Trichloroethylene poisoning

Attempts to diminish the overall metabolism of trichloroethylene might be useful (e.g., hypothermia, mixed-function oxidase inhibitors, competitive inhibitors of trichloroethylene metabolism [i.e., P-450 substrates]), if instituted soon enough after trichloroethylene exposure. Catecholamines (especially beta agonists) act in concert with trichloroethylene, increasing the risk of cardiac arrhythmias. Hence, catecholamines should be administered to patients only in the lowest efficacious doses and for certain limited presentations of trichloroethylene poisoning. Ethanol should also be avoided because concurrent exposure to trichloroethylene and ethanol can cause vasodilation and malaise and may potentiate central nervous system depression at high dosage levels of either compound. 

Bartonicek VJ, Brun A. 1970. Subacute and chronic trichloroethylene poisoning A neuropathological study in rabbits. Acta Pharm Toxicol 28 359-369. 

Buxton PH, Hayward M. 1967. Polyneuritis cranials associated with industrial trichloroethylene poisoning. J Neurol Neurosurg Psychiatry 30 511-518. 

Dhuner KG, Nordqvist P, Renstrom B. 1957. Cardiac irregularities in trichloroethylene poisoning. Acta Anaesthesiol Scand 1 121-135. 

Morreale SA. 1976. A case of acute trichloroethylene poisoning with myocardial infarction. Med Lav 67 176-182. 

Perbellini L, Olivato D, Zedde A, et al. 1991. Acute trichloroethylene poisoning by ingestion clinical and pharmacological aspects. Intensive Care Med 17 234-235. 

Todd J. 1954. Trichloroethylene poisoning with paranoid psychosis and Lilliputian halucination. Br Med J 1 439-440. 

A man of 56 years was found dead after exposure to trichloroethylene fumes. The following postmortem concentrations of trichloroethylene were reported blood about 90 pg/ml, brain about 270 pg/g, lung about 40 pg/g (A. A ha.etal., Bull. int. Ass.forens. Toxicol., 1974, 70(1), 14-15). In 19 cases of fatal trichloroethylene poisoning, the following postmortem concentrations were reported blood 1 to 41 pg/ml (mean 14, 15 cases), brain 4 to 74 pg/g (mean 31,5 cases), kidney 4 to 140 pg/g (mean 30, 8 cases), liver 1 to 250 pg/g (mean 64,9 cases), lung 1 to 15 pg/g (mean 7, 6 cases), urine a trace to 91 pg/ml (mean 35, 5 cases) (R. Bonnichsen and... 

We were able to confirm this condition in a 29-year-old female patient with severe acute trichloroethylene poisoning after taking 80-90 ml trichloroethylene perorally with suicidal intent. Despite a 6-day comatose state, intensive care produced a complete recovery. Throughout the 3-week period of treatment, all of the liver enzymes remained normal, and percutaneous liver biopsy yielded normal histology. (36)... 

Harenko A Two peculiar instances of psychotic disturbance in trichloroethylene poisoning. Acta Neurol Scand Suppl 31 139-140, 1967 Landrigan PJ, Stein GF, Kominsky JR, et al Common-source community and industrial exposure to trichloroethylene. Arch Environ Health 42 327-332, 1987 Lilis R, Stanescu D, Muica N, et al Chronic effects of trichloroethylene exposure. Med Lav 60 595-601, 1969... 

Harenko A Two peculiar instances of psychotic disturbance in trichloroethylene poisoning. Acta Neurol Scand Suppl 31 139-140,1967... 

Quantitative Determination of Trichloroacetic Acid as an Indicator of Trichloroethylene Poisoning. Methodological Review and Choice of a Gas Chromatographic Method G. Ital. Med. Lav. 2(1) 27-31 (1980) CA 93 198587h... 

Cardiovascular Effects. Chronic cardiovascular disease has not been reported in workers occupationally exposed to low levels of trichloroethylene (El Ghawabi et al. 1973), although deaths following acute high-level inhalation exposures to trichloroethylene have been attributed to cardiac arrhythmias. Case studies have described cardiac arrhythmias that in some instances led to death after occupational exposure (Bell 1951 Kleinfeld and Tabershaw 1954 Smith 1966), poisoning (Dhuner et al. 1957 Gutch et al. 1965), or... 

This section will describe clinical practice and research concerning methods for reducing toxic effects of exposure to trichloroethylene. However, because some of the treatments discussed may be experimental and unproven, this section should not be used as a guide for treatment of exposures to trichloroethylene. When specific exposures have occurred, poison control centers and medical toxicologists should be consulted for medical advice. The following texts provide specific information about treatment following exposures to trichloroethylene Bronstein and Currance 1988 Ellenhom and Barceloux 1988 Stutz and Janusz 1988. 

Kostrzewski P, Jakubowski M, Kolacinski Z. 1993. Kinetics of trichloroethylene elimination from venous blood after acute inhalation poisoning. Clin Toxicol 31 353-363. 

Ernst, A., and J.D.Zibrak. 1998. Carbon monoxide poisoning. N. Engl. J. Med. 339(22) 1603-1608. Ettema, J.H., R.L.Zielhuis, E.Burer, H.A.Meier, L.Kleerekoper, and M.A.de Graaf. 1975. Effects of alcohol, carbon monoxide and trichloroethylene exposure on mental capacity. Int. Arch. Occup. Environ. Health 35(2) 117—132. 

SAFETY PROFILE Confirmed carcinogen with experimental carcinogenic, neoplastigenic, and tumorigenic data. A deadly poison by intravenous route. Human systemic effects by inhalation lung fibrosis, dyspnea, and weight loss. Human mutation data reported. See also BERYLLIUM COMPOUNDS. A moderate fire hazard in the form of dust or powder, or when exposed to flame or by spontaneous chemical reaction. Slight explosion hazard in the form of powder or dust. Incompatible with halocarbons. Reacts incandescently with fluorine or chlorine. Mixtures of the powder with CCU or trichloroethylene will flash or spark on impact. When heated to decomposition in air it emits very toxic fumes of BeO. Reacts with Li and P. 

CONSENSUS REPORTS lARC Cancer Review Group 3 IMEMDT 7,56,87 Animal Limited Evidence IMEMDT 39,369,86. OSHA PEL CL 0.1 ppm ACGIHTLV CL 0.1 ppm DFG MAK Animal Carcinogen, Suspected Human Carcinogen DOT CLASSIFICATION Forbidden SAFETY PROFILE Confirmed carcinogen with experimental carcinogenic data. Poison by inhalation. Central nervous system effects. Can be formed by thermal decomposition (>70°) from trichloroethylene. Symptoms include a disabling nausea and intense jaw pain. 

Tetrachloroethylene and trichloroethylene are used for the cleaning of metals finely purified and for dry cleaning of clothes as the cleaning solvents. As they are very poisonous we have to take care not to pollute the environment with these compounds. When we accidentally litter the environment with these compounds, the cleaning methods which remove them effectively using bacteria may be helpful. 

Stress should again be laid on the importance of a thorough cleaning of the packing material before it is put into the column. It is not sufficient to rinse it a few times, say with carbon tetrachloride or trichloroethylene. The adhering layer can be removed by a treatment with hot benzene (poisonous use fume cupboard) followed by a rinse with trichloroethylene [14]. 

The symptoms of poisoning from oral intake of trichloroethylene are nausea, vomiting, diarrhea, and gastric disturbances. The acute oral toxicity, however, is low. The oral LD50 value in mice is in the range 2500 mg/kg. Trichloroethylene metabolizes to trichloroacetic acid, which is excreted in the urine. 

Between 1914 and 1918, solvent and general chemical production had been geared to the needs of war. At war s end, the chemical surpluses included, in addition to phenol and cellulose acetate, the acetone and butanol from the Weizmann fermentation process and chlorine from poison gas production. The latter, made by electrolysis of sodium chloride solution, became the basis of the British chlorinated solvents industry. Here the outstanding firm was Albright Wilson, which began manufacture of carbon tetrachloride in 1925. Cleaning and degreasing processes led to production of trichloroethylene, for which demand increased dramatically between 1928 and 1936. The principal manufacturer was Weston Co., later taken over by ICl. 

Carbon tetrachloride, trichloroethylene, and polyvinyl chloride (PVC) are well known hepatotoxins. Nephrotoxins are the chemicals that affect the kidneys. Since a large amount of blood circulates through the kidneys, they are susceptible to chemical attack if the blood contains a toxin. Heavy metals, chlorinated and fluorinated hydrocarbons, carbon disulfide, and ethylene glycol are some examples of kidney poisons. Many of these toxins can enter the body through inhalation or absorption. Toxins can be detected through medical surveillance, which monitors metabolites in the urine. Metabolites are the products formed by the toxin after it undergoes changes due to metabolism. 

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