid; DCVC, S-(1,2-dichlorovinyl)-L-cysteine; DCVG, S-(1,2-dichlorovinyl)glutathione; DCVT, S-(1,2-dichlorovinyl)thiol; GST, glutathione S-transferase; NAcDCVC, N-acetyl-S-(1,2-dichlorovinyl)-L-cysteine; TCA, trichloroacetic acid; TCE, trichloroethylene; TCE-O-CYP, trichloroethylene-oxide-cytochrome P-450 complex; TCOH, trichloroethanol; TCOG, trichloroethanol glucuronide. (From (1)).

Figure 1 presents a postulated scheme for the pathways of trichloroethylene metabolism, adapted from the work of Clewell et al. (2000), Lash et al. (2000a), and recent studies described below. Trichloroethylene metabolism occurs through two main, irreversible pathways---oxidation via the microsomal mixed-function oxidase system (cytochrome P-450s [CYPs]) primarily to chloral [C2HCl30]or chloral hydrate [CCl3CH(OH)2] and trichloroethylene oxide), and conjugation with glutathione by glutathione S-transferases to S-1,2-dichlorovinyl-L-glutathione. For trichloroethylene oxidation, CYP2E1 is thought to be most important in vivo. Subsequent important metabolic branch points include the production of trichloroethanol, regeneration of chloral and chloral hydrate from trichloroethanol, and further metabolism of S-1,2-dichlorovinyl-L-cysteine.


Up until 1977, trichloroethylene had direct uses for the human body. Used as a general anesthetic, skin wound and surgical disinfectant, and spice in coffee, human beings were ingesting and relying on trichloroethylene to sanitize their injuries. In 1977, these uses of trichloroethylene were banned by the FDA for their harm.

Today, there are different uses for trichloroethylene. As of 1986, 80% of the Trichloroethylene in the United States was used as vapor degreasing during production of metal parts. Trichloroethylene was also used as a chemical intermediate and some was even produced for export. Trichloroethylene's purpose in vapor degreasing of metal parts is highly important. Used by automotive and metal industries, trichloroethylene proves to be powerful in the removal of grease, oil, fat, wax and tar.

Trichloroethylene has also been used by textile industries. Their main use of trichloroethylene is to clean cotton, wool and other fabrics. It is also used as a solvent for waterless dying. Trichloroethylene is also found and used in products such as dyes, printing inks, paints, adhesives, paint removers, typewriter correction fluids, as well as spot removers.

About 10 million pounds of trichloroethylene are used each year in the manufacture of poly vinyl chloride.

It is an unstable and dangerous liquid that is non-flammable. When dealing with water, TCE is slightly soluble, while in most other organic Solvents - Chemical Profiles and External Links, TCE is very soluble. TCE is a colorless, or blue organic liquid, which has an odor somewhat like chloroform. The odor is sweet, and it has a sweet, yet burning taste.

Health Effects

Human Exposure
Trichloroethylene is a common environmental contaminant at Superfund sites, Department of Defense facilities, and certain manufacturing operations (e.g., aircraft, spacecraft). It has been found at approximately 852 of the 1,416 sites proposed for inclusion on the U.S. Environmental Protection Agency (EPA) National Priorities List. On the basis of data reported to the EPA Toxic Release Inventory, it was estimated that approximately 42 million pounds of trichloroethylene were released into the environment in 1994 (#Scott and Cogliano, 2000).

People can be exposed to trichloroethylene from contaminated air (outdoor and indoor), water, and soil. Data from 2004 on ambient air concentrations of trichloroethylene indicate an average of 0.37 µg/m3 (range, 0-6.32 µg/m3), a concentration that has remained fairly consistent since 1996 (#National Research Council, 2006). Mean concentrations at various land-use sites include 1.84 µg/m3 in commercial areas, 1.54 µg/m3 in industrial areas, 1.08 µg/m3 in agricultural areas, and 0.89 µg/m3 in residential areas Indoor air can become contaminated by certain consumer products (e.g., adhesives, tapes) and by volatilization from contaminated water supplies. Vapor intrusion through walls and floors can also be a source of indoor exposure when buildings are near contaminated groundwater.

Trichloroethylene is the most frequently reported organic contaminant in groundwater. The Agency for Toxic Substances and Disease Registry (ATSDR 1997a) estimates that between 9% and 34% of drinking water supply sources tested in the United States contain some trichloroethylene. This has lead the EPA to set standards for the amount of TCE that is allowed in the water samples. The goal standard is zero parts per billion, because this is the only level the EPA can prove to have no affects on the population. The realistic standard is 5 parts per billion, because that is as low as scientists feel is possible at present (#EPA, 2006). The release of TCE into the environment continues to rise. The states having the highest levels of the contaminant are Pennsylvania and Illinois. When levels were measures from 1987 to 1993, Pennsylvania showed the highest amount of TCE in drinking water with 33,450 pounds. West Virginia had the highest amount of TCE going directly into the water sources. TCE is a major contaminant found in almost one half of all Superfund Sites (#NIEHS, 2007). Those most at risk of exposure to TCE are people who work in factories that produce TCE or live near a TCE factory, an industrial waste site, or a military base (#EPA, 2007).

Metabolites and Exposure
Trichloroethylene toxicity comes primarily from its metabolites, but people may be exposed to the metabolites from sources other than trichloroethylene. For example, chlorination of drinking water produces the by-products chloral, chloral hydrate, monochloroacetic acid, dichloroacetic acid, and trichloroacetic acid. Chloral is used in the production of polyurethanes and as a chemical intermediate for the herbicide trichloroacetic acid. Chloral hydrate is a pharmaceutical used as a hypnotic and sedative. The metabolite monochloroacetic acid is used in pharmaceuticals, as an herbicide, and as a chemical intermediate in the production of indigoid dyes. Trichloroacetic acid is also used as a chemical intermediate and in the production of herbicides (#Simon, 2005).

Other chemical compounds have some of the same metabolites as trichloroethylene, including tetrachloroethylene, 1,1,1-trichloroethane, 1,2-dichloroethylene (cis-, trans-, and mixed isomers), 1,1,1,2-tetrachloroethane, and 1,1-dichloroethane. Tetrachloroethylene is used in textile dry cleaning, as part of the processing and finishing in cleaning and degreasing metals, and as a chemical intermediate in the synthesis of some fluorocarbons. 1,1,1-Trichloroethane is used as a solvent and in pesticides, textile processing, cutting oil formulations, and printing inks. 1,2-Dichloroethylene, 1,1,1,2-tetrachloroethane, and 1,1-dichloroethane are used primarily as solvents in cleaning, degreasing, and extracting processes (#Simon, 2005).

Trichloroethylene has shown reasonable evidence that it may increase risk of certain types of cancers in humans. Studies on experimental animals have shown that overexposure to TCE has caused a greater occurrence of renal and liver cell carcinomas, other studies may suggest an increased occurrence of testicular and lung cancers as well. Renal cell carcinoma studies provided adequate data suggesting that TCE acts on VHL, a tumor suppressing gene. Genotoxic effects were seen after an overexposure of TCE and damage to the VHL gene led to a higher occurrence of RCC (renal cell carcinoma). When the trichloroethylene is absorbed into the liver, it produces metabolites such as trichloroacetic acid and dichloroacetic acid. These have been shown responsible for the tumors in laboratory animals tested. The animal studies show that Trichloroethylene and its metabolites is a complete carcinogen, meaning it acts on both tumor initiation and progression. These findings suggest that high levels of exposure may lead to cancer in experimental animals and therefore the International Agency for Research on Cancer (IARC) has determined that trichloroethylene is probably carcinogenic to humans. Studies involving humans with long-term exposure of high levels of trichloroethylene in drinking water or in workplace air have increased incidences of cancer. Since most of these studies have strictly used experimental animals (mice and rats), it is not possible to predict whether human are more susceptible to the carcinogenic effects or not.

Trichloroethylene is metabolized in the body by two major pathways: the oxidative pathway and the glutathione-conjugation pathway. The metabolites these pathways generate are thought to be responsible for the toxicity and carcinogenicity observed in different organ systems. Key scientific issues for characterizing these hazards include identifying the metabolites responsible for the effects, elucidating the mode of action, and understanding the relevance of animal data for humans (#National Research Council, 2006).

Kidney Toxicity and Cancer
Trichloroethylene and some of its metabolites in the glutathione-conjugation pathway have been shown to be nephrotoxic and nephrocarcinogenic. There is concordance between animal and human studies. In bioassays, rats developed tubular toxicity before they developed tumors. Investigations of nephrotoxicity in human populations show that highly exposed workers exhibit evidence of damage to the proximal tubule. The magnitude of exposure needed to produce kidney damage is not clear (#National Research Council, 2006).

Trichloroethylene nephrotoxicity is associated with a multistep metabolic pathway. It is generally accepted that the metabolite S-(1,2-dichlorovinyl)-L-cysteine is the penultimate nephrotoxicant. The metabolite can undergo bioactivation by conjugation to reactive species that are genotoxic and cytotoxic and by sulfoxidation. Sulfoxides are more potent nephrotoxicants than their parent S-conjugates. Both S-(1,2-dichlorovinyl)-L-cysteine and S-(1,2-dichlorovinyl)-L-cysteine sulfoxide appear to play a role in renal tubular cell toxicity (#National Research Council, 2006).

Evidence from experimental, mechanistic, and epidemiologic studies supports the conclusion that trichloroethylene is a potential kidney carcinogen. In animal studies, the nephrocarcinogenic effects of trichloroethylene were more pronounced in male rats than in female rats and were absent in male and female mice. Studies on trichloroethylene metabolism in rodents and in humans indicate a bioactivation role in the development of nephrocarcinogenicity. This has been linked with the formation of S-(1,2-dichlorovinyl)-L-cysteine; however, there are no studies of the carcinogenic potential of this metabolite (#National Research Council, 2006).

Animal studies show that trichloroethylene acts as a complete carcinogen (at the stages of both tumor initiation and promotion and progression) in a dose-dependent manner, with nephrotoxicity as the promoter for cells initiated by a trichloroethylene metabolite. It is not possible to predict whether humans are more or less susceptible to the carcinogenic effects than other animals, because species differences in the extent of formation of S-(1,2-dichlorovinyl)-L-cysteine have not been fully characterized. Furthermore, the cytochrome P-450 enzyme isoforms that metabolize trichloroethylene have polymorphisms within national populations, resulting in considerable interindividual differences in enzyme expression. The committee ruled out the accumulation of ?2µ-globulin, peroxisome-proliferator activated receptor ? (PPAR?) agonism, and formic acid production as modes of action for the production of renal tumors in rodents (#National Research Council, 2006).

Renal clear cell carcinoma, the carcinoma most often induced by trichloroethylene, was shown to link with the homozygous inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene. The evidence indicates a strong association between trichloroethylene and VHL mutation, especially in protein expression, and kidney cancer in humans. Some studies have reported increased occurrence of mutations in renal cancer cells of patients exposed to high concentrations of trichloroethylene. The genotoxic effect of trichloroethylene metabolites likely results from bioactivation pathways in the kidney leading to renal VHL gene damage and renal cell carcinomas. However, there remains a lack of direct evidence that alterations in the VHL gene initiate renal tumors, but the alterations, especially in protein expression, might contribute to tumor progression. In the absence of information on the temporal relationship between VHL mutations and renal tumor initiation, it is prudent to assume that trichloroethylene-induced VHL mutations are initiating events. Direct evidence of alterations in the VHL gene in association with tumor progression remains to be determined (#National Research Council, 2006).

Liver Toxicity and Cancer
Animal data on trichloroethylene indicate that relatively high doses are needed to induce liver toxicity and cancer, even in susceptible strains of mice. The three major oxidative metabolites of trichloroethylene-trichloroacetic acid, dichloroacetic acid, and chloral hydrate-can contribute to liver toxicity and cancer in rodents. Trichloroethylene produces hepatotoxicity in experimental animals and humans that depends on generation of reactive intermediates by the enzyme cytochrome P-450 in the liver. Studies with laboratory animals indicate that trichloroethylene and its metabolites also produce liver effects independent of hepatotoxicity, including elevation in plasma bile acid concentration and accumulation of liver glycogen. The relevance and significance of these effects to humans remain to be elucidated (#National Research Council, 2006).

Trichloroethylene, chloral hydrate, and trichloroacetic acid induce liver cancer in mice when blood concentrations achieve millimolar concentrations. In contrast, dichloroacetic acid is active in rats as well and requires a much lower concentration to produce liver tumors. Trichloroethylene and its metabolites promote liver cancer. The mode of action for trichloroacetic acid in liver is principally as a liver peroxisome proliferator and agonist of PPAR? rather than as a genotoxicant. A significant lack of concordance in the sensitivity of human and rodent hepatocytes to peroxisome proliferators and early events associated with liver tumor promotion has been noted, with humans being much less sensitive. In addition, there is no supporting epidemiologic evidence of enhanced occurrence of liver tumors in humans administered potent rodent peroxisome proliferators. The weak carcinogenic activity in the liver of chloral hydrate in male B6C3F1 mice combined with lower rates of oxidation and higher rates of conjugation in humans compared with mice indicate that the mode of action for mice is not relevant to humans.
Species differences in susceptibility and phenotypic differences in tumors derived from trichloroethylene and its metabolites suggest that there are mechanistic differences in the way these chemicals cause tumors that cannot be fully explained by peroxisome proliferation. In rodents, the promotional activity of dichloroacetic acid includes a significant effect on cellular metabolism and cellular proliferation that encompasses a mitogenic mode of action. Assuming a mitogenic mode of action for dichloroacetic acid as a rodent liver carcinogen, genotypic species differences between mice and humans suggest that humans would be much less susceptible to liver carcinogenesis.

Respiratory Toxicity and Cancer
Trichloroethylene has been shown to induce lung tumors in rodents. It is well documented that the mode of action for this effect is localization of cytochrome P-450 metabolites of trichloroethylene in the Clara cells of the lungs and that pulmonary metabolism of trichloroethylene is species dependent. The proximate toxicant for the Clara cell, whether chloral, dichloracetyl chloride, or another metabolite, is still under study. The collective evidence indicates that rodents and humans are significantly different in their capacity to metabolize trichloroethylene in the lungs, with humans having less capacity. Results of most epidemiologic studies of occupational exposure to trichloroethylene do not show a strong association between trichloroethylene exposure and increased incidence of lung tumors. Thus, pulmonary cancer does not appear to be a critical end point in assessing human health risks to trichloroethylene.

Non-cancer Endpoints
The chlorinated hydrocarbon trichloroethylene (TCE) is used extensively in industry as an anesthetic and solvent, thus, this chemical has caused various harmful effects in human beings. When inhaled, trichloroethylene can cause headaches, dizziness, poor coordination, and potentially unconsciousness (similar effects as intoxication). Inhalation can also cause lung damage as well as heart, nerve, kidney and liver damage, followed by death. Consumption of this chemical also causes similar effects as inhalation along with nausea, a weakened immune system and a damaged fetal development in pregnant woman. TCE has also been shown to increase speech impairments for children under 10 years of age (#ATSDR NER, 1999). Skin contact with this chlorinated hydrocarbon causes a rash to form (#ATSDR Tox FAQs, 2007). Epidemiologically, trichloroethylene has also been seen to cause heart defects in children who have consumed water with high amounts of this chemical, which corresponds to the effects seen in laboratory animals (#ATSDR Public Health Statement, 2007).

Multiple animal studies have found decreased fetal growth after maternal exposure to trichloroethylene. Impaired fetal growth was also a consistent finding in different community studies of mothers exposed to drinking water contaminated with trichloroethylene or tetrachloroethylene, a compound that has some of the same metabolites as trichloroethylene. However, a mechanistic basis for this effect remains to be elucidated (#National Research Council, 2006).

Epidemiologic investigations of communities exposed to trichloroethylene have also reported mixed results. A 2- to 3-fold increase in risk of congenital heart defects was found in multiple studies, and the most frequently found defects were the same in animal and human studies (defects of the interventricular septae and the valves). In addition, mechanistic support is provided by studies in animals demonstrating altered proliferation in the endocardial cushions at low dose or alterations in endothelial cell activation and decreased expression of two markers of epithelial mesenchymal cell transformation, a key process in valve and septum formation. Evidence that trichloroacetic acid and dichloroacetic acid are as potent as trichloroethylene suggests that CYP2E1 metabolic activation, as well as the fractional formation of trichloroacetic acid from chloral, is important in trichloroethylene cardiac teratogenesis (#National Research Council, 2006).

Reproductive and Developmental Toxicity
Evidence from animal and epidemiologic studies suggests that several reproductive and developmental toxicity end points may be associated with trichloroethylene exposure, including infertility in males and females, impaired fetal growth, and cardiac teratogenesis. Multiple rodent studies
indicate that trichloroethylene affects spermatogenesis and the fertilizing capability of sperm in males and decreased fertilizability of oocytes in females. The effects appear to depend on metabolic activation of trichloroethylene by CYP2E1, but which oxidative metabolite is the proximate toxicant remains unknown. The relevance of these effects on rodent reproduction for predicting human outcomes also is not clear (#National Research Council, 2006).

Multiple animal studies have found decreased fetal growth after maternal exposure to trichloroethylene. Impaired fetal growth was also a consistent finding in different community studies of mothers exposed to drinking water contaminated with trichloroethylene or tetrachloroethylene, a compound that has some of the same metabolites as trichloroethylene. However, a mechanistic basis for this effect remains to be elucidated (#National Research Council, 2006).

Multiple studies in mammalian and avian models suggest that trichloroethylene or one or more of its metabolites (trichloroacetic acid and dichloroacetic acid) can cause cardiac teratogenesis. The avian studies are the most convincing. Rodent studies have had mixed results, suggesting either methodological or strain differences. The committee noted that the low-dose studies showing a positive correlation in trichloroethylene-induced cardiac teratogenesis showed unusually flat dose-response curves and came from a single laboratory. The results need to be replicated in another laboratory to clarify the dose-response relationship(#National Research Council, 2006).

Epidemiologic investigations of communities exposed to trichloroethylene have also reported mixed results. A 2- to 3-fold increase in risk of congenital heart defects was found in multiple studies, and the most frequently found defects were the same in animal and human studies (defects of the interventricular septae and the valves). In addition, mechanistic support is provided by studies in animals demonstrating altered proliferation in the endocardial cushions at low dose or alterations in endothelial cell activation and decreased expression of two markers of epithelial mesenchymal cell transformation, a key process in valve and septum formation. Evidence that trichloroacetic acid and dichloroacetic acid are as potent as trichloroethylene suggests that CYP2E1 metabolic activation, as well as the fractional formation of trichloroacetic acid from chloral, is important in trichloroethylene cardiac teratogenesis(#National Research Council, 2006).

Past evidence showed that inhalation of trichloroethylene causes neurotoxic effects in laboratory animals and humans that are similar in nature (e.g., massiter reflex latency, motor incoordination, changes in heart rate) and occur at comparable concentrations of exposure (7-16 parts per million [ppm]). New information has not added substantially to the understanding understanding the effects of chronic exposure to trichloroethylene. It is not yet possible to ascertain the extent of trichloroethylene-induced impairment of complex neurological functions such as learning, memory, and attention. Whether there is preferential vulnerability to trichloroethylene across these domains, what exposure parameters might be associated with the effects, the extent of their reversibility, and the impact of the developmental period of exposure on such effects remain to be elucidated. It has been suggested that exposure to trichloroethylene during early development could enhance its effects on the nervous system, but the available data are insufficient to draw firm conclusions. Aging appears to enhance susceptibility of the nervous system after exposure to trichloroethylene. Some studies suggest a contribution of trichloroethylene to Parkinson's disease. Multiple mechanisms appear to contribute to the neurotoxic action of trichloroethylene, and further study is needed to elucidate them more precisely (#National Research Council, 2006).

Among the immunotoxicity end points the committee evaluated, evidence for an effect of trichloroethylene was strongest for autoimmune disease. Studies in genetically susceptible rodents have shown that trichloroethylene exacerbates underlying autoimmune disease, and supporting information comes from multiple human studies of scleroderma and exposures to organic solvents. The metabolites and the mode of action involved have not been elucidated, but a role for chloral has been implicated in mouse models. Some individuals might be genetically susceptible to developing autoimmune disease; alterations in the CYP2E1 gene are suspected to play a role (#National Research Council, 2006).


The following is from the *Canadian Centre for Occupational Health and Safety (CCOHS) Profile for TCE*:

This material is a VERY TOXIC liquid (MUTAGEN, SKIN/EYE IRRITANT, SUSPECT CANCER HAZARD and POSSIBLE REPRODUCTIVE HAZARD). Before handling, it is extremely important that engineering controls are operating and that protective equipment requirements and personal hygiene measures are being followed. People working with this chemical should be properly trained regarding its hazards and its safe use. Maintenance and emergency personnel should be advised of potential hazards.

If trichloroethylene is released, immediately put on a suitable respirator and leave the area until the severity of the release is determined. In case of leaks or spills, escape-type respiratory protective equipment should be available in the work area.

Immediately report leaks, spills or ventilation failures.

Unprotected persons should avoid all contact with this chemical including contaminated equipment.

Closed handling systems for processes involving this material should be used. If a closed handling system is not possible, use in smallest possible amounts in well-ventilated area, separate from the storage area. Avoid generating vapours or mists. Prevent the release of vapours/mist into the workplace air. Do not use near welding operations, flames or hot surfaces because of the risk of formation of toxic hydrogen chloride or phosgene. Do not perform any welding, cutting, soldering, drilling or other hot work on an empty vessel, container or piping until all liquid and vapours have been cleared.

Follow the chemical supplier/manufacturer's advice regarding checking and maintaining appropriate levels of stabilizers.

Do not use with incompatible materials such as strong bases (e.g. sodium hydroxide) and alkali metals (e.g. sodium and its alloys). Never return contaminated material to its original container. Inspect containers for leaks before handling. Stand upwind of all opening, pouring and mixing operations. Prevent damage to containers. Label containers. Open containers on a stable surface. Keep containers tightly closed when not in use. Assume that empty containers contain residues which are hazardous. Never return contaminated material to its original container. Keeping work areas clean is essential. Use work surfaces that can be easily decontaminated. Follow handling precautions on Material Safety Data Sheet. Have suitable emergency equipment for fires, spills and leaks readily available. Practice good housekeeping. Maintain handling equipment. Comply with applicable regulations.

Current Events

In 2001 the Environmental Protection Agency (EPA) issued a draft report on the known health effects of TCE and recommended stringent cleanup protocols to be executed at both public and private sites and to be included as a chemical covered by the Superfund act. This sparked a major debate between the Department of Defense and the Department of Energy on whether TCE had the risks the EPA claimed, largely due to the fact many of their sites were contaminated by TCE. President Bush interceded and called for a National Academies of Science (NAS) report before any actions would be taken regulating TCE (#Associated Press, 2006). The NAS completed their assessment and filed their report in July of 2006. This study helped to further boost awareness and created a guideline on how much TCE was safe exposure for humans through a cost benefit analysis (#Henderson, et al, 2006). Residents in the San Gabriel and San Fernando Valleys in California are perhaps the most populated areas affected by TCE contamination in public water supplies. Over two million residents were potentially exposed to carcinogenic levels of TCE from aquifers contaminated by surrounding military bases (#Vartabedian, 2007). In August of this year, Senator Clinton of New York introduced legislation to amend the safe drinking water act focusing on TCE contamination. That bill has yet to leave committee to be voted upon (#Grayson and Strong, 2007).


Trichloroethylene was on the market in the 1950's as a degreaser, in food and in pharmaceutical industry. Once the toxicity was known it was slowly removed from the food and pharmaceutical market in the 1970's and total abandonment was reached in the 1980's. There are many different cases of contamination of ground water, the first two in Woburn, MA (1970's) and the military base, Camp Lejeune, NC (1980's). These incidents were caused by improper disposal of TCE. Woburn, MA had many cases of leukemia thought to be linked to the improper disposal of TCE by W. R. Grace and Company and Beatrice Foods, however nothing was proven at the time(#Fujita, et al, 2002). In Camp Lejeune the groundwater many different health effects were caused by the TCE (#Johnson, 2007). Other incidents occurred in 1916 involving animal feeds containing soybean meal defatted with TCE which caused the death of cattle (#Doherty, 2000).


Associated Press (AP). "Study points to cancer risks in common pollutant". 7/27/2006.

Agency for Toxic Substances and Disease Registry (ATSDR). "National Exposure Registry Trichloroethylene (TCE) Subregistry Baseline Through Followup 3 Technical Report October 1999 Disclaimer". March 1999. Accessed 13 Dec. 2007

Agency for Toxic Substances and Disease Registry (ATSDR). "Public Health Statement for Trichloroethylene". October 2007. Accessed 12 Dec. 2007.

Agency for Toxic Substances and Disease Registry (ATSDR). "Agency for Toxic Substances & Disease Registry Tox FAQs". 11 Sept. 2007. Accessed 12 Dec. 2007.

Richard E Doherty. "A History of the Production and Use of Carbon Tetrachloride, Tetrachloroethylene, Trichloroethylene and 1,1,1-Trichloroethane in the United States." Journal of Environmental Forensics (June, 2000).

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Hiroyoshi Fujita, Chiaki Nishitani, and Kazuhiro Ogawa. "Regulatory Heme and Trichloroethylene Intoxication: A Possible Explanation of the Case of '"A Civil Action'". Environmental Health and Preventive Medicine Vol. 7 (2002) , No. 3 p.103.

E. Lynn Grayson and Michale R. Strong. "Calls for increased TCE Regulation". Jener and Block: Environmental, Energy, and Natural Resources Law Practice. October 16, 2007.

Rogene F. Henderson, Mary E. Davis, Leslie Stayner. "Assessing the Human Health Risks of Trichloroethylene: Key Scientific Issues". July 27, 2006.

Kimberly Johnson. "23 military bases have tainted water". Marine Corps Times, Monday Jun 18, 2007.

Committee on Human Health Risks of Trichloroethylene, National Research Council. Assessing the Human Health Risks of Trichloroethylene: Key Scientific Issues. Washington, DC: National Academies Press, 2006.

United States National Institute of Health Sciences. "In situ Bioremediation of TCE". 20 August 2007.

Cheryl Siegel Scott and V. James Cogliano. "Trichloroethylene Health Risks--State of the Science." Environmental Health Perspectives Supplements Volume 108, Number S2, May 2000.

Suzanne E. Simon. "Editor's perspective: The prevalence of trichloroethylene metabolites in public drinking-water supplies." Remediation Journal, Volume 15, Issue 3 (Summer 2005, Pages: 1-4).

Ralph Vartabedian. "Panel questions failure to study tainted water". The Los Angeles Times. November 26, 2007.

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