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Carbon disulfide is a volatile organic solvent that is used industrially as a starting material in rayon manufacture in the viscose process. It was important historically in the cold vulcanization of rubber. Although no longer used in this form, carbon disulfide is still a major 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 (See Disulfiram) and a spontaneous breakdown by-product of the pesticide metam sodium.

  1. Mechanism of toxicity. 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 is widely reactive with a variety of biologic substrates.

  2. Toxic dose

    1. Carbon disulfide is highly volatile (vapor pressure, 297 mm Hg), and inhalation is a major route of exposure. The OSHA workplace limit (permissible exposure limit—ceiling [PEL-C]) for carbon disulfide is 30 ppm (the PEL is 20 ppm with an allowable 15-minute peak to 100 ppm). The ACGIH recommended workplace exposure limit (threshold limit value–8-hour time-weighted average [TLV-TWA]) is considerably lower at 1 ppm. The NIOSH recommended exposure limit (REL) is also 1 ppm, and the short-term exposure limit (STEL) is 10 ppm. Carbon disulfide is also well absorbed through the skin.

    2. Acute carbon disulfide overexposure via ingestion is unusual, but if ingested, it probably will be very 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.

  3. Clinical presentation

    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 lower-level exposure can cause parkinsonism and other poorly reversible CNS impairments, optic neuritis, peripheral neuropathy, and atherosclerosis. Epidemiologic studies indicate that carbon disulfide exposure is associated with adverse reproductive function and outcomes.

  4. Diagnosis 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 is not performed routinely.

    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.

  5. Treatment

    1. Emergency and supportive measures. Severe acute exposure would present as nonspecific CNS depression.

      1. Maintain an open airway and assist ventilation if necessary (See Airway and Breathing). 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 ...

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