The following information has been extracted from our CHEMINFO database, which also contains hazard control and regulatory information. [More about...] [Sample Record]

Access the complete CHEMINFO database by contacting CCOHS Client Services.

 
SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 103
CCOHS Chemical Name: Trichloroethylene

Synonyms:
Acetylene trichloride
1-Chloro-2,2-dichloroethylene
1,1-dichloro-2-chloroethylene
Ethinyl trichloride
Ethylene trichloride
Tri
Trichloroethene
1,1,2-Trichlorethylene

Chemical Name French: Trichloroéthylène

Trade Name(s):
Triclene
Trilene
Vitran

CAS Registry Number: 79-01-6
UN/NA Number(s): 1710
RTECS Number(s): KX4550000
EU EINECS/ELINCS Number: 201-167-4
Chemical Family: Halogenated aliphatic hydrocarbon / unsaturated halogenated hydrocarbon / halogenated alkene / haloalkene / trihaloalkene / chloroalkene / trichloroalkene
Molecular Formula: C2-H-Cl3
Structural Formula: Cl2C=CHCl

SECTION 2. DESCRIPTION

Appearance and Odour:
Clear, colourless liquid with an ethereal, sweet, chloroform-like odour.(1,33)

Odour Threshold:
A wide range of values have been reported; 0.5 to 167 ppm. Reliable values are 82 ppm (detection) and 110 ppm (recognition).(34) Some people may not smell trichloroethylene at higher concentrations because they become accustomed to the odour.

Warning Properties:
POOR - odour threshold is above the TLV. Irritation occurs above the TLV.

Composition/Purity:
Trichloroethylene is available commercially in a number of grades, including high-purity, electronic, metal degreasing and extraction grades. It typically has a purity above 99%. Impurities include other halogenated hydrocarbons such as tetrachloroethane, dichloroethylene, and trichloroethane.(22,35) Stabilizers are added to prevent decomposition by air and light, and to prevent trichloroethylene from becoming acidic and corrosive. Some 50 known stabilizers are used in trichloroethylene formulations and include amines, pyrroles, mixtures of epoxides and esters, phenols, and alcohols. Stabilizers are generally added at concentrations of 1% or less and to be effective must be present in both the liquid and vapour phases.(22,35) Epichlorohydrin has been used as a stabilizer in the past, but concern over its toxicity has led to elimination of its use.(29)

Uses and Occurrences:
Trichloroethylene is predominantly used for vapour degreasing of metal parts in the automotive and metal industries. It is also used as a component of adhesives and as a solvent in paint-strippers, lubricants, paints, varnishes, pesticides, cold metal cleaners, rubbers and elastomers. It is used as a low temperature heat-transfer medium and as a chemical intermediate in the production of pharmaceuticals, flame retardant chemicals and insecticides. It is used in metal phosphatizing systems, textile processing, the production of polyvinyl chloride and aerospace operations.(1,29,36)
Its historical use in foods, beverages (decaffeination of coffee), pet foods, medicine, pharmaceuticals and cosmetics has been banned because of its toxicity.(1,2,29)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Clear, colourless liquid with a sweet, ethereal, chloroform-like odour. Can probably burn if strongly heated, or be ignited by a high energy source. Can decompose at high temperatures forming toxic gases such as hydrogen chloride, chlorine and phosgene. Closed containers may rupture and explode if heated. May accumulate in low lying areas. Vapour causes irritation of the nose and throat. Central nervous system depressant. Vapour may cause headache, nausea, dizziness, drowsiness, incoordination, and confusion. High vapour concentrations may cause unconsciousness and death. Causes skin and eye irritation. Aspiration hazard. Swallowing or vomiting of the liquid may result in aspiration (breathing) into the lungs. SUSPECT CANCER HAZARD - may cause cancer, based on human information. MUTAGEN - may cause genetic damage, based on animal information.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Short-term exposure causes irritation of the nose and throat and central nervous system (CNS) depression, with symptoms such as drowsiness, dizziness, giddiness, headache, loss of coordination. High concentrations have caused numbness and facial pain, reduced eyesight, unconsciousness, irregular heartbeat and death.
Trichloroethylene is noticeable by smell at approximately 82 ppm and above. However, people can become accustomed to the odour and may not smell it until higher concentrations are reached. In one study, exposure to 110 ppm for 8 hours produced fatigue and drowsiness. Other studies have shown no significant effects following exposure to 200 or 300 ppm for less than 4 hours. At 160-250 ppm, the odour is persistent. Lightheadedness has been reported following exposure to 350-400 ppm for 3 hours. At 1000-1200 ppm, the odour is very strong and unpleasant. Lightheadedness, reduced hand-eye coordination and dizziness have been observed after several minutes. At 2000 ppm, the odour is difficult to tolerate, irritation of the nose and throat is strong, and drowsiness, dizziness and nausea occur within 5 minutes. Very high concentrations have produced death due to CNS effects, and, in rare cases, irregular heart beat. In one case, pulmonary edema (a potentially fatal accumulation of fluid in the lungs) was reported. The employee was welding a surface that had been washed in trichloroethylene. The pulmonary edema likely resulted from exposure to phosgene which is formed upon heating of trichloroethylene.(1,7,9,19,21,22)
Effects on behaviour and coordination have been observed in some studies. In one study, exposure to 110 ppm resulted in decreased performance in tests measuring reaction time, dexterity, perception, and memory. Similar effects were not observed when the study was repeated. In general, no significant effects have been observed with exposures to 100 ppm or below.(1,9,22,24)
Numbness and discomfort of the face and jaw weakness (trigeminal nerve effects) and serious visual disturbances, including reduced eyesight and blurred or double vision, have been reported following exposure to high concentrations. Some of the effects may persist for several months. These effects may actually be caused by other chemicals formed when trichloroethylene decomposes in the presence of strong alkaline materials (e.g. dichloroacetylene).(1,7,9,22)
Sometimes, permanent nervous system damage and/or liver injury have resulted from severe overexposure. In most cases, the individuals had intentionally inhaled very high concentrations of trichloroethylene for its intoxicating effects.(1,22)

Skin Contact:
Trichloroethylene is a severe skin irritant, based on human and animal evidence. A 58-year old man accidentally fell into a trichloroethylene reservoir bath head first during a degreasing operation. A fellow employee immediately pulled him out, so he was in the bath only 3-5 minutes. Chemical burns were observed on his face, buttocks and back. The burn area was estimated to be about 30% of his total body surface. The burns healed within 10 days without skin grafting.(59) Prolonged contact with the liquid has caused reddening of the skin, irritation and blister formation.
The concentrated vapour, especially at elevated temperatures, can also cause severe redness and irritation. Several cases of very severe skin irritation have been reported in employees exposed to unspecified or high concentrations (up to 165 ppm) of trichloroethylene for a relatively short time (up to 5 weeks). In most cases, liver impairment and exposure to other several other potentially harmful chemicals were also reported.(26,31,32)
Trichloroethylene can be absorbed through the skin. However, significant harmful effects are not expected to occur by this route of exposure.

Eye Contact:
The liquid is a severe eye irritant, based on limited human information and animal evidence. One report indicates that a splash drop of trichloroethylene caused smarting pain and injury to the surface tissue of the eye.(7)
Mild irritation has been reported by some volunteers exposed to 160 or 200 ppm vapour.(1,19) Other sources report no eye irritation at 350-400 ppm. Severe eye irritation, with temporary clouding of the cornea, has been reported in people exposed to vapour concentrations so high they became unconscious.(7,22)
Serious disturbances in eyesight, including reduced eyesight and blurred, double and tunnel vision, have been reported in people with high inhalation exposure. See "Inhalation", above, for additional information.

Ingestion:
Ingestion causes a burning sensation in the mouth and throat, followed by abdominal pain and signs and symptoms central nervous system (CNS) depression, as described for inhalation exposure above. Accidental ingestion of 30 mL to 500 mL (2 tbsp to 16 ozs) has caused muscle weakness, vomiting and unconsciousness or delirium, with recovery within 2 weeks. Effects on the heart, liver and kidneys have also been reported. In one case, ingestion of less than 50 mL was reported to be fatal due to kidney and liver failure.(1,19) Some of the harmful effects described, e.g. the liver effects, may be caused by other chemicals (stabilizers) added to trichloroethylene.(9)
Trichloroethylene can probably be aspirated, based on its physical properties. Aspiration is the inhalation of the chemical into the lungs during ingestion or vomiting. Severe lung irritation, damage to the lung tissues and death may result. Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

Nervous System:
Long-term occupational exposure may cause signs and symptoms of central nervous system (CNS) depression such as headaches, dizziness, altered mood, loss of memory and inability to concentrate or sleep. These effects have also been related to long-term occupational exposure to other organic solvents and are sometimes generally referred to as "organic solvent syndrome". It is difficult to draw specific conclusions regarding trichloroethylene from the available studies because, in general, a small number of people were studied, exposure levels were not defined, exposure to other potentially harmful chemicals may have occurred at the same time and, in some cases, comparisons were not made to unexposed individuals.(1,9,22) In general, symptoms of CNS depression are commonly reported in employees exposed to average trichloroethylene levels of 100 ppm and above.(9) One limited study reported symptoms such as dizziness, headache, insomnia, and altered mood in a small number of employees exposed to up to 40 ppm.(25)

Nerves of the face and head (cranial nerves) have been affected by long-term exposure to trichloroethylene or chemicals formed when it decomposes. In particular, the trigeminal nerve, which provides feeling and movement to part of the face, has been affected. To a lesser extent, the optic nerve, which provides sight, has also been affected.
In one study, some evidence of trigeminal nerve impairment was seen in employees with long-term exposure to no more than 35 ppm.(1) Evidence of trigeminal nerve damage was also observed in employees with long-term occupational exposure to approximately 40 ppm.(25) Effects were more pronounced with longer exposures. Several other studies, with higher exposures, have also reported trigeminal nerve effects. Symptoms such as facial numbness, jaw weakness, altered reflexes and facial discomfort have been reported.(1,7,9) In one study, trigeminal nerve disorders were not observed in employees with long- term exposure to 38 to 172 ppm.(1)
Vision disturbances, including blurred, double or tunnel vision and poor eyesight, have occasionally been reported following long-term exposure. These effects are caused by impairment of the optic nerve and other cranial nerves.(1,7,19)
The trigeminal and optic nerve effects may be caused by dichloroacetylene, a chemical formed when trichloroethylene decomposes in the presence of strong alkaline materials.(1,7,9,19)

A metal degreaser exposed to 1.5 to 32 ppm for 1 to 2 hours/day for over 20 years experienced loss of feeling in hands and feet persisting for 4 years after retirement. This individual also had several high level short-term exposures which may have contributed to his symptoms. Repeated skin contact (while cleaning contact lenses) resulted in a reduced sense of touch, decreased mobility of the fingers, and an inability to grasp small objects with thumb and forefinger. These effects were reversible after several months.(1,19)

Skin:
Repeated or prolonged contact can cause dry, red and chapped skin (dermatitis).(8,22)

Skin Sensitization:
A few case reports have described severe redness and irritation of the skin following relatively short exposures (up to 5 weeks) to unspecified or high vapour concentrations (up to 165 ppm). In most cases, impaired liver function and exposure to several other potentially harmful chemicals were also reported. In one case, the person later tested positive in a patch test, suggesting this person was allergic to trichloroethylene. However, it cannot be concluded that trichloroethylene is a skin sensitizer based on this one positive patch test.(26,31,32) Positive results were obtained in one animal study, but the trichloroethylene purity was not specified.

Heart/Blood Vessels:
A number of studies have investigated the effects of occupational exposure to trichloroethylene on the heart. Many of the studies are limited by factors such as the small number of people studied and lack of exposure information. In general, the studies suggest that workplace exposures to 100 ppm may cause irregular heart beat in a small number of people occupationally exposed.(9,22)

Kidneys/Urinary System:
There is limited evidence that exposure to trichloroethylene may cause kidney injury in some people following long-term occupational exposure. No firm conclusions can be drawn from the available studies because most only involved a very small number of exposed individuals, exposure levels were not defined and/or there may have been exposure to other potentially harmful chemicals.(1) Kidney effects were not observed following long-term occupational exposure at concentrations up to 40 ppm.(27)

Liver:
There is limited evidence that exposure to trichloroethylene may cause liver injury in some people following long-term occupational exposure. No firm conclusions can be drawn from the available studies because most only involved a very small number of exposed individuals, exposure levels were not defined and/or there may have been exposure to other potentially harmful chemicals.(1) Liver effects were not observed following long-term occupational exposure at concentrations up to 40 ppm.(27)

Hearing:
Limited information suggests that long-term exposure may harm hearing. Concentrations which have produced hearing effects are probably high enough to have also produced significant symptoms of central nervous system (CNS) depression.(9,22,23)

Carcinogenicity:

Trichloroethylene is probably a human carcinogen. Three well-designed studies of people with occupational exposure to trichloroethylene showed higher levels of liver and biliary tract cancers and non-Hodgkins lymphoma.(2) Numerous other studies were either negative or had significant limitations, including small sample size, limited exposure data and exposure to other chemicals.(2)
The International Agency for Research on Cancer (IARC) has concluded that there is limited evidence for the carcinogenicity of trichloroethylene in humans. IARC has also concluded that there is sufficient evidence that trichloroethylene is carcinogenic in experimental animals.(2)

The International Agency for Research on Cancer (IARC) has concluded that this chemical is probably carcinogenic to humans (Group 2A).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as not suspected as a human carcinogen (A5).

ACGIH has published a Notice of Intended Change to revise the carcinogenicity designation from A5 (not suspected as a human carcinogen) to A2 (suspected human carcinogen).

The US National Toxicology Program (NTP) has listed this chemical as reasonably anticipated to be a human carcinogen.

Teratogenicity and Embryotoxicity:
Very limited human information does not indicate that occupational exposure to trichloroethylene is harmful to the unborn child. There is some evidence that exposure to trichloroethylene in drinking water may cause certain types of birth defects. Although the available information is far from conclusive.(1) Some studies with women occupationally exposed to trichloroethylene have shown a slight increased frequency of miscarriages, while others have not.(1,2) It is not possible to draw firm conclusions from these studies due to factors such as the lack of exposure information, self-reporting biases and concurrent exposure to other potentially harmful chemicals.
The available animal information does not suggest that trichloroethylene causes developmental effects. Most studies have not shown harmful effects in the offspring or have shown effects, but only in the presence of significant toxicity in the mothers

Reproductive Toxicity:
It is not possible to conclude that occupational exposure to trichloroethylene causes harmful effects on reproductive function in men or women, based on the limited human information available. In a small-scale study, trichloroethylene and chemicals formed when trichloroethylene breaks down in the body were observed in the seminal fluid of men occupationally exposed to trichloroethylene. In another study, sperm parameters (sperm density and motility) were unaffected in men occupationally exposed to trichloroethylene, but a low percentage of sperm with normal shape was observed. Animal studies suggest that exposure to relatively high concentrations of trichloroethylene may produce effects on sperm, including reduced motility, changes in sperm shape and reduced sperm count. However, well-conducted studies have not shown reduced fertility following trichloroethylene exposure.
No changes in sperm count or sperm shape were observed in 15 men occupationally exposed to trichloroethylene for more than 20 hours/week. The exposed group had a small, but non-significant change, in mature spermatozoa, which may indicate Y-chromosomal non-disjunction.(1,2,30) Eight mechanics were selected from a group that had sought medical consultation for fertility problems. Exposure to trichloroethylene had occurred for at least 2 years, during cleaning and degreasing operations. All eight men had been diagnosed as infertile. Trichloroethylene and some of its breakdown products were detected in the seminal fluid samples of all eight men, while none were detected in the seminal fluid of 5 men who did not work with trichloroethylene.(50) This study is limited by factors such as the very small number of men studied, sperm parameters were not assessed and other potential causes of infertility were not evaluated.
In another study, analysis of semen samples from 85 male workers who were exposed to approximately 30 ppm trichloroethylene showed that the majority had normal semen volume, sperm density and motility. Exposed workers had a low percentage of normal sperm morphology (statistical significance not reported). Workers were divided into a "low exposure" and "high exposure" groups. There were no significant differences in mean sperm parameters, except sperm density. However, in both groups, sperm density was approximately double the World Health Organization standard normal sperm density.(49) In another study, increased miscarriages were not observed in the partners of men occupationally exposed to trichloroethylene.(2,30)
One study did not show more birth defects in the children of men occupationally exposed to trichloroethylene.(1,30)

Mutagenicity:
Trichloroethylene is considered mutagenic based on animal information. It is not possible to draw conclusions from mutagenicity studies of people with occupational exposure to trichloroethylene. Mutagenicity has been observed in some studies, but not in others. The studies had design limitations, including multiple chemical exposures and possible confounding factors such as smoking.(1,2) Positive results were obtained in the somatic cells of animals exposed to trichloroethylene with a purity of greater than 99%, using relevant routes of exposure.

Toxicologically Synergistic Materials:
When ethanol (commonly found in alcoholic beverages) is consumed shortly before or after exposure to trichloroethylene, the skin of the face and arms becomes very red. This condition is called "degreaser's flush".(1,8)

Potential for Accumulation:
Trichloroethylene is rapidly absorbed into the bloodstream following inhalation and ingestion and rapidly distributed to organs, including the liver, kidneys and cardiovascular and nervous systems. A small amount is absorbed through the skin. Some trichloroethylene is eliminated unchanged and as carbon dioxide in exhaled breath. Some trichlorethylene is broken down in the body mainly to trichloroacetic acid and trichloroethanol, which are excreted primarily in the urine. Trichloroethylene is excreted from the body at a moderate rate, mostly in the urine.(1,22,28)

Health Comments:
A number of studies have looked at health effects in human populations exposed to trichloroethylene in drinking water. For the most part, these studies have not been evaluated in this review due to difficulties with interpretation and their relevance to occupational exposures. Unstabilized trichloroethylene can decompose in the presence of air, light, heat, strong alkaline materials, and certain metals. Chemicals formed as a result of decomposition include phosgene, hydrogen chloride, and dichloroacetylene. These chemicals may contribute to or cause some of the harmful effects reported in workplaces where trichloroethylene was handled.(1,7,9,22,29)


SECTION 4. FIRST AID MEASURES

Inhalation:
Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment). Remove source of contamination or move victim to fresh air. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Immediately transport victim to an emergency care facility.

Skin Contact:
Avoid direct contact. Wear chemical resistant protective clothing if necessary. As quickly as possible, remove contaminated clothing, shoes and leather goods (e.g. watchbands, belts). Quickly and gently blot or brush away excess chemical. Wash gently and thoroughly with water and non-abrasive soap for 20 minutes or until the chemical is removed. Obtain medical attention immediately. Completely decontaminate clothing, shoes and leather goods before re-use or discard.

Eye Contact:
Avoid direct contact. Wear chemical resistant gloves, if necessary. Quickly blot or brush away excess chemical. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 20 minutes or until the chemical is removed, while holding the eyelid(s) open. Obtain medical attention immediately.

Ingestion:
NEVER give anything my mouth if victim is rapidly losing consciousness or is unconscious or convulsing. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 ozs) of water to dilute material in stomach. If vomiting occurs naturally, have victim lean forward to reduce risk of aspiration. Repeat administration of water. Obtain medical attention immediately.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest).
Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its condition of use in the particular workplace.

Note to Physicians:
Trichloroethylene decomposes to other toxic chemicals such as phosgene, dichloroacetylene and hydrogen chloride. Refer to Section 10 "Stability and Reactivity" for information on conditions which may lead to the formation of these chemicals. Depending on the circumstances in your workplace, it may be necessary to develop first aid procedures which also consider the effects of these chemicals.



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
None measured by conventional test methods. High concentrations of vapour mixed with air can be ignited by high-energy sources.(29,37)

Lower Flammable (Explosive) Limit (LFL/LEL):
8.0% at 25 deg C (1,37); 7.8% at 100 deg C (continuous contact with ignition source) (37)

Upper Flammable (Explosive) Limit (UFL/UEL):
Saturation vapour concentration (9.74% at 25 deg C)(29); 52% at 100 deg C (continuous contact with ignition source) (37)

Autoignition (Ignition) Temperature:
420 deg C (788 deg F) (37)

Sensitivity to Mechanical Impact:
Probably not sensitive; stable material.

Sensitivity to Static Charge:
Liquid can accumulate static charge by flow or agitation due to its low electrical conductivity (800 pS/m).(38) Probably not sensitive to static discharge because of large amount of energy required for ignition.

Combustion and Thermal Decomposition Products:
Hydrogen chloride gas, phosgene and other toxic and irritating compounds, such as chlorine and dichloracetyl chloride.(29,39)

Fire Hazard Summary:
Trichloroethylene is not flammable under most conditions of use. However, it can probably burn if strongly heated (high temperatures and a strong flame). No flash point has been measured by standard tests. However, under certain circumstances (e.g. ignition by a high-energy source such as a welding arc or hot wire ignition), trichloroethylene can form combustible vapour-air mixtures. Therefore, in hot work situations trichloroethylene should be regarded as flammable. Addition of small quantities of combustible substances or increasing oxygen content significantly increases flammability. The liquid can accumulate static charge by flow or agitation. During a fire, irritating and toxic hydrogen chloride gas, chlorine and phosgene may be generated. Trichloroethylene can accumulate in low lying areas. Closed containers can explode if exposed to the heat of a fire or excess heat for a sufficient period of time.

Extinguishing Media:
Trichloroethylene is generally not flammable. Use extinguishing media suitable for surrounding fire.(37,39) If trichloroethylene is burning, use carbon dioxide, dry chemical powder, foam or water fog.(33)

Fire Fighting Instructions:
Evacuate area and fight fire from a safe distance or a protected location. Approach fire from upwind to avoid hazardous vapours and toxic decomposition products.
If possible, isolate materials not yet involved in the fire, move containers from the fire area if this can be done without risk, and protect personnel. Otherwise, fire-exposed containers or tanks should be cooled by application of water spray. Application should begin as soon as possible and should concentrate on any unwetted portions of the container. Apply water from the side and from a safe distance until well after the fire is out. Stay away from the ends of tanks involved in the fire, but be aware that flying material from ruptured tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire. For a massive fire, it may be prudent to use unmanned hose holders or monitor nozzles.
If a leak or spill has not ignited, use water spray to disperse the vapours and to protect personnel attempting to stop a leak. Solid streams of water may be ineffective and spread material. Tanks or containers should not be approached directly after they have been involved in a fire or heated by exposure.
Trichloroethylene is a suspect carcinogen and its decomposition products are extremely toxic. Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical resistant suit with positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Health: 2 - Intense or continued (but not chronic) exposure could cause temporary incapacitation or possible residual injury.
NFPA - Flammability: 1 - Must be preheated before ignition can occur.
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 131.39

Conversion Factor:
1 ppm = 5.36 mg/m3; 1 mg/m3 = 0.186 ppm at 25 deg C (calculated)

Physical State: Liquid
Melting Point: Reported values vary; -73 deg C (-99.4 deg F) (2,33); -86.5 deg C (-124 deg F) (29,33)
Boiling Point: 87 deg C (189 deg F) (1,2,29,33)
Relative Density (Specific Gravity): 1.464 at 20 deg C (water=1) (2,29)
Solubility in Water: Slightly soluble (0.11 g/100 g at 20 deg C) (1,29,40)
Solubility in Other Liquids: Soluble in all proportions in ethanol, acetone, diethyl ether, chloroform, fixed and volatile oils, and most common organic solvents.(1,22,40)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log Poct = 2.42 (1); log Poct = 2.61 (2)
pH Value: Not available
Viscosity-Dynamic: 0.57 mPa.s (0.57 centipoise) at 20 deg C (29,40)
Viscosity-Kinematic: 0.39 m2/s (0.39 centistokes) at 20 deg C (calculated)
Surface Tension: 29.3 mN/m (29.3 dynes/cm) at 20 deg C (29)
Vapour Density: 4.53 (air=1) (2,41)
Vapour Pressure: 8 kPa (60 mm Hg) at 20 deg C (33); 9.87 kPa (74 mm Hg) at 25 deg C (1)
Saturation Vapour Concentration: Approximately 79000 ppm (7.9%) at 20 deg C; 97400 ppm (9.74%) at 25 deg C (calculated)
Evaporation Rate: 4.9 (n-butyl acetate = 1) (42); 3.0 (n-butyl acetate= 1) (41); 3.1 (diethyl ether = 1) (42)
Critical Temperature: 298-300 deg C (568.4-572 deg F) (29,40)
Critical Pressure: 4985 kPa (49.2 atm) (29); 5020 kPa (49.5 atm) (36)

SECTION 10. STABILITY AND REACTIVITY

Stability:
Moderately stable. Trichloroethylene is decomposed slowly by air forming phosgene, hydrogen chloride and dichloroacetyl chloride. Sunlight (especially ultraviolet light), heat and moisture accelerate this reaction. In the presence of water, corrosive dichloroacetic acid and hydrochloric acid are formed.(1,22,29,36)

Hazardous Polymerization:
Does not occur. The liquid can be polymerised by irradiation with cobalt 60 gamma rays or X-rays.(29)

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


ALKALI METALS (e.g. sodium or potassium and its alloys) - Mixtures are shock-sensitive and may explode with great violence on light impact. Forms spontaneously explosive and flammable monochloroacetylene or dichloroacetylene.(37,43)
STRONG BASES (e.g. sodium hydroxide or potassium hydroxide) or EPOXIDES (e.g. 1-chloro-2,3-epoxypropane and catalytic amounts of halide ions) - decompose trichloroethylene forming spontaneously explosive and flammable dichloroacetylene gas.(29,43)
STRONG OXIDIZING AGENTS (e.g. dinitrogen tetroxide, nitric acid, perchloric acid, oxygen, or peroxides) or STRONG REDUCING AGENTS (e.g. phosphorus, tin (II) chloride, metal hydrides) - may react violently with risk of fire and explosion.(22,29,33,37,39,43)
CHEMICALLY ACTIVE METALS (e.g. granular barium, lithium shavings, or beryllium, magnesium or titanium powder) - can ignite or explode violently.(37,43)
COPPER - can react with any dichloroethylenes present as an impurity, to form explosive acetylides.(36)
ALUMINUM POWDER - may react violently with ignition if traces of hydrochloric acid are present.(37,43)
ALUMINUM CHLORIDE - speeds up the polymerization of trichloroethylene, with production of hydrochloric acid and a very high release of heat.(37,43)
POTASSIUM NITRATE - may react violently.(22,43)
IRON, COPPER, ZINC or ALUMINUM - forms phosgene at 250-600 deg C.(35)

Hazardous Decomposition Products:
Hydrogen chloride gas, hydrochloric acid, phosgene, dichloroacetyl chloride and dichloroacetic acid.

Conditions to Avoid:
Excessive heat, open flames, sparks, electrical arcs, welding arcs, hot surfaces or other high temperature sources, sunlight, moisture, depletion of stabilizers.

Corrosivity to Metals:
Pure, dry, stabilized trichloroethylene is not corrosive to steel, cast iron, stainless steels, aluminum or nickel and its alloys. Trichloroethylene may attack aluminum, zinc and their alloys when it is unstabilized, uninhibited or lightly inhibited, heated or in the presence of water. No specific information is available on the corrosion rates. It can also attack brass and lead.(33,44)

Stability and Reactivity Comments:
Trichloroethylene stabilizers are stable to 130 deg C in the presence of air, moisture, light and construction metals. Stabilizers become less effective at higher temperatures.(22)


SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (rat): Approximately 8000 ppm (4-hour exposure) (5); 12500 ppm (4-hour exposure) (20)
LC50 (mouse): 8450 ppm (4-hour exposure) (3)

LD50 (oral, rat): 7200 mg/kg (cited as 4.92 mL/kg) (5)
LD50 (oral, male mouse): 2402 mg/kg (4)

LD50 (dermal, rabbit): Greater than 29000 mg/kg (cited as greater than 20 mL/kg (5)

Eye Irritation:

Trichloroethylene is a severe eye irritant.

Application of 0.1 mL of undiluted trichloroethylene caused severe injury in rabbits (scored over 5 where 5 is severe injury; graded 4/10).(5) In another study, application of undiluted trichloroethylene caused mild irritation in rabbits (scored 9/110).(6) Rabbits and guinea pigs exposed to 300-500 ppm trichloroethylene vapour over 6 weeks did not show signs of eye irritation.(7)

Skin Irritation:

Trichloroethylene is a severe skin irritant.

In an OECD-compliant test, application of 0.5 mL of trichloroethylene (greater than 99.95% pure) produced severe irritation in rabbits (primary irritation index: of 5.44/8; maximum average scores: 4/4 erythema and 2/4 edema at day 1).(55) Application of 0.01 mL of undiluted trichloroethylene (greater than 99.5% pure) produced severe irritation in rabbits (graded 5/10).(5) In a Draize test, application of undiluted trichloroethylene caused severe skin irritation in rabbits (scored 5.2/8).(6)

Effects of Short-Term (Acute) Exposure:

Signs of central nervous system (CNS) depression, such as incoordination and unconsciousness, have been observed in animals following inhalation or ingestion of high doses.(1,8,9,22) Reversible behavioural effects (e.g. avoidance behaviours) have been observed in rats exposed by inhalation to 200 ppm and above.(1,9) Kidney injury has been observed in rats exposed by inhalation to 1000 ppm or higher for less than 1 day. Kidney effects were not observed in mice and rats exposed by ingestion to up 2400 mg/kg/day for 3 weeks.(1) Reversible liver changes (e.g. increased liver weight) have been observed in mice, gerbils and rats exposed by inhalation to up to 300 ppm for 30 days. Slight liver effects have also been observed in rats exposed to 10000 ppm for 1 hour or 100 ppm for 6 hours. Liver injury (e.g. inflammation and tissue death) has been observed in mice that ingested 600 mg/kg/day for 4 weeks. Similar effects were not seen in male rats that ingested 1100 mg/kg/day for 3 weeks.(1,9) A few studies have reported harmful effects on hearing in rats in the mid- frequency range. High exposures were used in these studies (1000-4000 ppm) and it appears that exposures of 2000 ppm or higher are necessary to produce effects.(1,23) Sensitization of the heart to injected adrenaline has been observed in dogs and rabbits exposed by inhalation to very high concentrations (3000 to 10000 ppm) for up to 1 hour.(1,8,9)

Effects of Long-Term (Chronic) Exposure:

Rats have survived inhalation exposures of up to 2000 ppm for up to 6 months. The only harmful effects noted were signs of central nervous system (CNS) depression. Harmful effects were not observed in rats following exposure to 1000 ppm for 90 days or 770 ppm for 6 weeks, nor in monkeys exposed to 400 ppm for 7 months.(1,9) CNS effects have also been observed in animals following ingestion of large doses (e.g. 5600 mg/kg for 6 weeks).(9) Some studies have shown liver effects occasionally at 400-500 ppm, but more commonly at near lethal concentrations (approximately 3000 ppm). In one study, liver damage was observed in rats exposed to 372 ppm for 120 days.(9) Liver effects are generally not seen at lower concentrations.(1) Increased liver weights were observed in mice that ingested up to 800 mg/kg/day for 4 to 6 months.(8) Mice exposed by inhalation to 100, 300 or 600 ppm for 78 weeks had increased incidence of enlarged kidney cells at the two highest concentrations.(2) The kidney is a target organ in long-term feeding studies involving the administration of high doses to rats and mice.(1,2) In one study, enlarged kidney cells and kidney damage was observed in rats exposed to 500 or 1000 mg/kg/day for 103 weeks.(2) Rats exposed by inhalation to 2500 ppm for 13 weeks showed hearing loss in the mid-frequency range.(1)

Skin Sensitization:
In a Guinea Pig Maximization Test, trichloroethylene tested positive in 10/14 animals, indicating that it was a strong sensitizer.(60) However, the purity of trichloroethylene was not specified. Some 50 known stabilizers are used in trichloroethylene formulations, including amines, pyrroles, mixtures of epoxides and esters, phenols, and alcohols. Therefore, it is not possible to conclude that trichloroethylene is a skin sensitizer based on this study.

Carcinogenicity:
The International Agency for Research on Cancer (IARC) has determined that there is sufficient evidence for the carcinogenicity of trichloroethylene in experimental animals.
In two mouse feeding studies, significant increases in liver tumours were observed. In two rat feeding studies, kidney tumours were increased in male rats, and in one study, testicular tumours were increased. In mouse inhalation studies, an increased incidence of lymphomas was reported in one study, an increased incidence of liver tumours in one study, and increased incidences of lung tumours in three studies. In rat inhalation studies, an increased incidence of testicular tumours was observed in one study. Other studies were negative, or inconclusive due to limitations in study design.(2)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
The available information does not suggest that trichloroethylene causes developmental effects. Most studies have either not shown harmful effects in the offspring or have shown effects only in the presence of significant toxicity in the mothers.(1,2,8) Significant developmental effects were not observed in rats or mice exposed to trichloroethylene in a continuous breeding study.(54) Conclusions cannot be drawn from a study that showed delayed skeletal development (fetotoxicity) in the offspring of mothers exposed to high concentrations (1800 ppm) by inhalation. Effects were not observed in another group similarly exposed.(11) Maternal toxicity, as measured by weight gain and biochemical tests, was not reported, but central nervous system depression would be expected at the concentration used. In a limited study, abnormal heart development was reported in the offspring of rats exposed to 1100 ppm (estimated dose 100 mg/kg/day) in drinking water throughout pregnancy. There was no evidence of toxicity in the mothers.(10) This study is limited because the number of mothers/group was not specified, but was probably less than ten, based on the total number of females used. In addition, the trichloroethylene was mixed with tap water, which could have resulted in exposure of the mothers to other potentially harmful chemicals, and the purity of the trichloroethylene was not specified. In other studies, maternal toxicity was not evaluated and, therefore, these studies are not included in this review.

Reproductive Toxicity:
While some reproductive effects have been observed (e.g. abnormal sperm shape, reduced sperm motility), trichloroethylene has not been shown to reduce fertility in animals. A well-conducted continuous breeding study suggests that trichloroethylene is not a selective reproductive toxin. In mice, liver, kidney and lactational toxicity was more severe than the relatively moderate reductions in sperm motility. In rats, trichloroethylene produced general toxicity (reduced body weight, increased relative liver weight and kidney weights), with minimal effect on reproductive indices.
In a 2-generation continuous breeding study, mice were exposed to 0.15, 0.30 or 0.60% trichloroethylene (purity not specified) microencapsulated in a gelatin and sorbitol shell and added to the diet. Reported doses were 100, 300 or 700 mg/kg/day. Statistically significant effects were noted at the high dose only. In adult animals in both generations, there was evidence of liver damage (increased liver weight and centrilobular hypertrophy). In second-generation adults, evidence of kidney injury (increased weight and renal tubular degeneration) was observed. There was a 4% reduction in pup weight in the first generation. Maternal exposure during lactation was associated with a significant increase in perinatal mortality (61%). Reduced testis and prostate weights and reduced sperm motility were observed in the first-generation males. Increased epididymis weight, decreased sperm motility and an increased proportion of abnormal sperm were noted in second-generation males. However, there were no measurable effects on fertility.(54) In a related study, rats were exposed to 0.15, 0.30 and 0.60% trichloroethylene (purity not specified) microencapsulated in a gelatin and sorbitol shell and added to the diet. Reported doses were 76, 156 or 289 mg/kg/day. Adult female body weight was reduced at all doses, in both generations. Male body weight was reduced at the high dose in the first generation and at all doses in the second generation. Kidney weights were increased in first generation males and females. Liver weights were increased in first generation, high dose males and females, in all exposed males in the second generation and in females at the two higher doses in the second generation. The number of live pups/litter was decreased at the two highest doses in the first generation. Absolute testis weight was reduced in all exposed groups in the second generation. Sperm morphology was altered in low dose males in the second generation.(54) Male rats (6/group) were exposed to 376 ppm trichloroethylene (99% pure) for 12 or 24 weeks (4 hours/day; 5 days/week). A significant decrease in total epididymal sperm count, sperm motility, and serum testosterone levels was observed at weeks 12 and 24. This authors report that mating of the exposed rats produced maximum infertility, as judged by reproductive efficiency, percent pre-implantation and post implantation losses and litter size. However, no details are provided for evaluation.(52,53) Mice were exposed to a high concentration (1000 ppm) trichloroethylene (99% pure) for 4-19 days (6 hours/day; 5 days/week). Damage to the epididymis, as evidenced by sloughing of epithelial cells, was observed after 4 weeks exposure.(51) Mice exposed by inhalation to 2000 ppm trichloroethylene (purity not specified) for 5 days (4 hours/day) had abnormally shaped sperm 28 days after exposure.(13) A dose-related increase in abnormally shaped sperm was also observed in mice exposed by inhalation to 100 or 500 ppm trichoroethylene (99.9% pure) for 5 days (7 hours/day).(18) The biological significance of these observations is not clear. Rats exposed orally to up to 1000 mg/kg/day trichloroethylene (greater than 99.9% pure) for 6 weeks had normal sperm count, motility and shape.(14) Negative results were obtained in a dominant lethality study where male mice were exposed by inhalation to 450 ppm for 24 hours and then mated.(2, unconfirmed) Reproductive function was not affected in female rats exposed orally to up to 1000 mg/kg/day trichloroethylene (greater than 99.9% pure) or by inhalation to 1800 ppm trichloroethylene (99% pure with 0.2% epichlorohydrin) for 2 weeks prior to mating.(11,12)

Mutagenicity:
Trichloroethylene has been extensively studied for potential mutagenicity. Interpretation of the results from these tests is complicated, because the purity of the test substance is not always specified. Commercial trichloroethylene formulations may contain stabilizers (e.g. epichlorohydrin), which are mutagenic. Studies with impure trichloroethylene are not considered in this assessment. Positive results have been obtained in the somatic cells of live animals exposed by appropriate routes of exposure to highly pure trichloroethylene. Therefore, trichloroethylene is considered mutagenic.
A dose-related, statistically significant increase in micronuclei in bone marrow red blood cells was observed in mice exposed orally to two single doses of 375, 750, 1125, 1500, 2250 or 3000 mg/kg trichloroethylene (purity 99.5%).(16) The significance of this study is limited by the uncertainties of the scoring method used (micronuclei, including microbodies appearing to be of nuclear origin) and the unusually high frequency of micronucleated polychromatic erythrocytes in the control group. The micronucleus frequency in the untreated and vehicle control groups also differed significantly from each other.(58) Rats and mice were exposed to single 6-hour concentrations of 0, 5, 500 or 5000 ppm of reagent grade trichloroethylene (purity greater than 99%). A significant, dose-related increase in micronuclei was observed in rat bone marrow. At 5000 ppm, the increase was approximately 4-fold and was reproducible. Animal toxicity and cytotoxicity were observed at this concentration. No significant changes were observed in the mice. Groups of rats were also exposed to 0, 4, 50 or 500 ppm for 4 days (6 h/day). The number of micronuclei in bone marrow polychromatic erythrocytes was comparable to the 1-day study. However, the results were not statistically significant in this case due to an unusually high number of micronuclei in the control group.(15) A dose-related increase in DNA single strand breaks was observed in the liver cells of male mice and male rats administered single oral doses of epichlorohydrin-free trichloroethylene in Tween 80 in distilled water. Rats were dosed with 0, 510, 1500, 3010 or 3995 mg/kg (cited as 0, 3.9, 11.4, 22.9 or 30.4 mMol/kg). Mice were dosed with 0, 100, 760, 1500 or 3010 mg/kg (cited as 0, 0.76, 5.8, 11.4 or 22.9 mMol/kg). Statistically significant DNA strand breaks were observed at 3010 mg/kg and above for rats and 1500 mg/kg and above for mice.(17) In a non-standard test, male rats were given a single oral dose of 525 mg/kg (cited as 4 mMol/kg) trichloroethylene (99.5% pure). The rats were partially nephrectomized and injected intravenously with folic acid to increase the proliferative activity of the kidney cells. No lethality or severe toxic effects were observed in the animals. A statistically significant increase in the average frequency of micronucleated kidney cells was observed.(57) Mice were dermally exposed to 7, 14 or 28 g/kg trichloroethylene (plus 99% purity). Six days following single or repeated exposures, a statistically significant increase in aneupolid cells was observed in hematopoietic stem cells of the bone marrow.(56) Negative results (DNA damage, micronuclei, or chromosomal aberrations) were reported in several other animal studies.(1,2,18) In mice, effects on abnormal sperm shape were observed in two studies (13,18), but not in a third study (14). Although changes in sperm head shape may be genetically determined, it is uncertain whether they are due to genotoxicity or to other toxic effects. This effect can therefore not be taken as evidence of germ cell mutagenicity.
In general, negative results have been obtained in bacteria and cultured mammalian cells, but positive results have been obtained in some systems.(2)


SECTION 16. OTHER INFORMATION

Selected Bibliography:
(1) Agency for Toxic Substances an Disease Registry. Toxicological profile for trichloroethylene (Update). US Department of Health and Human Services, Sept. 1997
(2) International Agency for Research on Cancer. Trichloroethylene. In: IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 63. Dry cleaning, some chlorinated solvents and other industrial chemicals. World Health Organization, Feb. 1995. p. 75-158
(3) Friberg, L., et al. Toxicities of trichloroethylene and tetrachloroethylene and Fujiwara's pyridine-alkali reaction. Acta Pharmacologica et Toxicologica. Vol. 9 (1953). p. 303-312
(4) Tucker, A.N., et al. Toxicology of trichloroethylene in the mouse. Toxicology and Applied Pharmacology. Vol. 62, no. 3 (Mar. 15, 1982). p. 351- 357
(5) Smyth, Jr., H.F., et al. Range-finding toxicity data: list VII. American Industrial Hygiene Association Journal. Vol. 30 (1969). p. 470-476
(6) Duprat, P., et al. Pouvoir irritant des principaux solvents chlores aliphatiques sur la peau et les muqueuses oculaires du lapin. European Journal of Toxicology. Vol. 9, no. 3 (May-June 1976). p. 171-177
(7) Grant, W.M., et al. Toxicology of the Eye. 4th ed. Charles C. Thomas, 1993
(8) Torkelson, T.R. Halogenated aliphatic hydrocarbons containing chlorine, bromine, and iodine: unsaturated halogenated hydrocarbons: trichloroethylene, 1,1,2-trichloroethylene, tri, trilene [CAS # 79-01-6]. In: Patty's industrial hygiene and toxicology. 4th ed. Edited by G.D. Clayton, et al. Volume II. Toxicology. Part E. John Wiley and Sons, Inc., 1994. p. 4194-4207
(9) Fielder, R.J., et al. Trichloroethylene. Health and Safety Executive, 1982
(10) Dawson, B.V., et al. Cardiac teratogenesis of halogenated hydrocarbon- contaminated drinking water. Journal of the American College of Cardiology. Vol. 21, no. 6 (May 1993). p. 1466-1472
(11) Dorfmueller, M.A., et al. Evaluation of teratogenicity and behavioral toxicity with inhalation exposure of maternal rats to trichloroethylene. Toxicology. Vol. 14, no. 2 (1979). p. 153-166
(12) Manson, J.M., et al. Effects of oral exposure to trichloroethylene on female reproductive function. Toxicology. Vol. 32, no. 3 (Sept. 1984). p. 229-242
(13) Land, P.C., et al. Morphologic changes in mouse spermatozoa after exposure to inhalational anesthetics during early spermatogenesis. Anesthesiology. Vol. 54, no. 1 (Jan. 1981). p. 53-56
(14) Zenick, H., et al. Effects of trichloroethylene exposure on male reproductive function in rats. Toxicology. Vol. 31, no. 3 (June 1984). p. 237- 250
(15) Kligerman, A.D., et al. Inhalation studies of the genotoxicity of trichloroethylene to rodents. Mutation Research. Vol. 322, no. 2 (Aug. 1994). p. 87-96
(16) Duprat, P. et al. Cytogenetic effect of trichloroethylene in the mouse as evaluated by the micronucleus test. IRCS Medical Science. Vol. 8 (1980). p. 182
(17) Nelson, M.A., et al. Induction of strand breaks in DNA by trichloroethylene and metabolites in rat and mouse liver in vivo. Toxicology and applied Pharmacology. Vol. 94, no. 1 (June 15, 1988). p. 45-54
(18) Beliles, R.P., et al. Teratogenic-mutagenic risk of workplace contamination: trichloroethylene, perchloroethylene, and carbon disulfide. National Institute for Occupational Safety and Health, 1980
(19) Von Oettingen, W.F. The halogenated hydrocarbons of industrial and toxicological importance. Elsevier Publishing Company, 1964. p. 240-271
(20) Siegel, J., et al. Effects on experimental animals of acute, repeated and continuous inhalation to dichloroacetylene mixtures. Toxicology and Applied Pharmacology. Vol. 18, no. 1 (Jan. 1971). p. 168-174
(21) Stewart, R.D., et al. Observations on the concentrations of trichloroethylene in blood and expired air following exposure of humans. American Industrial Hygiene Association Journal. Vol. 23 (Mar.-Apr. 1962). p. 167-170
(22) Commission of the European Communities. Trichloroethylene. In: Organo- chlorine solvents: health risks to workers. Royal Society of Chemistry, 1986. p. 94-130
(23) Johnson, A.-C., et al. Effects of industrial solvents o hearing. Occupational medicine: state of the art reviews. Vol. 10, no. 3 (July- Sept. 1995). p. 623-640
(24) Salvini, M., et al. Evaluation of the psychophysiological functions in humans exposed to trichloroethylene. British Journal of Industrial Medicine. Vol. 28, no. 3 (July 1971). p. 293-295
(25) Barret, L. et al. Chronic trichloroethylene intoxication: a new approach by trigeminal-evoked potentials? Archives of Environmental Health. Vol. 42, no. 5 (Sept./Oct. 1987). p. 297-302
(26) Phoon, W.H., et al. Stevens-Johnson syndrome associated with occupational exposure to trichloroethylene. Contact Dermatitis. Vol. 10, no. 5 (1984). p. 270-276
(27) Nagaya, T., et al. Subclinical and reversible hepatic effects of occupational exposure to trichloroethylene. International Archives of Occupational and Environmental Health. Vol. 64, no. 8 (May 1993). p. 561-563
(28) Goeptar, A.R., et al. Metabolism and kinetics of trichloroethylene in relation to toxicity and carcinogenicity: relevance of the mercapturic acid pathway. Chemical Research Toxicology. Vol. 8, no. 1 (Jan./Feb. 1995). p. 3-21
(29) Mertens, J.A. Chlorocarbons and chlorohydrocarbons: trichloroethylene. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 6. John Wiley and Sons, 1993. p. 40-50
(30) Tas, S., et al. Occupational hazards for the male reproductive system. Critical Reviews in Toxicology. Vol. 26, no. 3 (1996). p. 261-307
(31) Goh, C.L., et al. A cutaneous manifestation of trichloroethylene toxicity. Contact Dermatitis. Vol. 18, no. 1 (1988). p. 59-61
(32) Nakayama, H., et al. Generalized eruption with severe liver dysfunction associated with occupational exposure to trichloroethylene. Contact Dermatitis. Vol. 19, no. 1 (1988). p. 48-51
(33) Emergency action guide for trichloroethylene. Association of American Railroads, Mar. 1995
(34) Odor thresholds for chemicals with established occupational health standards. American Industrial Hygiene Association, 1989
(35) HSDB database record for trichloroethylene. Last revision date: 97/05/08
(36) Dreher, E-L. Chlorinated hydrocarbons: trichloroethylene. In: Ullmann's encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 6. VCH Verlagsgesellschaft, 1986. p. 299-309
(37) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 325; NFPA 49
(38) Chemical safety sheets: working safely with hazardous chemicals. Kluwer Academic Publishers, 1991
(39) The Sigma-Aldrich library of chemical safety data. Edition II. Vol. 2. Sigma-Aldrich Corporation, 1988
(40) Dean, J.A. Lange's handbook of chemistry. 14th ed. McGraw-Hill, Inc., 1992
(41) Sullivan, D.A. Solvents, industrial. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 22. John Wiley and Sons, 1997. p. 538- 539, 550, 563
(42) Stoye, D., et al. Solvents. In: Ullman's encyclopedia of industrial chemistry. 5th revised ed. Vol. A 24. VCH Verlagsgesellschaft, 1993. p. 448-453, 476-484
(43) Urben, P.G., ed. Bretherick's handbook of reactive chemical hazards. 5th ed. Vol. 1. Butterworth-Heinemann Ltd., 1995
(44) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985
(45) NIOSH pocket guide to chemical hazards. National Institute Occupational Safety and Health, 1997
(46) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002
(47) European Communities (EC). Commission Directive 2001/59/EC. Aug. 6, 2001
(48) Report on Carcinogens. 11th ed. US Department of Health and Human Services, Public Health Service, National Toxicology Program
(49) Chia, S.E., et al. Semen parameters in workers exposed to trichloroethylene. Reproductive Toxicology. Vol. 10, no. 4 (1996). p. 295-299
(50) Forkert, P.G., et al. Identification of trichloroethylene and its metabolites in human seminal fluid of workers exposed to trichloroethylene. Drug Metabolism and Disposition. Vol. 31, no. 3 (Mar. 2003). p. 306-311
(51) Forkert, P.G., et al. Metabolism and toxicity of trichloroethylene in epididymis and testis. Toxicology and Applied and Pharmacology. Vol. 182, no. 3 (Aug. 2002). p. 244-54
(52) Kumar, P., et al. Steroidogenic alterations in testes and sera of rats exposed to trichloroethylene (TCE) by inhalation. Human and Experimental Toxicology. Vol. 19 (2000). p. 117-121
(53) Kumar, P., et al. Trichloroethylene induced testicular toxicity in rats exposed by inhalation. Human and Experimental Toxicology. Vol. 20 (2001). p. 585-589
(54) Lamb, J., et al. Trichloroethylene. Environmental Health Perspectives. Vol. 105, suppl. 1 (Feb. 1997). p. 357-360
(55) Technical report no. 66. Skin irritation and corrosion: reference chemicals data bank. European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC), Mar. 1995
(56) Giver, C.R., et al. Dermal benzene and trichloroethylene induce aneuploidy in immature hematopoietic subpopulations in vivo. Environmental and Molecular Mutagenesis. Vol. 37 (2001). p. 185-194
(57) Robbiano, L., et al. Increased frequency of micronucleated kidney cells in rats exposed to halogenated anaesthetics. Mutation Research. Vol. 413 (1998). p. 1-6
(58) National Industrial Chemicals Notification and Assessment Scheme. Trichloroethylene. Priority Existing Chemical Assessment Report No. 8. Commonwealth of Australia, Mar. 2000
(59) Yoshida, M., et al. Concentrations of trichloroethylene and its metabolites in blood and urine after acute poisoning by ingestion. Human and Experimental Toxicology. Vol. 15 (1996). p. 254-258
(60) Tang, X.-J., et al. Guinea pig maximization test for trichloroethylene and its metabolites. Biomedical and Environmental Sciences. Vol. 15 (2002). p. 113-118

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 1998-03-26

Revision Indicators:
TLV comments 1998-08-01
EU classification 2002-02-11
EU Risk 1998-11-01
EU safety 2002-02-11
ERPG 2001-03-01
EU risks 2002-02-11
EU comments 2002-02-11
TDG 2002-05-29
Mutagenicity 2003-03-27
WHMIS health effects 2003-03-27
Emergency overview 2003-03-27
Handling 2003-03-27
Engineering controls 2003-03-27
WHMIS classification comments 2003-05-25
PEL transitional comments 2003-12-19
PEL-TWA final 2003-12-19
PEL-STEL final 2003-12-19
Resistance of materials for PPE 2004-04-06
Toxicological info 2005-01-19
Long-term exposure 2005-01-19
Bibliography 2005-02-02
Teratogenicity/embryotoxicity 2005-10-07
Reproductive toxicity 2005-10-07
TLV-TWA 2006-02-16
TLV-STEL 2006-02-16
TLV definitions 2006-02-16
TLV proposed changes 2006-02-16
Carcinogenicity 2006-02-17
WHMIS detailed classification 2006-02-17



©2007 Canadian  Centre  for  Occupational  Health  &  Safety  
www.ccohs.ca  E-mail: clientservices@ccohs.ca  Fax: (905) 572-2206  Phone: (905) 572-2981  
Mail:  250  Main  Street  East,  Hamilton  Ontario  L8N  1H6