Intoxication with chlorinated hydrocarbons and benzene

Benzene

 * high danger → only used to a limited extent (production of benzene derivatives, pharmaceutical industry)
 * the work is under strict hygiene measures
 * source: oil, coke plants (during coke production)
 * lethal dose: 10–15&thinsp;ml p.o.
 * metabolism – it is oxidized to benzepoxide (carcinogen), reacts with DNA, approx. 15&thinsp;% is excreted unchanged through the lungs ; in urine – phenol ((it is there even without exposure as a breakdown product of AMK), phenyl mercapturic acid, urine is collected at the end of the shift

Clinical picture of intoxication

 * 1) acute intoxication – neurotoxic manifestations in the foreground
 * 2) long-term exposure – hematotoxic – effects dominate leukopenia, trombocytopenia, anemia, pancytopenia, there is an increased level of chromosomal aberrations in peripheral lymphocytes
 * 3) *after 10–20 years AML or CML may develop

Tetrachloromethane and chloroform

 * 50&thinsp;% is metabolized by the liver,  50&thinsp;% is exhaled unchanged
 * we have little data on metabolites

Central Nervous

 * excitation, disorientation, dizziness, drunkenness, nausea, drowsiness and even unconsciousness

Hepatotoxicity

 * dominates in oral poisoning, steatosis and necrosis occur, mainly in carbon tetrachloride
 * steatosis is caused by damage to the endoplasmic reticulum, which leads to disruption of lipid transport
 * necrosis is conditioned by the release of lysosomal enzymes by the action of free radicals
 * Thanks to cytochrome P450, CCl4 breaks down into Cl− and trichloromethyl radical, then HCl a  phosgene are formed – this damages
 * therefore, alcoholics are more susceptible (they have more active cytochrome P450)
 * with chloroform, damage used to be observed only at high concentrations

Nephrotoxicity

 * CCl4 damages tubule cells, glomeruli are not damaged

Related Articles

 * Organic solvents