Carbon disulfide is a volatile organic solvent used industrially as a starting material in rayon and cellophane manufacture in the viscose process. It was important historically as a pesticide fumigant and in the cold vulcanization of rubber. Although no longer used as a vulcanizing agent, carbon disulfide remains an industrial precursor in rubber industry chemical synthesis and has a number of other industrial applications. Carbon disulfide also is widely used as a solvent in a variety of laboratory settings. It is a metabolite of the drug disulfiram and a spontaneous breakdown by-product of the pesticides metam sodium and sodium tetrathiocarbamate.

Carbon disulfide toxicity appears to involve disruption of a number of metabolic pathways in various organ systems, including but not limited to the CNS. Although key toxic effects have been attributed to the functional disruption of enzymes, especially in dopamine-dependent systems, carbon disulfide reacts with a variety of biologic substrates.

1. Carbon disulfide is highly volatile (vapor pressure, 297 mm Hg), and inhalation is a major route of exposure. Carbon disulfide is also well absorbed through the skin. The Federal OSHA workplace limit (permissible exposure limit—ceiling [PEL-C]) for carbon disulfide is 30 ppm (the PEL is 20 ppm), but it also allows for exposure as high as 100 ppm for up to 15 minutes. The CAL OSHA PEL of 1 ppm is considerably lower, with a short term exposure limit (STEL) of 12 ppm. The ACGIH threshold limit value-8-hour time-weighted average (TLV-TWA) and the NIOSH recommended exposure limit (REL) for 10 hours are also 1 ppm, with a NIOSH STEL of 10 ppm. Various international standards are also in this range, far lower than Federal OSHA limits.
2. Acute carbon disulfide overexposure via ingestion is unusual, but if ingested, it is well absorbed. Chronic ingestion of therapeutic doses of disulfiram (200 mg/d) has been suspected to cause carbon disulfide-mediated toxicity, but this has not been firmly established.

1. Acute carbon disulfide exposure can cause eye and skin irritation and CNS depression.
2. Short-term (days to weeks) high-level exposure to carbon disulfide is associated with psychiatric manifestations ranging from mood change to frank delirium and psychosis.
3. Chronic exposure can cause parkinsonism and other poorly reversible CNS impairments, optic neuritis, peripheral neuropathy, and CNS and cardiac atherosclerosis. Epidemiologic studies indicate that carbon disulfide exposure also is associated with adverse reproductive function and outcomes.

Of carbon disulfide toxicity is based on a history of exposure along with consistent signs and symptoms of one of its toxic manifestations. Industrial hygiene data documenting airborne exposure, if available, are useful diagnostically and in initiating protective measures.

1. Specific levels. Biological monitoring for carbon disulfide can be performed using urinary 2-thiothiazolidine-4-carboxylic acid (TTCA) but this is not performed routinely in the United States.
2. Other useful laboratory studies can include nerve conduction studies if neuropathy is suspected and brain magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) to assess the CNS. Chronic carbon disulfide exposure is associated with altered lipid profiles.

1. Emergency and supportive measures. Severe acute exposure would present as nonspecific CNS depression.
   1. Maintain an open airway and assist ventilation if necessary. Administer supplemental oxygen.
   2. Start an IV line and monitor the patient's vital signs and ECG closely.
2. Specific drugs and antidotes. There are no specific antidotes for carbon disulfide.
3. Decontamination after high-level exposure
   1. Inhalation. Remove the victim from exposure and give supplemental oxygen if available.
   2. Skin and eyes. Remove contaminated clothing and wash exposed skin. Irrigate exposed eyes with copious amounts of tepid water or saline.
   3. Ingestion. Administer activated charcoal if it is available and the patient is alert. Consider gastric lavage if the ingestion occurred within 60 minutes of presentation.
4. Enhanced elimination. There is no role for these procedures.