belongs to the class of inorganic compounds known as other non-metal sulfides. These are inorganic compounds containing a sulfur atom of an oxidation state of -2, in which the heaviest atom bonded to the oxygen belongs to the class of other non-metals.
Carbon disulfide is a potent nerve toxin and also affect liver enzymes, particularly those related to lipid metabolism. The increases in serum cholesterol that are sometimes seen following carbon disulfide exposure may be a result of increased hepatic cholesterol synthesis. The primary target of carbon disulfide appears to be the nervous system. Neurophysiological and behavioral effects as well as pathomorphology of peripheral nervous system structures have been reported in humans. Moreover, carbon disulfide metabolites of the thiocarbamate type inhibit aldehyde anhydrase. (8, 7)
Metabolism
Nitrogenase reduces carbon disulfide and can also be inhibited by this toxin. Carbon disulfide binds (in the form of AL CS2) mainly to hemoglobin and to a small extent to other blood proteins, such as albumin and gamma-globulin. Carbon disulfide is bioactivated by cytochrome P-450 to an unstable oxygen intermediate. The intermediate may either spontaneously degrade to atomic sulfur and carbonyl sulfide or hydrolyze to form atomic sulfur and monothiocarbonate. The atomic sulfur generated in these reactions may either covalently bind to macromolecules or be oxidized to products such as sulfate. The carbonyl sulfide formed may be converted to monothiocarbonate by carbonic anhydrase. Monothiocarbonate may further spontaneously degrade, regenerating carbonyl sulfide or forming carbon dioxide and sulfide bisulfide ion (HS-). The HS- formed can subsequently be oxidized to sulfate or other nonvolatile metabolites. Dithiocarbamates are the products of the reaction of carbon disulfide with amino acids. Most of the carbon disulfude absorbed is metabolized. Small traces of unchanged can be found in the urine. Carbon disulfide or carbonyl sulfide can conjugate with endogenous glutathione to yield thiazolidine-2-thione-4-carboxylic acid and 2-oxythiazolidine-4-carboxylic acid, respectively. Carbonic anhydrase 2 mediates the metabolism of carbon disulfide. (8, 2, 3, 4, 5, 6)
No indication of carcinogenicity to humans (not listed by IARC).
Uses/Sources
Several industries use carbon disulfide as a raw material to make such things as rayon, cellophane, and carbon tetrachloride. Exposure to carbon disulfide can results from breathing air, drinking water, or eating foods that contain it. One can also be exposed by skin contact with soil, water, or other substances that contain it. (8)
Following inhalation, subtle and transient changes in pulmonary function can be manifested as reduced vital capacity and decreased partial pressure of arterial oxygen. Patients can developed normochromic and normocytic anemia, eosinopenia, and an increase in reticulocyte cell numbers after oral exposure . Carbon disulfide poisoning can result in central nervous system depression, coma, respiratory paralysis, and death. It also may accelerate coronary artery disease. Peripheral neuropathies, cranial nerve dysfunction, and neuropsychiatric changes are present in over 70% of chronic carbon sulfide victims. (8)
Symptoms
Dizziness, headache, nausea, shortness of breath, vomiting, weakness, irritability and hallucination can result from inhalation, ingestion or skin exposure to carbon disultfide. Skin and eye exposure can lead to pain, redness. Moreover, dermal exposure can lead to dryness of the skin; the carbon disulfide may be absorbed. Weak pulse, palpitations, fatigue, weakness in the legs, unsteady gait, vertigo, hyperesthesia, agitation, mania, hallucinations of sight, hearing, taste, and smell in acute are other symtoms of carbon disulfide poisoning. (9, 10)
Treatment
Following oral exposure, administer charcoal as a slurry (240 mL water/30 g charcoal). Consider gastric lavage after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Intravenous urea (0.5 to 1.5 g/kg) has been recommended to inactivate free carbon disulfide in the blood. The efficacy of this treatment is unknown. Following inhalation exposure, move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. If the exposure occurred through eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If the exposure occurred through dermal contact, remove contaminated clothing and wash exposed area thoroughly with soap and water. (11)
