Trichloroethylene

Hazardous Air Pollutants (HAPs)

Urban Hazardous Air Pollutants (HAPs) - EPA specified greatest potential health threat in urban areas

Carcinogens

Pesticide -> EPA IRIS

Volatile Organic Compound (VOC) (Pesticide/Volatile Organic Compound (VOC))

log Kow = 2.61

2.42

2.42

Ethereal odor

Sweet odor

Characteristic odor resembling that of chloroform

1.46 at 68 °F (USCG, 1999) - Denser than water; will sink

1.4642 at 20 °C/4 °C

Liquid heat capacity: 0.231 Btu/lb-F; saturated vapor pressure: 1.166 lb/sq in; saturated vapor density: 0.02695 lb/cu ft (all at 70 °F)

Saturated liquid density: 90.770 lb/cu ft; ideal gas heat capacity: 0.146 Btu/lb-F (All at 75 °F)

Relative density (water = 1): 1.5 (20 °C)

1.46

Colorless liquid (unless dyed blue)

Stable, low-boiling, colorless, photoreactive liquid

Danger

H315: Causes skin irritation [Warning Skin corrosion/irritation]

P203, P261, P264, P264+P265, P271, P273, P280, P302+P352, P304+P340, P305+P351+P338, P318, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Danger

H315 (100%): Causes skin irritation [Warning Skin corrosion/irritation]

P203, P261, P264, P264+P265, P271, P272, P273, P280, P302+P352, P304+P340, P305+P351+P338, P318, P319, P321, P332+P317, P333+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Chemical: Ethene, 1,1,2-trichloro-

Hazard Traits - Carcinogenicity; Cardiovascular Toxicity; Developmental Toxicity; Hepatotoxicity and Digestive System Toxicity; Nephrotoxicity and Other Toxicity to the Urinary System; Neurotoxicity; Ocular Toxicity; Reproductive Toxicity; Respiratory Toxicity

Ethene, 1,1,2-trichloro- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Ethene, 1,1,2-trichloro- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

R - indicates a substance that is the subject of a TSCA section 6 risk management rule.

Status: Active Update: 23-11-2021 https://echa.europa.eu/registration-dossier/-/registered-dossier/14485

Substance: Trichloroethylene

Special Hazards of Combustion Products: Toxic and irritating gases are produced in fire situations. (USCG, 1999)

· Some of these materials may burn, but none ignite readily.

Combustible under specific conditions. Gives off irritating or toxic fumes (or gases) in a fire.

Nonflammable, but high concentrations of trichloroethylene vapor in high-temperature air can be made to burn mildly if plied with a strong flame.

This chemical is a combustibe liquid.

At normal handling temperatures, trichloroethylene behaves as a non-flammable, non-burnable substance.

INHALATION: symptoms range from irritation of the nose and throat to nausea, an attitude of irresponsibility, blurred vision, and finally disturbance of central nervous system resulting in cardiac failure. Chronic exposure may cause organic injury. INGESTION: symptoms similar to inhalation. SKIN: defatting action can cause dermatitis. EYES: slightly irritating sensation and lachrymation. (USCG, 1999)

· Toxic by ingestion.

Trichloroethylene (TCE) is a nonflammable, colorless liquid with a somewhat sweet odor and a sweet, burning taste. It is used mainly as a solvent to remove grease from metal parts, but it is also an ingredient in adhesives, paint removers, typewriter correction fluids, and spot removers. Trichloroethylene is not thought to occur naturally in the environment. However, it has been found in underground water sources and many surface waters as a result of the manufacture, use, and disposal of the chemical.

Most of the trichloroethylene used in the United States is released into the atmosphere from industrial degreasing operations. Acute (short-term) and chronic (long-term) inhalation exposure to trichloroethylene can affect the human central nervous system (CNS), with symptoms such as dizziness, headaches, confusion, euphoria, facial numbness, and weakness. Liver, kidney, immunological, endocrine, and developmental effects have also been reported in humans. A recent analysis of available epidemiological studies reports trichloroethylene exposure to be associated with several types of cancers in humans, especially kidney, liver, cervix, and lymphatic system. Animal studies have reported increases in lung, liver, kidney, and testicular tumors and lymphoma. The Agency is currently reassessing the cancer classification of trichloroethylene.

TCE as Tri-lene was a popular self-administered obstetric anesthetic. It was discovered that alkali in rebreathing systems could lead to the production of dichloroacetylene, which produced cranial nerve injuries. Exposure to TCE concurrent with alcohol consumption can cause degreaser's flush, a temporary flushing of the neck and face. Hepatotoxicity has been associated primarily with intentional TCE inhalation abuse. Acute tubular necrosis, usually in conjunction with liver damage, has been reported. [ATSDR Case Studies: Trichloroethylene Toxicity] Liver toxicity can occur after prolonged inhalation of high concentrations of trichloroethylene. Ingestion of alcohol may increase this risk. However, liver effects have not been reported in acute-duration human exposure studies, although some older case reports have provided limited evidence of liver damage. [ATSDR Medical Management] Trichloroethylene is in the list of Some volatile substances which may be abused by inhalation published on the web site of the U.N. International Drug Control Programme, indicating its potential to cause narcosis in workers.[Flanagan et al. Volatile Substance Abuse] Suspected germ cell mutagen (3B); [MAK] A follow-up of 14,455 aircraft maintenance workers found no increased all-cause mortality or cancer mortality. Some previous occupational cohort studies have linked TCE exposure to liver cancer, kidney cancer, and non-Hodgkin's lymphoma. [PMID 19001957] For kidney cancer but not for non-Hodgkin lymphoma or liver cancer, TCE was classified as carcinogenic to humans (Group 1) by the Working Group in October 2012. [PMID 23323277]

Trichloroethylene (TCE) is a hazardous substance due primarily to its toxicity. Effects result from both high-level, acute and lower-level, chronic exposures. Protection must be afforded against both dermal contact and inhalation. Dermal protection is accomplished by routinely wearing neoprene constructed gloves, worksuit, apron, and shoes. Safety goggles or a face shield is necessary to protect against splash potential. The odor of chemically pure TCE is detectable at 21.4 ppm in air. Its clear, colorless appearance and liquid form do not serve similarly as warnings against dermal contact. The potential fire hazard from TCE alone is low. However, TCE, when exposed to flames or an electric arc in the presence of iron, copper, zinc, or aluminum, can form phosgene, a highly toxic gas. Also, TCE in the presence of heat and strong oxidizers (eg, tetraoxide) reacts violently. Even without a heat source, TCE can react with strong alkali (eg, sodium hydroxide) to form the dangerously toxic, flammable and explosive dichloroacetylene. Perchloric acid also reacts violently with TCE. Further TCE forms impact-explosive mixtures with finely divided aluminum, beryllium, lithium, magnesium or titanium. TCE should be packaged in steel drums. These drums should be stored in a cool, dry, well-ventilated area because TCE will slowly decompose to corrosive HCl when exposed to light and moisture. Should a TCE fire occur, it may be combated with water, fog, dry chemical, carbon dioxide or foam extinguisher. Spills of TCE should be isolated by flushing with water to an impoundment. Density stratification will cause the formation of a bottom TCE layer which can be pumped and containerized.

1710 160

1710 160

Trichloroethylene is an indirect food additive for use as a component of adhesives.

Tolerances are established for residues of trichloroethylene resulting from its use as a solvent in the manufacture of foods as follows: [Table#394]

Excerpt from ERG Guide 160 [Halogenated Solvents]:

In case of fire in the surroundings, use appropriate extinguishing media. In case of fire: keep drums, etc., cool by spraying with water.

Fresh air, rest. Artificial respiration may be needed. Refer immediately for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Do NOT induce vomiting. Refer immediately for medical attention.

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

General First Aid:

(General first aid procedures)

Vapors are heavier than air and will collect in low areas. Vapors may travel long distances to ignition sources and flashback. Vapors in confined areas may explode when exposed to fire. Containers may explode in fire. Storage containers and parts of containers may rocket great distances, in many directions.

· Wear positive pressure self-contained breathing apparatus (SCBA).

Biological Exposure Indices (BEI) [ACGIH] - Trichloroacetic acid in urine = 15 mg/L at end of shift at end of workweek; (See other BEIs and notations in ACGIH TLVs and BEIs.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

Approach fire from upwind to avoid hazardous vapors and toxic decomposition products. Use water spray to keep fire-exposed containers cool. Use water spray, dry chemical, foam, or carbon dioxide. Extinguish fire using agent suitable for surrounding fire.

Use dry chemical, carbon dioxide, or alcohol foam extinguishers. ... If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors or shows any signs of deforming), withdraw immediately to a secure position ... The only respirators recommended for fire fighting are self-contained breathing apparatuses that have full face-pieces and are operated in a pressure-demand or other positive-pressure mode.

Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage. Light sensitive. Handle and store under inert gas.

Store in cool, dry, well-ventilated location. Separate from active metals. Isolate from open flames and combustibles.

Store in a secure poison location. ... Before entering confined space where this chemical may be present, check to make sure that an explosive concentration does not exist. Trichloroethylene must be handled and stored away from operations which generate high temperatures, such as arc welding or cutting; unshielded resistance heating; open flames; and high-intensity ultraviolet light. It must also be handled to avoid contact with hot metals. Poisonous gases, such as phosgene, and hydrogen chloride are formed. Prevent contact of trichloroethylene with strong alkalis, such as sodium hydroxide or potassium hydroxide, because a highly flammable, toxic liquid is produced. Also prevent contact with aluminum in the presence of dilute hydrochloric acid, because a violent reaction will occur. Prevent contact with chemically active metals, powders, or shavings, such as barium, lithium, sodium, or magnesium; and titanium powders or shavings, since an explosion can occur. A regulated, marked area should be established where this chemical is handled, used, or stored in compliance with OSHA Standard 1910.1045.

Store trichloroethylene in cans or in dark glass bottles to minimize decomposition.

For more Storage Conditions (Complete) data for Trichloroethylene (9 total), please visit the HSDB record page.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.

Evacuate and restrict persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Establish forced ventilation to keep levels below explosive limit. Absorb liquids in vermiculite, dry sand, earth, peat, carbon, or a similar material and deposit in sealed containers. Keep this chemical out of a confined space, such as a sewer, because of the possibility of an explosion, unless the sewer is designed to prevent the buildup of explosive concentrations. It may be necessary to contain and dispose of this chemical as a hazardous waste. If materials or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters.

Contain and isolate spill by using clay/bentonite dams, interceptor trenches, or impoundments. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Construct swale to divert uncontaminated portion of watershed around contaminated portion. ... Density stratification and impoundment -- remove product from bottom layer by pumping through manifold or polyethylene rope mop collection or remove clarified upper portion by skimmers or siphon. Treatment is required for both clarified and concentrated fractions. Treatment alternatives include powdered activated carbon, granular activated carbon, and biodegradation. /Other/ treatment alternatives for contaminated soils include well point collection and treatment of leachates as for contaminated waters, bentonite/cement injection to immobilize spill.

Environmental considerations: Land spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash or cement powder.

For more Cleanup Methods (Complete) data for Trichloroethylene (8 total), please visit the HSDB record page.

Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D040, F002, U228, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.

Incineration, preferably after mixing with another combustible fuel. Care must be exercised to assure complete combustion to prevent the formation of phosgene. An acid scrubber is necessary to remove the halo acids produced. An alternative to disposal for trichloroethylene is recovery and recycling.

For more Disposal Methods (Complete) data for Trichloroethylene (20 total), please visit the HSDB record page.

Therapeutic or normal blood level 0.1-9 mg%

PERSONAL AIR: The exhaled breath of 73% of 26 smokers and 81% of 43 nonsmokers contained trichloroethylene at unreported concentrations(1). Breath of 12.5% of 50 individuals living in the Los Angeles area contained trichloroethylene(2). 51.2% of personal air samples collected from these 50 individuals contained trichloroethylene(2). Increased personal air exposures were reported following solvent use, household cleaning, furniture stripping, visiting a dry cleaning shop, photo developing and using paint remover of up to 220 ug/cu m from a baseline of <2 ug/cu m(3). Personal air samples from Los Angeles and Contra Costa residents contained trichloroethylene at concentrations of 7.8 ug/cu m (n = 110, Los Angeles residents, February 1984), 6.4 ug/cu m (n = 50, Los Angeles residents, May 1984) and 3.8 ug/cu m (n = 67, Contra Costa residents, June 1984)(4).

PERSONAL AIR: Personal air samples taken on 113 inner city school kids in Minneapolis, MN contained trichloroethylene in 90.3 and 72.7% at concentrations of 0.1-0.8 ug/cu m from samples taken in both the winter and spring of 2000(1). Personal air samples taken in the Boston Exposure Assessment Microenvironments study had a geometric mean of 0.17 ug/cu m in 55 nonsmoking participants, working in nonmanufacturing jobs, living in and around the greater Boston area, samples taken the summer of 2003 and winter of 2004 and 2005(2). Badge samplers worn for one week by 113 adults in 1990 and 1991 found trichloroethylene at an arithmetic mean of 2.7 and geometric mean of 1.2 ug/cu m(3). Personal air concentrations of trichloroethylene for 46 students from Philip Randolph Academy in Harlem, New York City were 2.62 and 0.51 ug/cu m in the winter and summer respectively(4). Personal air samples taken on 25 people from Battle Creek, 22 people from East St Paul and 24 people from Phillips contained an average of 0.2 ug/cu m on samples taken the spring and fall of 1999(5).

Blood samples from 179 of 277 people from the general population contained trichloroethylene at a mean concentration of 458 ng/L; a mean blood concentration of 763 ng/L was reported from 63 of 113 urban workers as compared to 180 ng/L from 82 of 127 workers(1). Blood samples collected from workers exposed to trichloroethylene in 4 dry-cleaning shops (air concentrations ranged from 25-40 ppm) contained this compound (median = 3.39 umol/L after work (range 0.46-12.71), 0.38 umol/L before work (range = 0.15-3.58)(2). Urine samples from the same workers contained the trichloroethylene metabolite, trichloroethanol (median 54.89 umol/mol creatine, range 5.30-177.67 after work; median = 9.70 umol/mol creatine, range 0.38-35.65 before work)(2). Kidney (n = 9), lung (n = 13), and muscle (n = 16) tissues collected from humans in Turku, Finland in 1987 contained trichloroethylene at 0.7, 0.02, and 0.2 ug/kg, respectively(3). Trichloroethylene was detected in 20% of composite adipose tissue samples collected in FY82 (n 46 composite samples)(4). Breathing air samples from 30 residents of Tokyo, Japan had a mean concentration of 2.0 ug/cu m trichloroethylene with a calculated daily intake due to breathing ambient air of 40 ug/person (men 24.9 ug/person; women 51.5 ug/person)(5). Breath samples of Los Angeles and Contra Costa residents contained trichloroethylene at concentrations of 1.6 (n = 110, Los Angeles residents, February 1984), 1.0 (n = 50, Los Angeles residents, May 1984) and 0.6 ug/L (n = 67, Contra Costa residents, June 1984)(6).

For more Body Burden (Complete) data for Trichloroethylene (6 total), please visit the HSDB record page.

Hematologic

[in animals: liver & kidney cancer]

Exposure to trichloroethene (TCE), a ubiquitous environmental contaminant, is known to induce autoimmunity both in humans and animal models. ... Previous studies ... in MRL+/+ mice suggest that oxidative stress may contribute to TCE-induced autoimmune response. The current study was undertaken to further assess the role of oxidative stress in TCE-induced autoimmunity by supplementing with an antioxidant N-acetylcysteine (NAC). Groups of female MRL+/+ mice were given TCE, NAC or TCE+NAC for 6 weeks (TCE, 10 mmol/kg, i.p., every 4th day; NAC, 250 mg/kg/day through drinking water). TCE exposure led to significant increases in serum levels of anti-nuclear, anti-dsDNA and anti-Sm antibodies. TCE exposure also led to significant induction of anti-malondiadelhyde (MDA)- and anti-hydroxynonenal (HNE)-protein adduct antibodies which were associated with increased ANA in the sera along with increased MDA-/HNE-protein adducts in the livers and kidneys, and increases in protein oxidation (carbonylation) in the sera, livers and kidneys, suggesting an overall increase in oxidative stress. Moreover, TCE exposure also resulted in increased release of IL-17 from splenocytes and increases in IL-17 mRNA expression. Remarkably, NAC supplementation attenuated not only the TCE-induced oxidative stress, IL-17 release and mRNA expression, but also the markers of autoimmunity, as evident from decreased levels of ANA, anti-dsDNA and anti-Sm antibodies in the sera. These results provide further support to a role of oxidative stress in TCE-induced autoimmune response. Attenuation of TCE-induced autoimmunity in mice by NAC provides an approach for preventive and/or therapeutic strategies.

Toxicological interactions with drugs have the potential to modulate the toxicity of trichloroethylene (TCE). Our objective is to identify metabolic interactions between TCE and 14 widely used drugs in human suspended hepatocytes and characterize the strongest using microsomal assays. Changes in concentrations of TCE and its metabolites were measured by headspace GC-MS. Results with hepatocytes show that amoxicillin, cimetidine, ibuprofen, mefenamic acid and ranitidine caused no significant interactions. Naproxen and salicylic acid showed to increase both TCE metabolites levels, whereas acetaminophen, carbamazepine and erythromycin rather decreased them. Finally, diclofenac, gliclazide, sulphasalazine and valproic acid had an impact on the levels of only one metabolite. Among the 14 tested drugs, 5 presented the most potent interactions and were selected for confirmation with microsomes, namely naproxen, salicylic acid, acetaminophen, carbamazepine and valproic acid. Characterization in human microsomes confirmed interaction with naproxen by competitively inhibiting trichloroethanol (TCOH) glucuronidation (Ki=2.329 mM). Inhibition of TCOH formation was also confirmed for carbamazepine (partial non-competitive with Ki=70 uM). Interactions with human microsomes were not observed with salicylic acid and acetaminophen, similar to prior results in rat material. For valproic acid, interactions with microsomes were observed in rat but not in human. Inhibition patterns were shown to be similar in human and rat hepatocytes, but some differences in mechanisms were noted in microsomal material between species. ...

Trichloroethylene (TCE), a nephrotoxicant is known to cause severe damage to the kidney. In this study, the nephroprotective potential of hesperidin was evaluated against TCE-induced nephrotoxicity in Wistar rats. Oral administration of TCE (1000 mg/kg b.wt) for 15 days enhanced renal lipid peroxidation and reduced antioxidant enzymes armory viz., reduced renal glutathione, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, catalase and superoxide dismutase. It also enhanced the levels of blood urea nitrogen, creatinine and kidney injury molecule (KIM-1). Caspase-3 and bax expression were found to be elevated, while that of bcl-2 reduced suggesting that TCE induces apoptosis. However, pretreatment with hesperidin at a dose of 100 and 200 mg/kg b.wt for 15 days significantly decreased lipid peroxidation, increased the levels of antioxidant enzymes and reduced blood urea, creatinine and KIM-1 levels. Hesperidin also modulated the apoptotic pathways by altering the expressions of caspase-3, bax and bcl-2 to normal. Our results suggest that hesperidin can be used as a nephroprotective agent against TCE-induced nephrotoxicity.

It /has been/ demonstrated that some drugs modulate in vitro metabolism of trichloroethylene (TCE) in humans and rats. The objective was to assess in vivo interactions between TCE and three drugs: naproxen (NA), valproic acid (VA), and salicylic acid (SA). Animals were exposed to TCE by inhalation (50 ppm for 6 h) and administered a bolus dose of drug by gavage, equivalent to 10-fold greater than the recommended daily dose. Samples of blood, urine, and collected tissues were analyzed by headspace gas chromatography coupled to an electron capture detector for TCE and metabolites (trichloroethanol [TCOH] and trichloroacetate [TCA]) levels. Coexposure to NA and TCE significantly increased (up to 50%) total and free TCOH (TCOHtotal and TCOHfree, respectively) in blood. This modulation may be explained by an inhibition of glucuronidation. VA significantly elevated TCE levels in blood (up to 50%) with a marked effect on TCOHtotal excretion in urine but not in blood. In contrast, SA produced an increase in TCOHtotal levels in blood at 30, 60, and 90 min and urine after coexposure. Data confirm in vitro observations that NA, VA, and SA affect in vivo TCE kinetics. ...

For more Interactions (Complete) data for Trichloroethylene (23 total), please visit the HSDB record page.

Cancer, Developmental (effects during periods when organs are developing), Hematological (Blood Forming), Hepatic (Liver), Immunological (Immune System), Neurological (Nervous System), Renal (Urinary System or Kidneys)

Developmental

Eyes, skin, respiratory system, heart, liver, kidneys, central nervous system

Chronic inhalation or ingestion of tricholoethylene causes nerve, kidney, and liver damage, impaired immune system function, impaired fetal development in pregnant women, and possibly death. It has also been linked to both kidney and liver cancer. (L14)

LC50; Species: Cyprinodon variegatus (Sheepshead minnow); Concentration: 20 mg/L for 96 hr /Conditions of bioassay not specified/

LC50; Species: Palaemonetes paludosus (Grass shrimp); Concentration: 2 mg/L/96 hr /Conditions of bioassay not specified/

EC50; Species: Xenopus laevis (Clawed toad) embryo; Conditions: freshwater, renewal, 23 °C, pH 7.0; Concentration: 36200 ug/L for 96 hr (95% confidence interval: 30800-42600 ug/L); Effect: increased developmental malformations /formulation/

LC50; Species: Xenopus laevis (Clawed toad) embryo; Conditions: freshwater, renewal, 23 °C, pH 7.0; Concentration: 43400 ug/L for 96 hr (95% confidence interval: 38100-49300 ug/L) /formulation/

For more Ecotoxicity Values (Complete) data for Trichloroethylene (18 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an average Koc value of 101, based on measurements in 32 soils(2), indicates that trichloroethylene is expected to have high mobility in soil(SRC). Volatilization of trichloroethylene from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 9.02X10-3 atm-cu m/mole(3). Trichloroethylene is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 69 mm Hg at 25 °C(4). Trichloroethylene can exist in soil in the gas, liquid and adsorbed phases(5). The initial percentage of trichloroethylene in the gas (24, 52, 57%), liquid (5, 3, 4%) and adsorbed (71, 45, 39%) phases was determined in three soils, respectively: (Rindge, 11.2% organic matter, 35.4% moisture; Yolo, 2.2% organic matter, 11.7% moisture; Reiff, 1.4% organic matter, 13.9% moisture)(5). A 2.4% of theoretical BOD using activated sludge in the Japanese MITI test indicates that trichloroethylene is not readily biodegradable(6). Trichloroethylene is resistant to aerobic biodegradation although biodegradation may proceed cometabolically(5,7). Under anaerobic conditions, as might be seen in soil microsites, flooded soils or aquifer sites, trichloroethylene is slowly biodegraded via reductive dechlorination; the extent and rate of degradation is dependent upon the strength of the reducing environment(8). Anaerobic half-lives of 0.144 to 3.3 years have been reported(9).

AQUATIC FATE: Based on a classification scheme(1), an average Koc value of 101, based on measurements in 32 soils(2), indicates that trichloroethylene is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 9.02X10-3 atm-cu m/mole(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 3.5 hours and 4.6 days, respectively(SRC). Trichloroethylene volatilization half-lives from a mesocosm field experiment in Narragansett Bay ranged from 10.7 to 28 days(5). According to a classification scheme(6), BCFs of 17(3), 4-17(7) and 39(3) in bluegill sunfish, carp and rainbow trout, respectively, suggest bioconcentration in aquatic organisms is low to moderate(SRC). A 2.4% of theoretical BOD using activated sludge in the Japanese MITI test indicates that trichloroethylene is not readily biodegradable(7). Trichloroethylene is resistant to biodegradation under aerobic conditions although cometabolic biodegradation has been reported under conditions where additional nutrients have been added(8-10). Under anaerobic conditions, as might be seen in sediments or groundwater, trichloroethylene is slowly biodegraded via reductive dechlorination; the extent and rate of degradation is dependent upon the strength of the reducing environment(11). Hydrolysis is not expected to be an important environmental fate process since the hydrolysis half-life of trichloroethylene at 25 °C has been approximated to be 1X10+5 to 1X10+6 years(12,13). Although trichloroethylene reacts with other photo-oxidants in surface waters exposed to sunlight, hydroxyl radicals are expected to be the dominant photo-oxidant in water(14). The indirect photolysis half-life of trichloroethylene in some surface waters may be as short as 50 days(14).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), trichloroethylene, which has a vapor pressure of 69 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase trichloroethylene is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 8 days(SRC), calculated from its rate constant of 2.00X10-12 cu cm/molecule-sec at 25 °C(3). Vapor-phase trichloroethylene is also degraded by reaction with nitrate radicals and ozone; the half-lives for these reactions are estimated to be 111 and >190days(SRC), calculated from their respective rate constants of 2.90X10-16 and <5.0X10-20 cu cm/molecule-sec at 25 °C(4). Phosgene, dichloroacetyl chloride, chloroform and formyl chloride are formed from the reaction of trichloroethylene with hydroxyl radicals(5-7). Monitoring has detected trichloroethylene in rain and snow samples(8,9), therefore, trichloroethylene may be removed from the air by wet deposition(SRC). Trichloroethylene does not absorb at wavelengths >290 nm(10,11) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

Trichloroethylene was detected in the following food samples: intermediates grain-based food (1984): 9 varieties, 44.4% pos, 0.77-2.7 ppb, 1.9 ppb (max concentration in yellow corn meal; wheat, corn, oats (1984)), 10, 2, and 1 samples, respectively: not detected(1). Sampling table-ready foods showed trichloroethylene concentrations as follows: 19 varieties, 47% pos, 1.7-8.0 ppb, 1.5 ppb avg, max concentration in plain granola; butter, 7 samples, 100% pos; 1.6-20 ppb, 9.7 ppb avg; margarine, 7 samples, 100% pos, 3.7-980 ppb, 4.3 ppb avg of pos, max concentration in Mozzarella cheese(2). Trace amounts of trichloroethylene were detected in extracted edible oils(1). It was also detected in meat, beverages, dairy products, fruits and vegetables, oil and fats, range 0.02-60 ug/kg(1). Concentrations of trichloroethylene in food samples were as follows: Cheshire cheese: 3 mg/kg; English butter: 10 mg/kg; eggs: 0.6 mg/kg; shin of beef: 16 mg/kg; beef fat: 12 mg/kg; pig liver: 22 mg/kg; margarine: 6 mg/kg; olive oil (Spanish): 9 mg/kg; cod liver oil: 19 mg/kg; vegetable oil for frying: 7 mg/kg; fruit juices: 5 mg/kg; light beer: 0.7 mg/kg; freeze-dried coffee: 4 mg/kg; tea in bags: 60 mg/kg; Yugoslavian wine: 0.02; potatoes: 3 mg/kg; apples: 5 mg/kg; pears: 5 mg/kg; fresh bread: 7 mg/kg(3).

Trichloroethylene was detected in 5 of 372 samples of food obtained from the Food and Drug Administration's "market basket" collections at concentrations of 2-94 ng/g (mean = 49 ng/g)(1). Trichloroethylene was present in samples of butter from not detected to 0.3 ug/kg, in margarine at concentrations from not detected to 0.4 ug/kg, in peanut butter at concentrations from not detected to 0.7 ug/kg, and in pastry mix at a concentration of 0.2 ug/kg(2). Floured chickpeas contained trichloroethylene at unreported concentrations(3). Trichloroethylene has been reported as a component of chicken meat volatiles(4).

Trichloroethylene was detected in the following foods during the US FDA total diet program that was run 1996 to 2000 with samplings done four times a year(1).[Table#396]

According to the US FDA total diet program that was run 1996 to 2000 with samplings done four times a year, trichloroethylene was not detected in graham crackers, sour cream, olive/safflower oil, sugar cookies, fruit flavored sherbert, popsicle, sandwich cookies, scrambled eggs, raw strawberries, carbonated cola beverage and pork bacon.

The substance can be absorbed into the body by inhalation, by ingestion and through the skin.

inhalation, skin absorption, ingestion, skin and/or eye contact

Oral (L14) ; inhalation (L14)

Trichloroethylene is an indirect food additive for use as a component of adhesives.

Tolerances are established for residues of trichloroethylene resulting from its use as a solvent in the manufacture of foods as follows: [Table#394]

U228; As stipulated in 40 CFR 261.33, when trichloroethylene, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5).

D040; A solid waste containing trichloroethylene may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste.

F002; When trichloroethylene is a spent solvent, it is classified as a hazardous waste from a nonspecific source (F002), as stated in 40 CFR 261.31, and must be managed according to state and/or federal hazardous waste regulations.

Trichloroethylene (TCE) is a volatile organic compound widely used in industrial and commercial processes and has some limited uses in consumer and commercial products. EPA identified significant health risks associated with TCE use in vapor degreasing and EPA's proposed determination is that these risks are unreasonable risks. To address these unreasonable risks, EPA is proposing under section 6 of the Toxic Substances Control Act (TSCA) to prohibit the manufacture (including import), processing, and distribution in commerce of TCE for use in vapor degreasing; to prohibit commercial use of TCE in vapor degreasing; to require manufacturers, processors, and distributors, except for retailers of TCE for any use, to provide downstream notification of these prohibitions throughout the supply chain; and to require limited recordkeeping.

Trichloroethylene (TCE) is a volatile organic compound widely used in industrial and commercial processes and has some limited uses in consumer and commercial products. EPA identified significant health risks associated with TCE use in aerosol degreasing and for spot cleaning in dry cleaning facilities. EPA has preliminarily determined that these risks are unreasonable risks. To address these unreasonable risks, EPA is proposing under section 6 of the Toxic Substances Control Act (TSCA) to prohibit the manufacture, processing, and distribution in commerce of TCE for use in aerosol degreasing and for use in spot cleaning in dry cleaning facilities; to prohibit commercial use of TCE for aerosol degreasing and for spot cleaning in dry cleaning facilities; to require manufacturers, processors, and distributors, except for retailers of TCE for any use, to provide downstream notification of these prohibitions throughout the supply chain; and to require limited recordkeeping.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Trichloroethylene is produced, as an intermediate or a final product, by process units covered under this subpart.

Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Trichloroethylene is included on this list.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations.

Trichloroethylene is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

(DE) DELAWARE 1 ug/L

(FL) FLORIDA 3 ug/L

(NJ) NEW JERSEY 1 ug/L

(AZ) ARIZONA 3.2 ug/L

(CT) CONNECTICUT 5 ug/L

(ME) MAINE 32 ug/L

(MN) MINNESOTA 5 ug/L

Maximum contaminant levels (MCL) for organic contaminants apply to community and non-transient, non-community water systems: Trichloroethylene, MCL 0.005 mg/L.

EPA 5 ug/L

N - Nervous system

QN - Nervous system

Trichloroethylene (TCE), dichloroacetic acid (DCA), and trichloroacetic acid (TCA) are environmental contaminants that are carcinogenic in mouse liver. 5-Methylcytosine (5-MeC) in DNA is a mechanism that controls the transcription of mRNA, including the protooncogenes, c-jun and c-myc. ... TCE decreased methylation of the c-jun and c-myc genes and increased the level of their mRNAs. Decreased methylation of the protooncogenes could be a result of a deficiency in S-adenosylmethionine (SAM), so that methionine, by increasing the level of SAM, would prevent hypomethylation of the genes. For 5 days, female B6C3F1 mice were administered, daily by oral gavage, either 1000 mg/kg bw of TCE or 500 mg/kg DCA or TCA. At 30 min after each dose of carcinogen, the mice received, by ip injection, 0, 30, 100, or 450 mg/kg methionine. Mice were euthanized at 100 min after the last dose of DCA, TCA, or TCE. Decreased methylation in the promoter regions of the c-jun & c-myc genes and increased levels of their mRNA and proteins were found in livers of mice exposed to TCE, DCA, and TCA. Methionine prevented both the decreased methylation & the increased levels of the mRNA and proteins of the two protooncogenes. The prevention by methionine of DCA- TCA-, and TCE-induced DNA hypomethylation supports the hypothesis that these carcinogenes act by depleting the availability of SAM. Hence, methionine would prevent DNA hypomethylation by maintaining the level of SAM. Furthermore, the results suggest that the dose of DCA, TCA, or TCE must be sufficient to decrease the level of SAM in order for these carcinogens to be active.

Kidney tumors (renal-cell carcinomas) from workers occupationally exposed to high levels of TCE exhibited somatic mutations of the von Hippel-Landau (VHL) tumor suppressor gene, a gene that has been associated with renal-cell carcinoma. Mutations in the VHL gene were found in 75% of renal-cell carcinomas from 44 TCE-exposed persons. DNA sequencing analysis showed that 39% of these tumors had a specific mutation, a C to T transition at nucleotide (nt) 454, resulting in a Pro to Ser amino acid change at codon 81. In four patients, the nt 454 mutation also was found in the nearby noncancerous kidney tissue. Moreover, this mutation was specific to TCE exposure, because it was not found in renal-cell carcinomas from patients not exposed to TCE, and it was related to the disease, because it was not found in germline DNA from either diseased or nondiseased individuals. It is reasonable from a biological perspective that the kidney tumors observed in humans are related to TCE exposure because (1) the site and histopathological characteristics of the tumors in humans and experimental animals are similar, (2) a portion of the molecular mechanism of this type of cancer (nephrocarcinogenicity) has been discovered, (3) the metabolites derived from TCE (the likely ultimate electrophilic intermediates of its bioactivation) are identical in humans and experimental animals, and (4) taking the key urinary metabolites (mercapturic acids) as an indicator of the bioactivation of TCE, humans seem to be more sensitive than rats in developing the primary biochemical lesion that precedes kidney cancer.

Whole body: 53 hours; for trichloroethanol in blood: 12 hours; for trichloroacetic acid in urine: 75 hours; [TDR, p. 1181]

The biological half-lives of the urinary metabolites of humans occupationally exposed to trichloroethylene /is/ approx 41 hours.

The half-life of trichloroethylene in exhaled air & in the blood depends on the length of exposure & on the time of sampling after exposure. ... Maximum concentration /of trichloroethanol/ in blood & urine /is reached/ almost directly after exposure. ... concentration decreases with a half-life of about 10-15 hr. ... Concentration of trichloroacetic acid in both the blood & urine increases for up to 20-40 hr after /a single/ exposure. ... concentration decreases with a half-life of about 70-100 hr.

Trichloroethanol and its glucuronide are rapidly eliminated in urine, with half-lives of about 10 hr, and trichloroacetic acid is eliminated slowly, with a half-life of about 52 hr (range, 35-70 hr).

... Trichloroethylene has an estimated half- life in humans in venous blood of 21.7 hours ... .

For more Biological Half-Life (Complete) data for Trichloroethylene (8 total), please visit the HSDB record page.

... We collected urine from Hartley male and female guinea pigs 24 hours after intracutaneous injection of trichloroethylene (TRI), trichloroethanol (TCE) or trichloroacetic acid (TCA) during a guinea pig maximization test and measured the urinary metabolites by gas chromatography-mass spectrometry. After TRI treatment, the amount of TCA was significantly greater in females than males, while there was no sex difference in the total amount (TCA + TCE). TCA was only detected in urine after TCA treatment. Interestingly, not only TCE but also TCA was detected in urine of both sexes after TCE treatment, and the amount of TCA was also greater in females than males. An additional experiment showed that TCE treatment did not result in the detection of urinary TCA in cytochrome P450 (CYP)2E1-null mice TCE but did in wild-type mice, suggesting the involvement of CYP2E1 in the metabolism from TCE to TCA. The constitutive expression of CYP2E1 in the liver of guinea pigs was greater in females than males. The sex difference in urinary TCA excretion after TRI and TCE treatments may be due to variation of the constitutive expression of CYP2E1.

Toxicological interactions with drugs have the potential to modulate the toxicity of trichloroethylene (TCE). Our objective is to identify metabolic interactions between TCE and 14 widely used drugs in human suspended hepatocytes and characterize the strongest using microsomal assays. Changes in concentrations of TCE and its metabolites were measured by headspace GC-MS. Results with hepatocytes show that amoxicillin, cimetidine, ibuprofen, mefenamic acid and ranitidine caused no significant interactions. Naproxen and salicylic acid showed to increase both TCE metabolites levels, whereas acetaminophen, carbamazepine and erythromycin rather decreased them. Finally, diclofenac, gliclazide, sulphasalazine and valproic acid had an impact on the levels of only one metabolite. Among the 14 tested drugs, 5 presented the most potent interactions and were selected for confirmation with microsomes, namely naproxen, salicylic acid, acetaminophen, carbamazepine and valproic acid. Characterization in human microsomes confirmed interaction with naproxen by competitively inhibiting trichloroethanol (TCOH) glucuronidation (Ki=2.329 mM). Inhibition of TCOH formation was also confirmed for carbamazepine (partial non-competitive with Ki=70 uM). Interactions with human microsomes were not observed with salicylic acid and acetaminophen, similar to prior results in rat material. For valproic acid, interactions with microsomes were observed in rat but not in human. Inhibition patterns were shown to be similar in human and rat hepatocytes, but some differences in mechanisms were noted in microsomal material between species. ...

... In this study we have compared the renal toxicity of TCE and /its major metabolite trichloroethanol/ (TCE-OH) in rats to try and ascertain whether the glutathione pathway or formic aciduria can account for the toxicity. Male rats were given TCE (500 mg/kg/day) or TCE-OH at (100 mg/kg/day) /by oral gavage/ for 12 weeks and the extent of renal injury measured at several time points using biomarkers of nephrotoxicity and prior to termination assessing renal tubule cell proliferation. The extent of formic aciduria was also determined at several time points, while renal pathology and plasma urea and creatinine were determined at the end of the study. TCE produced a very mild increase in biomarkers of renal injury, total protein, and glucose over the first two weeks of exposure and increased Kim-1 and NAG in urine after 1 and 5 weeks exposure, while TCE-OH did not produce a consistent increase in these biomarkers in urine. However, both chemicals produced a marked and sustained increase in the excretion of formic acid in urine to a very similar extent. The activity of methionine synthase in the liver of TCE and TCE-OH treated rats was inhibited by about 50% indicative of a block in folate synthesis. Both renal pathology and renal tubule cell proliferation were reduced after TCE and TCE-OH treatment compared to controls. Our findings do not clearly identify the pathway which is responsible for the renal toxicity of TCE but do provide some support for metabolism via glutathione conjugation.

Extraplacental membranes define the gestational compartment and provide a barrier to infectious microorganisms ascending the gravid female reproductive tract. We tested the hypothesis that bioactive metabolites of trichloroethylene (TCE) decrease pathogen-stimulated innate immune response of extraplacental membranes. Extraplacental membranes were cultured for 4, 8, and 24 hr with the TCE metabolites trichloroacetate (TCA) or S-(1,2-dichlorovinyl)-l-cysteine (DCVC) in the absence or presence of lipoteichoic acid (LTA) or lipopolysaccharide (LPS) to simulate infection. In addition, membranes were cocultured with DCVC and Group B Streptococcus (GBS). DCVC (5-50 uM) significantly inhibited LTA-, LPS-, and GBS-stimulated cytokine release from tissue cultures as early as 4 hr (P </= 0.05). In contrast, TCA (up to 500 uM) did not inhibit LTA-stimulated cytokine release from tissue punches. Because cytokines are important mediators for host response to infectious microorganisms these findings suggest that TCE exposure could potentially modify susceptibility to infection during pregnancy.

For more Metabolism/Metabolites (Complete) data for Trichloroethylene (24 total), please visit the HSDB record page.

Trichloroethylene has known human metabolites that include Chloral hydrate.

Liquids that dissolve other substances (solutes), generally solids, without any change in chemical composition, as, water containing sugar. (Grant &amp; Hackh&apos;s Chemical Dictionary, 5th ed)

Gases or volatile liquids that vary in the rate at which they induce anesthesia; potency; the degree of circulation, respiratory, or neuromuscular depression they produce; and analgesic effects. Inhalation anesthetics have advantages over intravenous agents in that the depth of anesthesia can be changed rapidly by altering the inhaled concentration. Because of their rapid elimination, any postoperative respiratory depression is of relatively short duration. (From AMA Drug Evaluations Annual, 1994, p173)

Blood and urine samples were collected in 1990 from 10 people working in four dry cleaning shops in Croatia, where trichloroethylene was used as the cleaning solvent. The concentration of trichloroethylene in the air was 25-40 ppm [134-215 mg/cu m]. The mean blood levels of trichloroethylene were 0.38 umol/L [50 ug/L] on Monday morning (range, 0.15- 3.58 umol/L) (20-70 ug/L) and 3.39 umol/L [445 ug/L] on Wednesday afternoon (range, 0.46- 12.71 umol/L (60-1670 ug/L]. ...

TCE is rapidly absorbed into the systemic circulation via the oral and inhalation routes. The majority of TCE undergoes oxidation in the liver by CYPs, with a small proportion being conjugated with glutathione (GSH) via glutathione S-transferases (GSTs). Thus, two distinct metabolic pathways exist for TCE. ... TCE may be oxidized to yield one of three initial metabolites: chloral, TCE-epoxide, and dichloroacetylchloride. These metabolites rapidly undergo oxidation and/or reduction to yield trichloroacetate (TCA) and trichloroethanol (TCOH), the major end products of the oxidative pathway. TCOH is either oxidized to TCA or glucuronidated. TCOH glucuronide is excreted via the urine and bile. That in the bile may undergo enterohepatic recirculation by hydrolysis to TCOH in the gut, with reabsorption and the possibility of conversion to TCA. TCA accumulates in the body due to strong plasma protein binding and slow excretion. In contrast, blood levels of DCA, formed by TCA dechlorination or from TCOH, are very low or nondetectable in humans. Relatively small amounts of TCE can be conjugated in the liver with GSH to form S-(1,2-dichlorovinyl)glutathione (DCVG). DCVG is then effluxed from the hepatocyte into plasma and bile for translocation to the kidney and small intestine, respectively. The plasma DCVG is intrarenally converted by gamma-glutamyltransferase and dipeptidases to the cysteine conjugate S-(1,2-dichlorovinyl)-L-cysteine (DCVC). The DCVG secreted into the bile can undergo extrarenal processing to DCVC, that is subsequently delivered to the kidney by enterohepatic recirculation. DCVC represents a branch point in the pathway. It may be detoxified through N-acetylation or bioactivated to reactive thiols via renal beta-lyase located in renal proximal tubular cells (or to a lesser extent, bioactivated to DCVC sulfoxide via flavin-containing monooxygenases).

TCE is rapidly and extensively absorbed by all routes of environmental exposure, including oral ingestion, inhalation and skin contact. Absorbed TCE is distributed throughout the body, where it can accumulate in fat and other tissues.

... The pharmacokinetics of trichloroethylene (TCE) in male Sprague-Dawley (S-D) rats were characterized (1) during and after inhalation exposure to 50 or 500 ppm TCE, (2) following administration of 8 mg/kg TCE PO, and (3) following intra-arterial injection of 8 mg/kg TCE. Blood and tissues (including liver, kidney, fat, skeletal muscle, heart, spleen, gastrointestinal tract, and brain) were collected at selected time-points from 5 min up to 24 hr post initial exposure. The fat compartment was modified to be diffusion-limited to predict the observed slow release of TCE from the fat. The addition of a deep liver compartment was necessary to accurately predict the slower hepatic clearance of TCE for all three exposure routes. Simulations of liver concentrations following gavage of male B6C3F1 mice with 300-2000 mg/kg TCE were also improved with the addition of a deep liver compartment. Liver predictions were calibrated and validated using a cross-validation technique novel to PBPK modeling. Splitting of compartments did not significantly affect predictions of TCE concentrations in the liver, fat, or venous blood. ...

For more Absorption, Distribution and Excretion (Complete) data for Trichloroethylene (23 total), please visit the HSDB record page.

The main use of trichloroethylene is in the vapor degreasing of metal parts. Trichloroethylene is used in consumer products such as typewriter correction fluids, paint removers/strippers, adhesives, spot removers, and rug-cleaning fluids.

Used extensively form 1920s through 1970s as a degreaser in metal fabrication, but use declined because of concerns about environmental pollution and cancer; TCE used in about 50% of vapor degreasing in 1970s and about 33% in 1980s. Increased EPA regulations in 1990s further limited its use. Other industries using TCE: dry cleaning, textile, electronics, leather, and rubber; Also used in adhesives, drugs, paints, and inks; [Reference #2]

Banned in the US in 1977 as a pet food additive, grain fumigant, wound disinfectant, obstetrical anesthetic, and extractant to make decaffeinated coffee; [ATSDR ToxProfile] In US industries, the process use of TCE ended in the mid-1980s; [PMID 24224613]

Metal Degreasing [Category: Clean]

Preparing and mounting animal skins (taxidermy) [Category: Hobbies]

For trichloroethylene (USEPA/OPP Pesticide Code: 081202) there are 0 labels match. /SRP: Not registered for current use in the U.S., but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

Acidity (as hydrochloric acid), 0.0005% max; alkalinity (as sodium hydroxide), 0.001% max; residue on evaporation, 0.005% max; antioxidants, such as amine (0.001-0.01% or more) or combinations of epoxides such as epichlorohydrin & esters (0.2-2% total)

Apart from added stabilizers, commercial grades of trichloroethylene should not contain more than the following amounts of impurities: water, 100 ppm; acidity (as HCl), 5 ppm; insoluble residue, 10 ppm. Free chlorine should not be detectable.

Impurities that have been found in commercial trichloroethylene products include: carbon tetrachloride, chloroform, 1,2-dichloroethane, trans-1,2-dichloroethylene, cis-1,2-dichloroethylene, pentachloroethane, 1,1,1,2-tetrachloroethane, 1,1,2,2-tetrachloroethane, 1,1,1-trichloroethane, 1,1,2-trichloroethane, 1,1-dichloroethylene, tetrachloroethylene, bromodichloromethane, bromodichloroethylene, and benzene.

(1985) 1.06X10+10 g

Exports were 65 million pounds during 1996, but averaged 83 million pounds per year in the 1992-1996 period.

(1985) 1.98X10+10 g

Imports last year totaled approximately 10 million pounds, averaging 12 million pounds during the period.

2023: 50,000,000 - <100,000,000 lb

USA production: (1981): 258,182 pounds.

Production quantities (1976): 610X10+6 pounds.

(1985) 7.72X10+10 g /Estimated/

(1991) 320 million lb

For more U.S. Production (Complete) data for Trichloroethylene (9 total), please visit the HSDB record page.

Demand: (1982): 240 million pounds; (1983): Est 235 million pounds; 1987: Est 215 million pounds.

Vapor degreasing of fabricated metal parts, 80%; chemical intermediate, 5%; miscellaneous used, 5%; exports, 10% (1985)

Vapor degreasing of fabricated metal parts, 66%; chemical intermediates, miscellaneous domestic uses, 5%; exports, 22%.

Vapor degreasing of fabricated metal parts, 65%; chemical intermediates and miscellaneous uses, 35%.

Demand: 1996: 180 million pounds; 1997: 190 million pounds; 2001: 230 million pounds (includes exports)

The production of trichloroethylene is mainly based on acetylene or ethylene. The acetylene route comprises acetylene chlorination to 1,1,2,2-tetrachloroethane followed by dehydrochlorination to trichloroethylene. In the ethylene-based processes, ethylene or ethylene-based chlorohydrocarbons, preferably 1,2-dichloroethane, are chlorinated or oxychlorinated and dehydrochlorinated in the same reactor. Tetrachloroethylene is obtained as a byproduct in substantial amounts. Some production is based on the catalytic hydrogenation of tetrachloroethylene coming from the chlorinolysis of C1 to C3 chlorohydrocarbons.

Until 1968, about 85% of United States production capacity of trichloroethylene was based on acetylene. The acetylene-based process consists of two steps: acetylene is first chlorinated to 1,1,2,2-tetrachloroethane, with a ferric chloride, phosphorus chloride or antimony chloride catalyst, and the product is then dehydrohalogenated to trichloroethylene. The current method of manufacture is from ethylene or 1,2-dichloroethane. In a process used by one plant in the United States, trichloroethylene is produced by noncatalytic chlorination of ethylene dichloride and other C2 hydrocarbons with a mixture of oxygen and chlorine or hydrogen chloride.

Prepn from sym-tetrachlorethane by elimination of /hydrochloric acid/ (by boiling with lime) ... ; by passing tetrachloroethane vapor over /calcium chloride/ catalyst at 300 °C ... ; without catalyst at 450-470 °C ... .

From tetrachloroethane by treatment with lime or alkali in the presence of water, or by thermal decomposition, followed by steam distillation.

Medicinal trichloroethylene may contain thymol as a preservative; industrial grades may contain stabilizers such as triethylamine.

Grade: USP, technical, high purity, electronic, metal degreasing, extraction.

Commercial grades of trichloroethylene, formulated to meet use requirements, differ in the amount and type of added inhibitor. Typical grades contain >99% trichloroethylene; they include a neutrally inhibited vapor-degreasing grade and a technical grade for use in formulations.

Stabilizers that have been used in formulations of trichloroethylene include neutral inhibitors and free-radical scavengers, amyl alcohol, n-propanol, isobutanol, 2-pentanol, diethylamine, triethylamine, dipropylamine, diisopropylamine, diethanolamine, triethanolamine, morpholine, N-methylmorpholine, aniline, acetone, ethyl acetate, borate esters, ethylene oxide, propylene oxide, 1,2-epoxybutane, cyclohexene oxide, butadiene dioxide, styrene oxide, pentene oxide, 2,3-epoxy-1-propenol, 3-methoxy-1,2-epoxypropane, stearates, 2,2,4-trimethyl-1-pentene, 2-methyl-1,2-epoxypropanol, epoxycyclopentanol, epichlorohydrin, tetrahydrofuran, tetrahydropyran, 1,4-dioxane, dioxalane, trioxane, alkoxyaldehyde hydrazones, methyl ethyl ketone, nitromethanes, nitropropanes, phenol, ortho-cresol, thymol, para-tert-butylphenol, para-tert-amylphenol, isoeugenol, pyrrole, N-methylpyrrole, N-ethylpyrrole, (2-pyrryl)trimethylsilane, glycidyl acetate, isocyanates and thiazoles.

Chemical Classes -> Volatile organic compounds

Food Additives -> EXTRACTION_SOLVENT -> JECFA Functional Classes

Food Additives -> EXTRACTION_SOLVENT -> JECFA Functional Classes