Trichloroethylene

131.39

131.39

1736782

201-167-4

TSCA listed

Clear colorless

29032200

0

Clear, colorless, watery-liquid with a chloroform-like odor. Odor threshold concentrations determined in air were 21.4 ppmv(Leonardos et al., 1969) and 3.9 ppmv(Nagata and Takeuchi, 1990). The average least detectable odor threshold concentrations in water at 60 °C and in air at 40 °C were 10 and 2.6 mg/L, respectively (Alexander et al., 1982).

Reactivity with Water No reaction; Reactivity with Common Materials: No reaction; Stability During Transport: Stable; Neutralizing Agents for Acids and Caustics: Not pertinent; Polymerization: Not pertinent; Inhibitor of Polymerization: Not pertinent.

2.5017

Colorless transparent liquid, with the same odor as a chloroform

1.463 g/mL at 25 °C(lit.)

-86 °C

87 °C

90°C

n20/D1.476(lit.)

Slightly soluble. 0.11 g/100 mL

Storage Room low temperature ventilation drying ,Separate storage with food additives

61 mm Hg ( 20 °C)

4.5 (vs air)

Extended exposure (e.g., occupational exposure) to a chlorinated solvent like TCE typically results in signs of central nervous system (CNS) disturbance and hepatotoxicity. The primary target tissues for the carcinogenicity of TCE identified in animal studies are the liver, lung, and kidney. For each of these target tissues there is evidence that the carcinogenicity of TCE may be associated with one or more of its metabolites: TCA and dichloroacetic acid (DCA) in the liver, chloral in the lung, and S-(1,2-dichlorovinyl)-L-cysteine (DCVC) in the kidney.TCA acts as a peroxisome proliferator, and hepatic neoplasms in mice may arise through this mechanism. TCE metabolism via cytochrome P450 generates the metabolites DCA and TCA, which are associated with hepatotoxicity and liver cancer. DCA and TCA may induce hepatic tumorigenesis by (1) modification of signaling pathways; (2) cytotoxicity, cell death, and reparative hyperplasia; and (3) direct DNA damage.TCE metabolism via glutathione (GSH) conjugation generates DCVC, which is associated with nephrotoxicity and kidney cancer. DCVC can be both bioactivated and detoxified by different enzymes. The enzyme that is primarily responsible for renal bioactivation of nephrotoxic cysteine S-conjugates is the b-lyase. The reactive thiol and subsequent species generated from b-lyase-catalyzed metabolism of DCVC may induce renal tumorigenesis by (1) peroxisome proliferation, (2) a-2uglobulin nephropathy, (3) genotoxicity leading to somatic mutation, and (4) acute cytotoxicity and necrosis leading to cell proliferation.

Non flammable

vol% in air: 7.9 100

Chloroform-like; ethereal.

Sweet burning taste

3.14 at 1.8 °C, 8.47 at 21.6 °C, 19.0 at 40.0 °C, 26.5 at 50 °C, 35.8 at 60 °C, 56.6 at 70 °C (EPICS-GC, Shimotori and Arnold, 2003)

Slightly soluble in water.

Trichloroethylene has been determined experimentally that mixtures of finely divided barium metal and a number of halogenated hydrocarbons possess an explosive capability. Specifically, impact sensitivity tests have shown that granular barium in contact with monofluorotrichloromethane, trichlorotrifluoroethane, carbon tetrachloride, Trichloroethylene, or tetrachloroethylene can detonate (ASESB Pot. Incid. 39. 1968; Chem. Eng. News 46(9):38. 1968). Trichloroethylene has been determined experimentally that a mixture of beryllium powder with carbon tetrachloride or with Trichloroethylene will flash or spark on heavy impact (ASESB Pot. Incid. 39. 1968). A mixture of powdered magnesium with Trichloroethylene or with carbon tetrachloride will flash or spark under heavy impact (ASESB Pot. Incid, 39. 1968).

770°F

2-8°C

III

6.1

UN 1710 6.1/PG 3

3

T,F

53-45-61-36/37-16-7

KX4550000

T

Separated from metals, strong bases, food and feedstuffs, combustible substances and ignition sources. See Chemical Dangers. Dry. Keep in the dark. Keep in a well-ventilated room. Cool.

Stable. Incompatible with oxidizing agents, aluminium, magnesium, strong bases, reducing agents. Light-sensitive. Reacts violently with many metals, ozone, potassium nitrate, potassium hydroxide, sodium hydroxide.

P201-P308 + P313

45-36/38-52/53-67-68-39/23/24/25-23/24/25-11

Contact with strong caustics causes decomposition and the production of highly toxic and flammable dichloroacetylene. Violent reaction with chemically active metals; powders, or shavings, such as aluminum, barium, lithium, sodium, magnesium, and titanium. Violent reaction with aluminum in the presence of dilute hydrochloric acid. Thermal decomposition of trichloroethylene, due to contact with hot metal or UV radiation, forms hazardous products including chlorine gas, hydrogen chloride; and phosgene. Keep this chemical away from high temperatures, such as arc welding or cutting, unshielded resistance heating; open flames; and high intensity UV light. Slowly decomposed by light in presence of moisture, with formulation of hydrochloric acid.

UN 1710

P201; P261; P273; P281; P305 + P351 + P338; P308 + P313

Special Hazards of Combustion Products: Toxic and irritating gases are produced in fire situations.

Trichloroethylene is a chlorinated hydrocarbon used as a detergent or solvent for metals, oils, resins, sulfur, and as general degreasing agent. It can cause irritant contact dermatitis, generalized exanthema, Stevens-Johnson- like syndrome, pustular or bullous eruption, scleroderma, as well as neurological and hepatic disorders.

TLV-TWA 50 ppm (～270 mg/m3) (ACGIH), 100 ppm (MSHA and OSHA); TLV-STEL 200 ppm (ACGIH); ceiling 200 ppm (OSHA); carcinogenicity: Animal Lim ited Evidence, Human Inadequate Evidence (IARC).

The toxic effects manifested in humansfrom inhaling trichloroethylene vapors areheadache, dizziness, drowsiness, fatigue, andvisual disturbances. A 2-hour exposure to a1000-ppm concentration affected the visualperception. Higher concentrations can pro duce narcotic effects. Heavy exposures maycause death due to respiratory failure or car diac arrest. A 4-hour exposure to 8000 ppmwas lethal to rats. Chronic exposure causedincrease in kidney and liver weights in testanimals.The symptoms of poisoning from oralintake of trichloroethylene are nausea, vom iting, diarrhea, and gastric disturbances. Theacute oral toxicity, however, is low. Theoral LD50 value in mice is in the range2500 mg/kg. Trichloroethylene metabolizesto trichloroacetic acid, which is excreted inthe urine.Although trichloroethylene exhibits lowtoxicity, its metabolite trichloroethanol, andoxidative degradation products phosgene,COCl2, and chlorine, can cause severe unex pected health hazards. Kawakami andassociates (1988) reported a case of Steven–Johnson syndrome in a worker in a printingfactory. In another case, fire on a stove in ametal-degreasing workplace produced phos gene and chlorine inhalation, which causeddyspnea, fever, and fatigue.Trichloroethylene exhibited evidence ofcarcinogenicity in laboratory animals. Oraladministration produced liver tumors, whileinhalation caused lung and blood tumors inmice and rats.