1,1,2,2-tetrachloroethane (TeCA), also known by the brand names Bonoform, Cellon and Westron, is an organic compound. It is colorless liquid and has a sweet odor. It is used as an industrial solvent and as a separation agent. TeCA is toxic and it can be inhaled, consumed or absorbed through the skin. After exposure, nausea, dizziness or even liver damage may occur.
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Chemical compound
History.
1,1,2,2-Tetrachloroethane and 1,1,1,2-Tetrachloroethane were discovered by Auguste Laurent in 1836.
1,1,2,2-tetrachloroethane was used in large amounts to produce other chemicals like trichloroethylene, tetrachloroethylene, and 1,2-dichloroethylene.
Because 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. It is however still generated as a byproduct and as an intermediate product during manufacturing, where low levels of the chemical have been detected in the air.
Uses.
1,1,2,2-Tetrachloroethane has been used as an industrial solvent since the 1910s when it was widely used in cellulose acetate "dope" formulations, under the name "Cellon". Its use in dope formulations decreased towards the 1920s as its toxicity became more known.
Other uses for the substance include paint stripping, acting as a denaturation agent for alcohol, as a solvent for waxes &amp; varnishes, and in the extraction of oils and degreasing of metals.
1,1,2,2-Tetrachloroethane is currently used as a feedstock in the production of 1,2-dichloroethylene,trichloroethylene and tetrachloroethylene.
Synthesis.
There are a few different ways to synthesise 1,1,2,2-tetrachloroethane. 1,1,2,2-tetrachloroethane can be produced by the catalytic addition of chlorine to acetylene (ethyne) which yields the highest purity. 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 is always produced in closed systems to obtain the highest yield. 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).
Toxicity.
Alcohol increases the metabolism of 1,1,2,2-tetrachloroethane (TeCA) and it will intensify the effects of TeCA. Humans who consume alcohol might be at an increased risk for all toxic effects from TeCA. This is also a case for several other chlorinated aliphatic hydrocarbons. An investigation showed when you combine alcohol with TeCA it increases the relative weight of the experimented rats, indicating an enlarged activity of TeCA.
Metabolism.
The metabolism is believed to involve cytochrome (CYP) P450. Experiments showed that biotransformation reactions increased with chronic ethanol consumption and fasting.
Mechanism of action.
1,1,2,2,-Tetrachloroethane (TeCA) can be rapidly and extensively absorbed from oral and inhalation exposure. In animal studies the oral take up was reported as 70-100% and 40-97% oral uptake in human inhalation. TeCA is a small, volatile, lipophilic molecule; TeCA can be readily absorbed from respiratory and gastrointestinal tracts. Absorption with passive diffusion is the most likely mechanism.
After TeCA is absorbed in the body, it is readily distributed throughout the body via passive diffusion. TeCA will most likely accumulate in lipid-rich tissues, such as the 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. In rats, microsomal and nuclear cytochrome P450 enzymes are implicated in the metabolism with TeCA, releasing biologically active compounds as; aldehydes, alkenes, acids and free radicals. Formation of active metabolites is likely the mechanism for the toxicity.
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 in TeCA's carcinogenic effect 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.
Health effects.
1,1,2,2-tetrachloroethane (TeCA) has a vast array of effects spread throughout the whole body. Effects have been investigated on different systems on both humans and animals, stated respectively.
Gastrointestinal Effects.
4 studies on humans after TeCA exposure determined gastrointestinal distress in the participants. Two humans exposed to 2.9 ppm TeCA for 30 minutes showed symptoms of vomiting and nausea. These symptoms also caused weight loss.
A study by Horiuchi et al. showed that a monkey frequently exposed to 1.9 ppm TeCA got anorexic and developed regular diarrhea.
Hematological Effects.
Workers in an artificial silk factory that had regularly inhaled TeCA, showed elevated white blood cell levels and slight anemia.
In 1962, a study showed that ;templatestyles src="Fraction/styles.css" / ;2⁄3 of the investigated rats exposed to 9000 ppm TeCA for 29 days had decreased red blood cells and hemoglobin levels.
Hepatic Effects.
Autopsies on humans who died due to TeCA exposure showed that some humans developed hepatic failure from the TeCA, they showed jaundice and an enlarged liver. The liver is the most affected system with TeCA poisoning, causing for example apoptosis of the liver tissue.
After 60 ppm exposure rats show fatty liver degeneration. Another study determined the limit for acute hepatic failure to be at 102ppm for four hours, indicated by increases in hepatic ascorbic acid and serum glutamate dehydrogenase and decreases in serum triglycerides.
Ocular Effects.
The vapors of TeCA can cause eye irritation, stinging, squinting and lacrimation in both humans and animals. This is due to direct contact of the skin and vapor rather than inhalation or digestion.
Neurological effects.
Inhalation of TeCA vapor can cause dizziness, headache and tremors.
Acute symptoms in rats showed in the form of 50% motor loss when exposed to 360ppm for one hour.
Carcinogenic Effects.
The National Cancer Institute performed experiments on the tumorigenicity of TeCA in rats and mice via the oral exposure route. Liver tumors were found in both species. Other studies on the tumorigenic mode of action revealed that it acts both as initiator and promoter.
Lethal dose.
Due to several case study reports on individuals who died after ingesting TeCA, the approximate lethal dose was possible to be established. Since the amount consumed varied this was difficult to exactly determine. One report was shown to be 4100 mg/kg, the second 357 mg/kg and the third 1100–9600 mg/kg. Death following the ingestion occurred within 3–20 hours.