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Priority Existing Chemical Assessment Reports - Trichloroethylene
CHEMICAL IDENTITY Chemical Name
Synonyms
Trade Names
Molecular Formula: C2HCl3 Chemical Abstracts Service (CAS) Number: 79-01-6 EINECS Number: 2011674 *Trademark of The Dow Chemical CompanyAPPLICANTS
Overview of Trichloroethylene AssessmentTrichloroethylene has been assessed as a Priority Existing Chemical (PEC) under the National Industrial Chemicals Notification and Assessment Scheme. Trichloroethylene is a chlorinated solvent used mainly in metal cleaning. The most common form of metal cleaning using trichloroethylene is vapour degreasing, while cold cleaning, such as dipping and wiping, occurs to a lesser extent. Trichloroethylene is either used as a solvent neat or as an ingredient of products such as adhesives, electrical equipment cleaners, waterproofing agents, paint strippers and carpet shampoos. Most of these products are used for industrial purposes, although some are available for consumer use. Exposure to trichloroethylene is mainly by inhalation, with skin contact significant in some cases, particularly cold cleaning. In a comprehensive NICNAS survey conducted in industry to investigate current uses, exposure levels, control technologies and environmental exposure, there was little evidence of routine exposure monitoring. Consequently, a special project was commissioned to undertake atmospheric and biological monitoring of workers using trichloroethylene as a neat solvent in cold cleaning and in products for various purposes. From the study and other exposure data, it was concluded that exposure to trichloroethylene vapours could be high during vapour degreasing and cold cleaning. Trichloroethylene is absorbed via inhalational, dermal and oral routes, with the most significant uptake being through inhalation of the vapour. Absorbed trichloroethylene is distributed throughout the body and is deposited mainly in adipose tissue and liver. It readily crosses the placental and blood brain barriers. The liver is the primary site of metabolism. The major metabolites are trichloroethanol, trichloroacetic acid and trichloroethanol glucuronide. Other minor metabolites that have been identified are chloral hydrate, monochloroacetic acid, dichloroacetic acid and N-acetyl dichlorovinyl cysteine. A second pathway identified in humans and animals is conjugation with glutathione with the formation of dichlorovinyl cysteine in the kidneys. The major part of the absorbed trichloroethylene is excreted in urine as metabolites while a small amount is exhaled unchanged. There are some species differences in the metabolism of trichloroethylene. The rate of metabolism of trichloroethylene to trichloroacetic acid in mice is more rapid than in rats. Saturation of the oxidative pathway has also been reported in rats at 200 to 500 mg/kg while in mice saturation is only seen at 2000 mg/kg. Saturation in humans has been predicted by physiologically based pharmacokinetic (PBPK) models to occur at 2000 mg/kg. The predominant effect of acute exposure to trichloroethylene in humans is CNS depression. It is a skin and eye irritant but not a skin or respiratory sensitiser. The critical effect on repeated exposure is kidney toxicity, with an inhalational No Observed Adverse Effect Level (NOAEL) of 100 ppm observed in a two year study. Other affected systems are the lungs, nervous system and hearing. In animal reproductive toxicity studies, adverse effects were only observed at maternally toxic doses. Trichloroethylene is weakly mutagenic in vitro. In the presence of metabolic activation, trichloroethylene tested positive in several bacterial and fungal gene mutation assays. Trichloroethylene also tested positive in a mouse lymphoma gene mutation assay, and unscheduled DNA synthesis (UDS) was reported in several studies. In somatic cell studies in vivo, both positive and negative results were obtained in micronucleus tests, with negative results obtained in studies for chromosome aberrations, sister chromatid exchange and UDS. Trichloroethylene induced DNA single strand breaks in the liver of rats and mice in one study, and in mice liver and kidneys in a second study. A mouse spot test was equivocal, however, a preliminary test for pink-eyed unstable mutation test was clearly positive. In germ cell assays, dominant lethal tests were either negative or inconclusive. Studies in occupationally-exposed groups of workers were inconclusive. However, a study of somatic mutations in the von Hippel-Lindau gene in tissue from renal cancer patients reported that trichloroethylene acts on the gene. Further work is underway in Europe to confirm the effects of trichloroethylene on the VHL gene. Trichloroethylene has been shown to induce tumours in mouse liver and lung and rat kidney and testis with all but the rat kidney tumours considered not relevant to humans. Peroxisomal proliferation is thought to be the mechanism of liver tumour formation and this has not been seen in humans. Lung tumours in mice are related to the accumulation of chloral hydrate in the Clara cells of the lung. Testicular tumours were observed only in one strain of rats with a high incidence in the control group. These tumours are rare in men and are often associated with peroxisomal proliferators. A number of epidemiological studies have investigated the carcinogenic potential of trichloroethylene. Most studies that were large enough to detect an effect individually did not show any association between cancer and occupational exposure to trichloroethylene. However two other studies, with some weaknesses in their conduct, indicated an apparent association between cancer and occupational exposure to trichloroethylene. The kidney tumours are thought to be related to the metabolism of trichloroehtylene and are considered to be of concern to humans. The mechanism by which trichloroethylene causes rat kidney cytotoxicity is uncertain and is currently under investigation. It has been proposed that the likely mechanism of kidney tumours in rats is repeated cytotoxicity and regeneration. Some workers have postulated that kidney toxicity is due to formic acid while others have attributed it to the metabolite dichlorovinyl cysteine. Dichlorovinyl cysteine has been identified in the urine of workers exposed to trichloroethylene. Based on the assessment of health effects, trichloroethylene meets the Approved Criteria for Classifying Hazardous Substances for classification as a skin and eye irritant (risk phrases R36/38 - irritating to eyes and skin), mutagen category 3 (R40(M3) Possible risk of irreversible effects, mutagen category 3) and carcinogen category 2 (R45 - May cause cancer). The occupational risk assessment found that during formulation of products the risk of kidney effects is considered to be minimal. However, there is a concern during vapour degreasing as workers may be exposed to high vapour concentrations for prolonged periods. Use of trichloroethylene in cold cleaning is of concern as workers may be exposed to the vapour as well as absorption of liquid through the skin. Use of trichloroethylene products usually involves work activities of short duration. However there is a concern if workers are exposed on a prolonged basis to products containing high concentrations of trichloroethylene, especially if they are used as aerosols. It is recommended that greater research and development be directed to substitute processes and non-hazardous substances because of concern that workers may be exposed to high trichloroethylene concentrations during vapour degreasing and cold cleaning. To control worker exposure during vapour degreasing it is recommended that the vapour degreasing tank must conform to the requirements of the Australian Standard AS 2661 - 1983 (Standards Association of Australia, 1983). This standard also describes the safety requirements for the operation of a vapour degreaser plant. Use of trichloroethylene in cold cleaning is not supported by this assessment, and a phase out period of two years is recommended. The use of trichloroethylene may be unnecessary and/or excessive for some processes. Alternative processes and the substitutes available for some of the uses should be used. During the period where alternatives are being identified, for other uses, appropriate engineering controls such as local exhaust ventilation must be used to minimise exposure. Use of trichloroethylene products in an aerosol form is not supported by this assessment. Local exhaust ventilation will help to minimise exposure of workers to trichloroethylene during use of other products. Gross deficiencies were noted in the MSDS and labels provided for assessment and it is recommended that suppliers amend these in accordance with regulatory requirements. The deficiencies and the recommendations to rectify them are detailed in the full report. Trichloroethylene is not expected to present a risk to public health provided consumer products containing trichloroethylene are labelled in accordance with the requirements of the Standard for the Uniform Scheduling of Drugs and Poisons and the label instructions are followed. The risk to the environment is expected to be low in Australia. Based on the available data it is predicted that trichloroethylene will not occur at concentrations potentially harmful to the aquatic environment or the atmosphere. There is no manufacture of trichloroethylene in Australia, and measures for handling and storing bulk trichloroethylene are in place, therefore except in the case of a major spill, contamination of groundwater is unlikely.
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