the body via passive diffusion. TeCA will most likely accumulate in lipid-rich tissues, liver. Urinary elimination occurs as metabolites, including formic acid, glyoxalic acid, trichloroacetic acid and trichloroethanol. Already mentioned before passive diffusion is an important mechanism, because it is most likely the major mechanism of excretion. TeCA metabolism to reactive products plays a key role in the toxicity of TeCA. Microsomal and nuclear cytochrome P450 enzymes are implicated in the metabolism with TeCA, releasing biologically active compounds as; aldehydes, alkenes, acids and free radicals. Experiments of Hanley, Milman and Mitoma obtained evidence of this metabolism in rats. Thus, metabolic capacity for tissues high, liver, formation of active metabolites is a likely mechanism for the toxicity. [PDF] Mechanism for neurological effects is not yet determined and therefore can not be described, TeCA might play a role. The property of the readily passive diffusion to lipid-rich tissues allows it to interfere with neural membrane function, central nervous system depression, behavioral changes and anesthesia. but there are no studies of TeCA's mechanism of neuronal effects. Mode of action of the carcinogenic effect of TeCA is not completely determined. Several studies of TeCA have reported increases in the number of hepatocytes in mitosis, but the role these effects might have of TeCA on carcinogenicity is not evaluated. It suggests that TeCA may have promoting and initiating activity. Toxicokinetics The most common health effect was found to be on the liver following 1,1,2,2-tetrachloroethane (TeCA) exposure. The studies for this have been divided into the four different Toxicokinetic phases: Adsorption, Distribution, Metabolism and Excretion (ADME). Three exposure routes have been studied to examine the effects depending on the entry route of TeCA into the body. Oral exposure: The experiment for the oral exposure was done by administering oral doses of radioactively labeled TeCA by gavage in corn oil to rats and mice. Followed by measuring the radioactivity in the expired air and urine. a) Adsorption: With a measured radioactivity of 65%-73% the conclusion made was that the compound is almost completely absorbed orally. b) Distribution: Hepatic protein binding was observed by purifying the liver protein. Furthermore adverse effects were seen in liver, kidney and testes leading to the conclusion that TeCA is distributed to these tissues. c) Metabolism: see experiments on Metabolism routes d) Excretion: After 72h more than 90% of the dose was excreted in metabolized or unchanged form. The largest part was excreted