The most common health effect was found to be on the liver following 1,1,2,2-tetrachloroethane (TeCA) exposure. It suggests that TeCA may have promoting and initiating activity. 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. Mode of action of the carcinogenic effect of TeCA is not completely determined. but there are no studies of TeCA’s mechanism of neuronal effects. 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. Mechanism for neurological effects is not yet determined and therefore can not be described, TeCA might play a role. Thus, metabolic capacity for tissues high, liver, formation of active metabolites is a likely mechanism for the toxicity. Experiments of Hanley, Milman and Mitoma obtained evidence of this metabolism in rats.
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Microsomal and nuclear cytochrome P450 enzymes are implicated in the metabolism with TeCA, releasing biologically active compounds as aldehydes, alkenes, acids and free radicals. TeCA metabolism to reactive products plays a key role in the toxicity of TeCA. Īlready mentioned before passive diffusion is an important mechanism, because it is most likely the major mechanism of excretion. Urinary elimination occurs as metabolites, including formic acid, glyoxalic acid, trichloroacetic acid and trichloroethanol. TeCA will most likely accumulate in lipid-rich tissues, liver. Absorption with passive diffusion is the most likely mechanism.Īfter TeCA is absorbed in the body, it is readily distributed throughout the body via passive diffusion.
TeCA is a small, volatile, lipophilic molecule it appears that TeCA readily be absorbed from respiratory and gastrointestinal tracts. In animal studies the oral take up was reported bij 70-100% and 40-97% oral uptake in human inhalation.
Looking at the chemical and physical properties the 1,1,2,2,-tetrachloroethane (TeCA) might be rapidly and extensively absorbed, which results in oral and inhalation exposures. Proposed metabolism of 1,1,2,2-Tetrachloroethane Toxicity Mechanism of action Common side products that are created during the synthesis of 1,1,2,2-tetrachloroethane are 1,2-dichloroethane and trichloroethylene (in the presence of heat). 1,1,2,2-Tetrachloroethane is always produced in closed systems to obtain the highest yield. It is also produced by direct chlorination or oxychlorination utilizing ethylene as feedstock and by catalytic chlorination of ethane or chlorination of 1,2- dichloroethane. 1,1,2,2-tetrachloroethane can be produced by the catalytic addition of chlorine to acetylene (ethyn) which yields the highest purity. There are a few different ways to synthesise 1,1,2,2-tetrachloroethane. It is however still generated as a by-product and as a intermediate product during manufacturing, where low levels of this toxigenic where detected in the air Synthesis It also found its function as a industrial solvent and was used in paint removers and pesticides.īecause of its possible carcinogen effects on humans, the production of 1,1,2,2-tetrachloroethane has decreased significantly and is no longer widely used as an end-product. 1,1,2,2-tetrachloroethane was used in large amounts to produce other chemicals like trichloroethylene, tetrachloroethylene, and 1,2,-dichloroethylene.
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