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CARBON DISULFIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Carbon disulfide is an industrial solvent and, in its gaseous form, is an insecticide.

Specific Substances

    1) Carbon disulfide
    2) Carbon bisulfide
    3) Carbonei sulfidum
    4) Carboneum sulfuratum
    5) Dithiocarbonic anhydride
    6) Schwefelkohlenstoff
    7) CAS 75-15-0
    8) CABONEUM SULFURATUM
    9) CARBINIO (SOLFURO DI) (ITALIAN)
    1.2.1) MOLECULAR FORMULA
    1) C-S2

Available Forms Sources

    A) FORMS
    1) Carbon disulfide is found in technical and reagent grades and is a clear, colorless or faintly yellow liquid (HSDB, 2004)
    a) Modern plants can manufacture the chemical to about 99.99% purity (HSDB, 2004).
    B) SOURCES
    1) Carbon disulfide is a metabolite of disulfiram and other dithiocarbamate compounds (Baselt, 2000).
    a) Carbon disulfide occurs naturally from coal tar, crude petroleum, the ocean, microbial reductions of sulfates in the soil, emissions from volcanoes and marshlands, inland soil, some plants, and tree roots (Budavari, 2000).
    b) It can also be manufactured by the following methods:
    1) Preheating natural gas and mixing it with vaporized sulfur and passing it over a catalyst (Ashford, 1994a; HSDB, 2004).
    2) Metallurgical coke and sulfur; coproduced with hydrogen sulfide (Ashford, 1994a).
    3) Natural gas and hydrogen sulfide is mixed at a high temperature (using the plasma process) (Lewis, 1997a).
    4) Heating sulfur and charcoal and condensing the carbon disulfide vapors (Lewis, 1997a).
    5) Hydrogen sulfide and carbon at 900 degrees C produces carbon disulfide at approximately 70% purity (HSDB, 2004).
    6) Methane and sulfur dioxide mixed at 850 degrees C in the presence of a catalyst, yields a product at approximately 84% purity (HSDB, 2004).
    C) USES
    1) Carbon disulfide is utilized as a solvent for bromine, fats, iodine, phosphorus, resins, rubbers, selenium, sulfur, and waxes. It is also used in the production of cellophane, carbon tetrachloride, electronic vacuum tubes, soil disinfectants, xanthogenates, a chemical intermediate for adhesives used in food packaging, flotation agents, viscose rayon, and optical glass. Additionally, it has been employed as an insecticide, a parasiticide, a fumigant for grain, a polymerization inhibitor (for vinyl chloride), a corrosion inhibitor, and in the destructive distillation of coal (Bingham et al, 2001; Budavari, 2000; HSDB, 2004; Lewis, 1998; Sittig, 1991a).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Carbon disulfide is a volatile organic solvent used most commonly in the rubber industry, but used in a variety of laboratory settings. It is also a metabolite of disulfiram and other dithiocarbamates.
    B) TOXICOLOGY: Acute topical exposure can cause topical irritation to skin and mucosa and, in severe cases, full thickness burns. It can also cause a defatting injury. Short term inhalation exposures can present with headache, nausea, vomiting, and dizziness. It can initially cause central nervous system excitement followed by CNS depression. Chronic exposure can lead to parkinsonian effects, ototoxicity, visual impairment and optic neuritis, peripheral neuropathy, and hepatotoxicity. It has also been associated with male infertility.
    C) EPIDEMIOLOGY: Exposure to carbon disulfide is common in certain industries. Toxicity is most common after inhalation, but can occur with topical exposure or ingestion. However, with proper personal protective equipment (PPE) regulations, severe toxicity is uncommon/rare, but deaths have been reported.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild toxicity from topical exposures consists of skin, eye, and mucosal irritation. Patients can develop dizziness, headache, fatigue, nervousness, restlessness, and nausea and vomiting after inhalation.
    2) SEVERE TOXICITY: CNS excitation (seizures) and depression (coma) can occur. Agitation, delirium, hallucinations, tremor, muscle spasticity, and psychosis can also develop. Cardiopulmonary effects can include dyspnea, dysrhythmias, respiratory failure, and cardiovascular collapse. Long-term severe toxicity may result in a parkinsonian-like syndrome (speech disturbances, spasticity, tremor), neuropathy, fatigue, and irritability. Severe topical exposures can result in vesicular formation, and possibly partial and full thickness burns. Ingestion of small amounts can cause respiratory failure, mydriasis, tremors, seizures, coma, and death.
    3) CHRONIC: Chronic exposures can produce permanent central and peripheral nervous system damage. Other consequences include atherosclerotic tendencies, ECG abnormalities, gastrointestinal disturbances, fatty degeneration of the liver (with jaundice), renal damage, fatigue, memory loss, insomnia, melancholia, mania, hallucinations, increased suicide rate, sexual dysfunction, cranial nerve damage, hearing loss, visual disturbances, altered pupillary reaction to light, retinal microaneurysms, optical, otic, and peripheral neuropathies, loss of reflexes, tremors, and blood dyscrasias.
    0.2.3) VITAL SIGNS
    A) Respiratory failure may occur after exposure to high concentrations.
    0.2.4) HEENT
    A) Chronic systemic exposure may result in degenerative changes of the retina and optic nerve. Nystagmus, diplopia, xanthopsia and minimal visual field constriction have been observed. Ocular exposure may cause irritation.
    0.2.5) CARDIOVASCULAR
    A) Chest pain and angina have been significantly related to carbon disulfide exposure. Atherosclerosis and ischemic heart disease have been associated with long term exposure.
    0.2.6) RESPIRATORY
    A) Coughing and dyspnea are common. Respiratory failure may occur following exposure to high concentrations.
    0.2.7) NEUROLOGIC
    A) In acute exposure, headache, dizziness, nervousness, tremor, seizures, and coma may be noted. Chronic exposure may lead to encephalopathy, psychosis, and polyneuritis.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting may occur after acute exposure. Chronic exposure is associated with gastritis and dyspepsia.
    0.2.9) HEPATIC
    A) Fatty degeneration as well as other pathological changes have been noted.
    0.2.14) DERMATOLOGIC
    A) Carbon disulfide is a strong skin irritant and dermal exposure may result in severe burns.
    0.2.18) PSYCHIATRIC
    A) Carbon disulfide may cause psychosis. Extreme irritability, uncontrolled anger, mania, memory deficits, suicidal tendencies, severe insomnia and loss of libido are possible symptoms.
    0.2.20) REPRODUCTIVE
    A) Acute and prolonged exposure may produce adverse effects in males and females. Reported female adverse effects include menstrual abnormalities, spontaneous abortions and premature births. In males, changes in spermatogenesis and libido were reported.
    B) Teratogenic effects reported in humans include heart defects, CNS effects, and inguinal hernia. Teratogenic effects reported in experimental animals include developmental abnormalities of the eye, ear, and craniofacial area, and changes in viability index and growth statistics.

Laboratory Monitoring

    A) Monitor vital signs, neurologic exam, and mental status.
    B) Obtain serum electrolytes, and monitor renal function and liver enzymes in symptomatic patients.
    C) Monitor pulse oximetry and obtain a chest radiograph in any patient with respiratory symptoms.
    D) Carbon disulfide blood concentration and urinary metabolites can be measured, but will require reference laboratories and is not helpful in an acute exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Dermal irritation should be treated with irrigation and supportive measures for dermatitis. Headaches can be treated with fresh air and analgesics.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Management is similar as with any CNS depressant. Ensure airway is protected. If altered mental status and/or inability to protect airway, intubate and mechanically ventilate. Support volume status with intravenous fluids if cardiovascular collapse occurs. Use benzodiazepines for seizures.
    C) DECONTAMINATION
    1) PREHOSPITAL: Wash topical exposures with water. Pre-hospital gastrointestinal decontamination is not recommended due to the potential for decreased mental status or seizures and subsequent aspiration.
    2) HOSPITAL: With large ingestions, administer activated charcoal if patient is alert and can protect airway or is intubated.
    D) AIRWAY MANAGEMENT
    1) Endotracheal intubation and mechanical ventilation may be needed if CNS depression, seizures, or respiratory distress develop.
    E) ANTIDOTE
    1) None
    F) ENHANCED ELIMINATION
    1) There is no role for hemodialysis or other methods of enhanced elimination.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Asymptomatic patients with minor dermal or inhalation exposures can be monitored at home.
    2) OBSERVATION CRITERIA: Any symptomatic patient, those with deliberate exposure, and any patient who ingests carbon disulfide should be sent to a healthcare facility for evaluation and treatment.
    3) ADMISSION CRITERIA: Patients with large exposures, persistent or severe symptoms should be admitted for further care.
    4) CONSULT CRITERIA: Consult a medical toxicologist or poison center in large and/or symptomatic exposures.
    H) PITFALLS
    1) Lack of decontamination, not recognizing as a potential exposure in someone who works with carbon disulfide, and not monitoring exposure in work place environment.
    I) TOXICOKINETICS
    1) Carbon disulfide is highly volatile, so it is primarily rapidly absorbed via inhalation. Rapid absorption is also expected with ingestion. Dermal absorption is also reported. The majority of carbon disulfide is metabolized; 5% to 30% is excreted unchanged by the lungs, and trace amounts (0.05%) by the kidney.
    J) DIFFERENTIAL DIAGNOSIS
    1) CNS depressants; other common solvents, such as hydrocarbons; other agents that can cause parkinsonism, such as carbon monoxide, MPTP.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: 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 an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: As little as 10 mL by mouth has caused toxicity and death. The lowest reported lethal oral dose is 14 mg/kg. The 8-hour TLV-TWA is 1 part per million (ppm). Five hundred ppm is considered immediately dangerous to life and health.

Clinical Effects

Summary Of Exposure

    A) USES: Carbon disulfide is a volatile organic solvent used most commonly in the rubber industry, but used in a variety of laboratory settings. It is also a metabolite of disulfiram and other dithiocarbamates.
    B) TOXICOLOGY: Acute topical exposure can cause topical irritation to skin and mucosa and, in severe cases, full thickness burns. It can also cause a defatting injury. Short term inhalation exposures can present with headache, nausea, vomiting, and dizziness. It can initially cause central nervous system excitement followed by CNS depression. Chronic exposure can lead to parkinsonian effects, ototoxicity, visual impairment and optic neuritis, peripheral neuropathy, and hepatotoxicity. It has also been associated with male infertility.
    C) EPIDEMIOLOGY: Exposure to carbon disulfide is common in certain industries. Toxicity is most common after inhalation, but can occur with topical exposure or ingestion. However, with proper personal protective equipment (PPE) regulations, severe toxicity is uncommon/rare, but deaths have been reported.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Mild toxicity from topical exposures consists of skin, eye, and mucosal irritation. Patients can develop dizziness, headache, fatigue, nervousness, restlessness, and nausea and vomiting after inhalation.
    2) SEVERE TOXICITY: CNS excitation (seizures) and depression (coma) can occur. Agitation, delirium, hallucinations, tremor, muscle spasticity, and psychosis can also develop. Cardiopulmonary effects can include dyspnea, dysrhythmias, respiratory failure, and cardiovascular collapse. Long-term severe toxicity may result in a parkinsonian-like syndrome (speech disturbances, spasticity, tremor), neuropathy, fatigue, and irritability. Severe topical exposures can result in vesicular formation, and possibly partial and full thickness burns. Ingestion of small amounts can cause respiratory failure, mydriasis, tremors, seizures, coma, and death.
    3) CHRONIC: Chronic exposures can produce permanent central and peripheral nervous system damage. Other consequences include atherosclerotic tendencies, ECG abnormalities, gastrointestinal disturbances, fatty degeneration of the liver (with jaundice), renal damage, fatigue, memory loss, insomnia, melancholia, mania, hallucinations, increased suicide rate, sexual dysfunction, cranial nerve damage, hearing loss, visual disturbances, altered pupillary reaction to light, retinal microaneurysms, optical, otic, and peripheral neuropathies, loss of reflexes, tremors, and blood dyscrasias.

Vital Signs

    3.3.1) SUMMARY
    A) Respiratory failure may occur after exposure to high concentrations.
    3.3.2) RESPIRATIONS
    A) Respiratory failure may occur after exposure to high concentrations (Gosselin et al, 1984).
    3.3.4) BLOOD PRESSURE
    A) A direct, linear relationship has been shown between diastolic blood pressure and the level of chronic exposure to carbon disulfide. Alternatively, carbon disulfide exposure did not correlate with systolic blood pressure (Harbison, 1998).

Heent

    3.4.1) SUMMARY
    A) Chronic systemic exposure may result in degenerative changes of the retina and optic nerve. Nystagmus, diplopia, xanthopsia and minimal visual field constriction have been observed. Ocular exposure may cause irritation.
    3.4.3) EYES
    A) IRRITATION
    1) Exposure to vapors causes eye irritation (Sittig, 1985).
    2) Splashes of liquid carbon disulfide in the eye cause immediate and severe irritation (Hathaway et al, 1996).
    B) NYSTAGMUS and diplopia have been observed (Grant, 1993; Hathaway et al, 1996).
    C) RETINA: Chronic exposure may lead to retinal microaneurysms (Gosselin et al, 1984; Hathaway et al, 1996) and discrete pigmentary changes in the posterior pole (Vale & Meredith, 1983).
    D) XANTHOPSIA: And minimal visual field constriction have been noted (Grant, 1993; Hathaway et al, 1996).
    E) OPTIC NERVE: Pallor of the temporal portion of the optic nerve heads and extensive atrophy of the optic nerve may occur. Blindness has rarely been seen (Grant, 1993).
    F) RETINOPATHY - Retinopathy has been reported after long-term occupational exposure (a viscose rayon manufacturing plant) to toxic levels of carbon disulfide (Klemmer & Harris, 2000).
    3.4.4) EARS
    A) Reported effects of exposure to carbon disulfide include hearing loss to high-frequency tones (Hathaway et al, 1996).

Cardiovascular

    3.5.1) SUMMARY
    A) Chest pain and angina have been significantly related to carbon disulfide exposure. Atherosclerosis and ischemic heart disease have been associated with long term exposure.
    3.5.2) CLINICAL EFFECTS
    A) CARDIOTOXICITY
    1) WITH POISONING/EXPOSURE
    a) Studies suggest that carbon disulfide has a reversible, direct, dose-related cardiotoxic and/or thrombotic effect (Sweetnam et al, 1987; Harbison, 1998; Hathaway et al, 1996).
    b) OCCUPATIONAL EXPOSURE
    1) There is considerable epidemiological evidence that workers exposed to carbon disulfide have higher rates of atherosclerotic cardiovascular disease (Lewis et al, 1999). Rayon and rubber industry workers are historically most exposed and seem to have a higher incidence of coronary artery disease (Campbell et al, 1985). In a retrospective cohort of the US rayon industry, atherosclerosis was associated with long-term exposure(Wilcosky & Tyroler, 1983).
    2) A prospective cohort study of 251 Japanese carbon disulfide-exposed rayon workers (140 formerly exposed) and 359 non-exposed workers found a statistical association between carbon disulfide exposure and an increase in subclinical ischemic findings. The mean carbon disulfide and 2-thiothiazolidine-4-carboxylic acid (TTCA) concentrations were 5.0 ppm and 1.6 mg/g/creatinine respectively. The authors concluded that the current exposure limit of 10 ppm in Japan would be high to prevent subclinical cardiovascular effects in this study (Takebayashi et al, 2004).
    3) Chest pain and angina were significantly related to carbon disulfide exposure in workers, controlling for age and smoking (Oliver & Weber, 1984; Harbison, 1998).
    4) A study of 2291 carbon disulfide workers found elevated mortality from cardiovascular and ischemic heart disease in both males and females (Peplonska et al, 1996).
    5) An excess of deaths from arteriosclerotic heart disease has been reported among the men most heavily exposed men to carbon disulfide (MacMahon & Monson, 1988). A historical review of carbon disulfide exposure in the rayon industry suggested that the risk of cardiovascular effects is not increased with workplace exposures of less than 15-20 ppm (less than or equal to 8 hours/day times 5 days/week). The high levels of exposure reported in earlier studies existed in the 1940's through the 1960's and are no longer found in the workplace (Price et al, 1997).
    6) Twenty-two women exposed to carbon disulfide were compared to non-exposed workers and demonstrated adverse effects on lipid profiles and changes in coagulation factors suggestive of enhanced coagulability (Stanosz et al, 1998).
    B) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) A study, conducted 12 years after a carbon disulfide mass poisoning incident in a Korean viscose rayon factory, involved 198 workers from that exposure in order to evaluate ECG findings in those patients as compared to a reference group (n=198). Comparison of the ECG components in the two groups showed that the only significant difference was a shorter PQ interval in the case group as compared with the reference group (161.24 +/- 22.93 msec vs. 165.16 +/- 24.30 msec; p<0.05). However, the overall prevalence of ECG abnormalities was greater in the case group (40.4%) as compared with the reference group (33.8%). The clinical significance of these findings is unclear (Jhun et al, 2007).
    C) CARDIOVASCULAR FINDING
    1) WITH POISONING/EXPOSURE
    a) A direct, linear relationship has been shown between diastolic blood pressure and the level of exposure to carbon disulfide. Alternatively, carbon disulfide exposure did not correlate with systolic blood pressure (Harbison, 1998).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Carbon disulfide is the only industrial chemical reported to cause atherosclerosis in animals without supplemental cholesterol in diets (Clayton & Clayton, 1993).
    b) Atherosclerosis and arterial fatty deposits can be induced in the C57BL/6 mouse by inhalation of 500 to 800 ppm carbon disulfide for 20 weeks. The effect was subtle with a low fat diet, but strikingly enhanced by a high fat diet (Lewis et al, 1999).

Respiratory

    3.6.1) SUMMARY
    A) Coughing and dyspnea are common. Respiratory failure may occur following exposure to high concentrations.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) In a study of acute carbon disulfide exposure, there were some reports of shortness of breath (Harbison, 1998).
    B) APNEA
    1) WITH POISONING/EXPOSURE
    a) Deaths from carbon disulfide exposure usually result from respiratory paralysis after exposure to high concentrations (Gosselin et al, 1984; Baselt, 2000a). Cough, cyanosis, and dyspnea are common.
    C) CHEYNE-STOKES RESPIRATION
    1) WITH POISONING/EXPOSURE
    a) Cheyne-stokes respirations have preceded coma and death in cases of carbon disulfide ingestion (Harbison, 1998).

Neurologic

    3.7.1) SUMMARY
    A) In acute exposure, headache, dizziness, nervousness, tremor, seizures, and coma may be noted. Chronic exposure may lead to encephalopathy, psychosis, and polyneuritis.
    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) The primary symptoms of acute exposure are manifested in the central nervous system and may include seizures (Spyker et al, 1982), tremors, or coma (Davidson & Feinleib, 1972; Peters et al, 1988; Spyker et al, 1982; Baselt & Cravey, 2000).
    B) COMA
    1) WITH POISONING/EXPOSURE
    a) Coma has been noted after acute oral exposures (Davidson & Feinleib, 1972).
    C) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Dizziness is a symptom of exposure (Peters et al, 1988; Harbison, 1998).
    D) NEUROPATHY
    1) WITH POISONING/EXPOSURE
    a) Polyneuritis was seen in 88% of 100 cases of carbon disulfide poisoning in workers exposed to 60 to 500 ppm (Vigliani, 1954). Subclinical polyneuropathy (believed irreversible) is seen in long term, moderate exposures (Seppalainen & Tolonen, 1974; Aaserud et al, 1990).
    b) Conduction velocity of slow motor fibers was decreased at low levels of carbon disulfide exposure in a study of 45 workers (20 years mean exposure) and 37 controls (Ruijten et al, 1990). No sural nerve function impairment or color discrimination was observed.
    c) CASE REPORT: Peripheral neuropathy has been reported after a 15-year occupational exposure (air sample levels detected as high as 200 to 500 ppm) to carbon disulfide in a viscose rayon manufacturing plant(Klemmer & Harris, 2000).
    E) DEMENTIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 46-year-old nondiabetic man had clinical features that were characteristic of diabetic triopathy (i.e., peripheral and central nervous system abnormalities which included progressive dementia, memory failure, homicidal ideation and peripheral neuropathy as well as retinopathy, dyslipidemia, cardiovascular and renal disease) after toxic occupational exposure to carbon disulfide (Klemmer & Harris, 2000). Past medical history was negative. The patient was employed in a viscose rayon manufacturing plant for 15 years and air samples were as high as 200 to 500 ppm (normal 20 ppm) for carbon disulfide (the plant was later closed by the USEPA and became part of a Superfund Cleanup site).
    1) Over a 5-year period, the patient developed progressive dementia and renal failure. The family stopped dialysis due to severe dementia, and the patient died of uremia.
    F) ATROPHY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT : A 60-year-old man developed cerebellar and pontine atrophy which progressed following long term occupational (worked in a viscose rayon manufacturing plant for approximately 34 years) exposure to carbon disulfide (Frumkin, 1998). The patient developed progressive dysphagia, dysarthria, and ataxia with loss of independent function (i.e., walking, bladder control). A repeat MRI obtained at age 68 showed advanced cerebellar atrophy and prominent atrophy in the posterior region of the pons; the patient died at age 69.
    G) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache is a common finding after acute exposure (Spyker et al, 1982; Harbison, 1998; Donoghue, 1998).
    H) FATIGUE
    1) WITH POISONING/EXPOSURE
    a) Fatigue was reported in a worker approximately 20 hours after acute dermal exposure to carbon disulfide after mixing xanthate reagent; symptoms gradually improved over a 4-day period (Donoghue, 1998).
    I) EXTRAPYRAMIDAL DISEASE
    1) WITH POISONING/EXPOSURE
    a) Varying degrees of Parkinsonism characterized by speech disturbances, muscle spasticity, tremor, and memory loss, are noted in 20% to 30% of rayon workers exposed chronically (Ku et al, 2003; Hathaway et al, 1996; Quarelli, 1928; Lewey, 1941) .
    1) These patients tend to be younger with more frequent mental impairment than those with idiopathic parkinsonism. Patients with carbon disulfide induced parkinsonism do not respond well to antiparkinsonian medications. This may be explained by a dopamine transporter SPECT study that demonstrated normal uptake in the basal ganglia (Huang, 2004).
    J) NEUROLOGICAL FINDING
    1) WITH POISONING/EXPOSURE
    a) In a study of former carbon disulfide-exposed workers, a statistically significant increase (p<0.022) of cerebral lacunae was found on magnetic resonance imaging (MRI) in the high-exposure group. The study was performed to determine the relationship between neuropsychological deficits and MRI findings in a low-exposure group versus the high-exposure group (actual exposure levels unreported). Intelligence testing was also performed and no significant differences were found between the groups. The study was limited by the small sample size and that there was no control group. The authors suggest that further studies using MRI to assess carbon disulfide-related neuropsychological defects would be useful (Cho et al, 2002).
    b) CASE REPORT: Diffuse lesions in the subcortical white matter, brain stem and basal ganglia were found on magnetic resonance imaging (MRI) in a 56-year-old man who had worked in a viscose rayon plant for 27 years. These changes were thought to be comparable with the changes found in cerebral microangiopathy. The patient also had progressive cognitive dysfunction, polyneuropathy, cerebellar and pyramidal signs, as well as parkinsonian features (Ku et al, 2003).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) Exposure of mice to 800 ppm of carbon disulfide, 6 hours/day, 5 days/week for 20 weeks produces gait alteration and impaired function on the inverted screen test. Anconal neuropathy was noted in both peripheral and spinal neurons, accompanied by neurofibrillary tangles. Erythrocyte spectrin cross-linking was demonstrated and the authors suggest that neurofibrillary cross-linking by carbon disulfide may be the primary lesion in carbon disulfide induced neuropathy (Sills et al, 2000)
    2) Dose related behavioral effects were noted using the NIEHS/EPA Functional Observational Battery in Fisher 344 rats exposed to 0, 50, 500, or 800 ppm carbon disulfide for 6 hours per day, five days per week, for 2, 4, 8, or 13 weeks. Findings were noted even in the lowest dose (50 ppm, 2 weeks) exposure group (Moser et al, 1998).
    a) Related studies using the same dosing regimen demonstrated decreased nerve conduction velocity and action potential in the tail in animals exposed at 500 and 800 ppm for 13 weeks, but not at lower doses (Herr et al, 1998). Using this same model, pathological changes in the peripheral nerves and spinal cord have been described in detail (Sills et al, 1998).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting may occur after acute exposure. Chronic exposure is associated with gastritis and dyspepsia.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting have been noted following acute exposure (Spyker et al, 1982; Harbison, 1998).
    b) A 32-year-old worker came in contact with liberated carbon disulfide during xanthate reagent mixing (both xanthate powder and aqueous xanthate solution), and within 20 hours began to develop symptoms of nausea, vomiting, dyspepsia and epigastric burning (Donoghue, 1998). Symptoms gradually resolved over a 4-day period, with no long-term effects reported.
    B) GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) CHRONIC: In chronic exposure, chronic gastritis, dyspepsia, and achlorhydria may occur (Gosselin et al, 1984; Hathaway et al, 1996).

Hepatic

    3.9.1) SUMMARY
    A) Fatty degeneration as well as other pathological changes have been noted.
    3.9.2) CLINICAL EFFECTS
    A) STEATOSIS OF LIVER
    1) WITH POISONING/EXPOSURE
    a) Fatty degeneration as well as other pathological changes have been noted (Brieger, 1961; Cavallero et al, 1967; Lewey, 1941).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE TOXIC NEPHROPATHY
    1) WITH POISONING/EXPOSURE
    a) CHRONIC TOXICITY
    1) CASE REPORT: A 45-year-old nondiabetic man had clinical features that were characteristic of diabetic triopathy (i.e., peripheral and central nervous system abnormalities which included progressive dementia, memory failure, homicidal ideation and peripheral neuropathy as well as retinopathy, dyslipidemia, cardiovascular and renal disease) after toxic occupational exposure to carbon disulfide (Klemmer & Harris, 2000). Past medical history was negative.
    a) The patient was employed in a viscose rayon manufacturing plant for 15 years with documented elevated air levels of carbon disulfide. An initial renal biopsy showed lipoid nephrosis which resolved 5 years after leaving work. Over the subsequent 5 years, the patient developed progressive azotemia requiring hemodialysis. Dialysis was eventually withdrawn by the family due to severe dementia; the patient died of uremia.

Dermatologic

    3.14.1) SUMMARY
    A) Carbon disulfide is a strong skin irritant and dermal exposure may result in severe burns.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) WITH POISONING/EXPOSURE
    a) Carbon disulfide is thought to be one of the strongest skin irritants of all the organic solvents. Systemic symptoms from cutaneous exposure are usually preceded by severe local irritation. If contact is brief the usual effect is slight erythema.
    b) If the liquid is kept in contact with the skin over a prolonged period, it may lead to second and third degree burns (Vale & Meredith, 1983).
    c) LACK OF EFFECT: A 32-year-old worker came in contact with liberated carbon disulfide during xanthate reagent mixing (both xanthate powder and aqueous xanthate solution) (Donoghue, 1998). Immediately after exposure the patient showered and noted that his chest was stained green. Although the patient experienced systemic effects (i.e., gastrointestinal and CNS symptoms), he did not experience skin irritation and only mild pruritus.
    B) ECZEMA
    1) WITH POISONING/EXPOSURE
    a) Carbon disulfide dissolves the fatty layer of the skin resulting in dry, cracked skin on which eczematous lesions may appear (HSDB, 2004).

Reproductive

    3.20.1) SUMMARY
    A) Acute and prolonged exposure may produce adverse effects in males and females. Reported female adverse effects include menstrual abnormalities, spontaneous abortions and premature births. In males, changes in spermatogenesis and libido were reported.
    B) Teratogenic effects reported in humans include heart defects, CNS effects, and inguinal hernia. Teratogenic effects reported in experimental animals include developmental abnormalities of the eye, ear, and craniofacial area, and changes in viability index and growth statistics.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) In a study on 682 female synthetic fiber workers exposed to carbon disulfide for at least 6 months prior to and during pregnancy, the incidence of birth defects was 2.6-fold higher than in unexposed women; spontaneous abortion, prematurity, stillbirths, low birth weight, and neonatal and perinatal deaths, were not affected. The most frequent birth defects seen involved the heart, followed by inguinal hernia and CNS defects (Bao et al, 1991).
    B) ANIMAL STUDIES
    1) In the rat, fetal death, fetotoxicity, specific developmental abnormalities of the eye and ear and craniofacial area (including nose and tongue), changes in the viability index, growth statistics, and homeostasis as well as behavioral changes were observed (Schardein, 1993; RTECS, 2004).
    2) Increased pre-implantation mortality and smaller litter size was observed in the mouse (RTECS, 2004).
    3) In the rabbit, developmental abnormalities were detected (Schardein, 1993; RTECS, 2004).
    3.20.3) EFFECTS IN PREGNANCY
    A) ABORTION
    1) Adverse effects of both male and female reproductive function have been reported. Menstrual abnormalities, spontaneous abortions and premature births have occurred (Dixon, 1986; Schardein, 1993).
    B) MENSTRUAL DISORDER
    1) Menstrual disturbances and toxemia of pregnancy were seen in women occupationally exposed to 37 to 56 mg/m(3) (HSDB, 2004).
    C) UTERINE CONTRACTILITY INCREASED
    1) Carbon disulfide appears to increase uterine contractility in response to a variety of in vitro stimuli (Tsai et al, 2000).
    D) ANIMAL STUDIES
    1) Pre-implantation mortality was observed in rat and mouse studies. In rabbit studies, post-implantation mortality was observed(RTECS, 2004) .
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Carbon disulfide can cross the human placenta. It also has been found in the breast milk from exposed nursing mothers (HSDB, 2004).
    3.20.5) FERTILITY
    A) FERTILITY DECREASED MALE
    1) In humans, carbon disulfide induced changes in spermatogenesis(RTECS, 2004) .

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS75-15-0 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) Carbon disulfide did not show a carcinogenic potential in animals chronically exposed for periods of less than one year. Epidemiologic studies do not support a carcinogenic risk from moderate exposure to carbon disulfide (Hathaway et al, 1996).

Genotoxicity

    A) Carbon disulfide is a genotoxin, inducing mutations in bacteria and human cells.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs, neurologic exam, and mental status.
    B) Obtain serum electrolytes, and monitor renal function and liver enzymes in symptomatic patients.
    C) Monitor pulse oximetry and obtain a chest radiograph in any patient with respiratory symptoms.
    D) Carbon disulfide blood concentration and urinary metabolites can be measured, but will require reference laboratories and is not helpful in an acute exposure.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Obtain serum electrolytes, and monitor renal function and liver enzymes in symptomatic patients.
    2) Carbon disulfide in the blood is indicative of exposure; its concentration can give some indication of the severity of the exposure (Clayton & Clayton, 1993).
    a) Carbon disulfide blood concentration can be measured, but will require reference laboratories and is not helpful in an acute exposure.
    3) A direct, linear relationship has been shown between low-density lipoprotein concentration (LDLc) and the level of exposure to carbon disulfide. However, carbon disulfide exposure did not correlate with high-density lipoprotein concentration (HDLc), triglyceride or fasting glucose concentrations (Harbison, 1998).
    4) Twenty-two women exposed to carbon disulfide were compared to non-exposed workers and demonstrated adverse effects on lipid profiles and changes in coagulation factors suggestive of enhanced coagulability (Stanosz et al, 1998).
    4.1.3) URINE
    A) URINARY LEVELS
    1) Carbon disulfide in the urine is indicative of exposure; its concentration can give some indication of the severity of the exposure (Clayton & Clayton, 1993).
    a) Carbon disulfide urinary metabolites can be measured, but will require reference laboratories and is not helpful in an acute exposure.
    2) A study found that the concentration of the carbon disulfide metabolite 2-thiothiazolidine-4-carboxylic acid (TTCA) in the urine increased on the second and third day of the work week in 29 workers processing viscose rayon fibers (Meuling et al, 1990).
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor vital signs, neurologic exam, and mental status.
    b) Research suggests that monitoring of altered hemoglobin (Valentine et al, 1998) or spectrin (Lewis et al, 1999) may be a useful index of exposure, however, this has not been validated in humans.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Monitor pulse oximetry and obtain a chest radiograph in any patient with respiratory symptoms.

Methods

    A) OTHER
    1) Specific chemical tests (urinary) are available to evaluate exposure, particularly the metabolite 2-thiothiazolidine-4-carboxylic acid (TTCA). When evaluating exposures to carbon disulfide by workers, measuring TTCA in end of shift urine samples appeared to be a better measure of exposure than either bound carbon disulfide in blood or breath carbon disulfide (Campbell et al, 1985).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with large exposures, persistent or severe symptoms should be admitted for further care.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Asymptomatic patients with minor dermal or inhalation exposures can be monitored at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist or poison center in large and/or symptomatic exposures.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Any symptomatic patient, those with deliberate exposure, and any patient who ingests carbon disulfide should be sent to a healthcare facility for evaluation and treatment.

Monitoring

    A) Monitor vital signs, neurologic exam, and mental status.
    B) Obtain serum electrolytes, and monitor renal function and liver enzymes in symptomatic patients.
    C) Monitor pulse oximetry and obtain a chest radiograph in any patient with respiratory symptoms.
    D) Carbon disulfide blood concentration and urinary metabolites can be measured, but will require reference laboratories and is not helpful in an acute exposure.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Wash topical exposures with water. Prehospital gastrointestinal decontamination is not recommended due to the potential for decreased mental status or seizures and subsequent aspiration.
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Monitor vital signs, neurologic exam, and mental status.
    2) Obtain serum electrolytes, and monitor renal function and liver enzymes in symptomatic patients.
    3) Monitor pulse oximetry and obtain a chest radiograph in any patient with respiratory symptoms.
    4) Carbon disulfide blood concentration and urinary metabolites can be measured, but will require reference laboratories and is not helpful in an acute exposure.
    B) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2010; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    C) EXPERIMENTAL THERAPY
    1) UREA
    a) Intravenous urea (0.5 to 1.5 g/kg) has been recommended to inactivate free carbon disulfide in the blood, but the efficacy of this procedure has not been established (Gosselin et al, 1984).
    2) PYRIDOXINE
    a) Vitamin B6 in large parenteral doses has been recommended since carbon disulfide reacts with pyridoxamine to produce pyridoxamine-dithiocarbamic acid (Gosselin et al, 1984).
    b) DOSE: There is no specific recommended dose for carbon disulfide poisoning. Doses of 25 mg/kg intravenously have been well tolerated. However, established dosage recommendations employed in ISONIAZID poisoning are to give an equal amount of pyridoxine - up to 4 grams intravenously followed by 1 gram intramuscularly every 30 minutes. Pyridoxine can be toxic, but doses of 70 to 357 milligrams/kilogram have been administered without incident (Wason et al, 1981).
    c) ADVERSE REACTIONS: A single acute dose of 10 grams pyridoxine has been reported to produce neuropathy in an adult (Harati & Niakan, 1986).
    d) ANIMAL STUDIES have indicated that neural toxicity of pyridoxine is significantly reduced by a highly mineralized diet (Scheel, 1967).
    D) CONTRAINDICATED TREATMENT
    1) Avoid catecholamines and indirect-acting adrenergic agents because of probable monoamine oxidase inhibition by carbon disulfide (eg, amphetamine, reserpine) (Gosselin et al, 1984).

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) If burns or blisters appear, treat them as if they were thermal burns.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) HEMODIALYSIS
    1) There is no role for hemodialysis or other methods of enhanced elimination.

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) INHALATION: In one report of 27 patients exposed to carbon disulfide from a leaking railroad tank car, 59% experienced headache and dizziness (Spyker et al, 1982).

Range Of Toxicity

Summary

    A) TOXICITY: As little as 10 mL by mouth has caused toxicity and death. The lowest reported lethal oral dose is 14 mg/kg. The 8-hour TLV-TWA is 1 part per million (ppm). Five hundred ppm is considered immediately dangerous to life and health.

Minimum Lethal Exposure

    A) ADULT
    1) ORAL EXPOSURE
    a) In humans, the lowest reported lethal dose of carbon disulfide is 14 mg/kg via the oral route (Bingham et al, 2001a).
    b) Lethal doses by the oral route are between 0.5 and 5 g/kg (1 ounce to 1 pint (or pound)) for a 70-kg human (Bingham et al, 2001a; Gosselin et al, 1984).
    c) Adult ingestion of 10 mL (OHM/TADS, 2004) to 15 mL of carbon disulfide may be fatal (HSDB, 2004).
    2) INHALATION EXPOSURE
    a) Human exposure to an airborne concentration of 4800 ppm for 30 minutes causes coma and may be fatal (Hathaway et al, 1996).
    b) Exposure to an airborne concentration of 5000 ppm is rapidly fatal (Sweetnam et al, 1987).
    c) Exposures to carbon disulfide vapors at 15 mg/L can be lethal (OHM/TADS, 2004).

Maximum Tolerated Exposure

    A) ADULT
    1) Effects of Various Concentrations of Carbon Disulfide on Humans (Bingham et al, 2001a):
    CONCENTRATIONEFFECTS
    4815 ppmFatal in 1/2 hour
    3210-3850 ppmDangerous to life after 1/2 hour
    1150 ppmSerious symptoms after 1/2 hour
    420-510 ppmSymptoms after 1/2 hour
    320-390 ppmSlight symptoms after a few hours
    160-230 ppmSlight or no effect

    2) The ATSDR recommends a minimal risk level of 0.3 ppm for chronic (365 days and longer) inhalation exposures ((ATSDR, 2000)).
    3) 0.01 mg/kg/day is the minimal risk level recommended by the ATSDR for an acute (1-14 days) oral exposure ((ATSDR, 2000)).
    4) Acute exposures are rare, and are characterized by nausea, vomiting, dizziness, fatigue, delirium, and CNS depression. Chronic exposure can result in irritability, nervousness, indigestion, insomnia and strange dreams, headaches, changes in perception, loss of appetite, fatigue, and neurological deficits (ACGIH, 1991; Bingham et al, 2001a; Harbison, 1998; Hathaway et al, 1996).
    a) Exposure to airborne concentrations of 40 to 50 ppm was associated with headache, fatigue, anorexia, and psychiatric problems (Toyama & Sukurai, 1967).
    b) Exposure to airborne concentrations of 60 to 120 ppm was associated with mental fatigue, sleepiness, and headaches (Paluch, 1948).
    c) Exposure to an airborne concentration of 1000 ppm may cause acute psychosis (Sweetnam et al, 1987).
    d) No irritant symptoms were detected at 480 ppm inhaled for 1 hour (OHM/TADS, 2004).

Workplace Standards

    A) ACGIH TLV Values for CAS75-15-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Carbon disulfide
    a) TLV:
    1) TLV-TWA: 1 ppm
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A4
    2) Codes: BEI, Skin
    3) Definitions:
    a) A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    b) BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.
    c) Skin: This refers to the potential significant contribution to the overall exposure by the cutaneous route, including mucous membranes and the eyes, either by contact with vapors or, of likely greater significance, by direct skin contact with the substance. It should be noted that although some materials are capable of causing irritation, dermatitis, and sensitization in workers, these properties are not considered relevant when assigning a skin notation. Rather, data from acute dermal studies and repeated dose dermal studies in animals or humans, along with the ability of the chemical to be absorbed, are integrated in the decision-making toward assignment of the skin designation. Use of the skin designation provides an alert that air sampling would not be sufficient by itself in quantifying exposure from the substance and that measures to prevent significant cutaneous absorption may be warranted. Please see "Definitions and Notations" (in TLV booklet) for full definition.
    c) TLV Basis - Critical Effect(s): PNS impair
    d) Molecular Weight: 76.14
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS75-15-0 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Carbon disulfide
    2) REL:
    a) TWA: 1 ppm (3 mg/m(3))
    b) STEL: 10 ppm (30 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: [skin]
    1) Indicates the potential for dermal absorption; skin exposure should be prevented as necessary through the use of good work practices and gloves, coveralls, goggles, and other appropriate equipment.
    f) Note(s):
    3) IDLH:
    a) IDLH: 500 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS75-15-0 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Carbon disulfide
    a) A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Carbon disulfide
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Carbon disulfide
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS75-15-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Carbon disulfide
    2) Table Z-1 for Carbon disulfide:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3:
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed
    3) Table Z-2 for Carbon disulfide (Z37.3-1968):
    a) 8-hour TWA:20 ppm
    b) Acceptable Ceiling Concentration: 30 ppm
    c) Acceptable Maximum Peak above the Ceiling Concentration for an 8-hour Shift:
    1) Concentration: 100 ppm
    2) Maximum Duration: 30 minutes
    d) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Lewis, 2000 OHM/TADS, 2001 RTECS, 2004
    1) LD50- (ORAL)MOUSE:
    a) 2780 mg/kg (RTECS, 2004)
    2) LD50- (ORAL)RAT:
    a) 3188 mg/kg (Lewis, 2000)
    b) 0.1-0.99 g/kg (grade 2) (CHRIS, 2001)
    c) 1200 mg/kg (RTECS, 2004)
    3) TCLo- (INHALATION)HUMAN:
    a) 0.08 mg/m(3) - changes in sensation of smell (RTECS, 2004)
    b) 0.04 mg/m(3) - Changes in CNS and sense organs (RTECS, 2004)
    c) 1500 mg/m(3) for 30M - headache, nausea or vomiting (RTECS, 2004)
    d) 3600 mg/m(3) - paresthesias and cough (RTECS, 2004)
    e) Male, 40 mg/m(3) for 91W prior to mating -- affected sperm genetic material, morphology, count, and motility (RTECS, 2004)
    4) TCLo- (INHALATION)MOUSE:
    a) Female, 10 mg/m(3) for 2H 3W prior to mating - fertility effects (RTECS, 2004)
    b) 114 mg/m(3) for 8H/20W- intermittent -- gastrointestinal changes; affected weight loss and weight gain; death (RTECS, 2004)
    c) Female, 2000 mg/m(3) for 2H at 1-21D of pregnancy -- affected litter size; increased pre-implantation mortality (RTECS, 2004)
    5) TCLo- (INHALATION)RAT:
    a) 2000 ppm for 4H/2W- intermittent -- changes in psychophysiological behavior; death (RTECS, 2004)
    b) 800 ppm for 6H/15W-intermittent -- decrease in weight gain or weight loss; affected recordings from specific areas of CNS (RTECS, 2004)
    c) 114 mg/m(3) for 8H/20W- intermittent -- changes in kidney tubules; acute renal failure and acute tubular necrosis; splenic changes; death (RTECS, 2004)
    d) 10 mg/m(3) for 5H/13W- intermittent -- changes to endocrine system; degenerative changes to the brain; affected dopamine levels at other sites (RTECS, 2004)
    e) 800 mg/m(3) for 5H/1Y- intermittent -- changes in phosphatases and other enzymes (RTECS, 2004)
    f) 500 ppm for 24H/25W- continuous -- decreased weight gain or weight loss; affected recording from afferent and peripheral motor nerves(RTECS, 2004)
    g) 1500 mg/m(3) for 5H/26W- intermittent -- biochemical changes including phosphatases, transport lipid, and other enzymes (RTECS, 2004)
    h) 100 mg/m(3) for 17W-intermittent -- changes in vascular vessels and coronary arteries (RTECS, 2004)
    i) 800 ppm for 6H/12W-intermittent -- transaminases and other biochemical changes; weight loss or weight gain were decreased (RTECS, 2004)
    j) Female, 30 mcg/m(3) for 8H at 1-22D of pregnancy -- affected newborn behavior (RTECS, 2004)
    k) Female, 10 mg/m(3) for 8H at 1-22D of pregnancy -- abnormal development of the eyes and ears; affected newborn viability index (RTECS, 2004)
    l) Female, 200 mg/m(3) for 24H at 1-21D of pregnancy -- increased pre-implantation mortality (RTECS, 2004)
    m) Female, 100 mg/m(3) for 8H at 1-21D of pregnancy -- abnormal development of craniofacial features, including the nose and tongue; homeostasis abnormalities; increased fetal deaths (RTECS, 2004)
    n) Female, 100 mg/m(3) for 8H at 1-22D of pregnancy -- reduced weight gain in newborns (RTECS, 2004)
    o) Male, 600 ppm for 6H at 50D prior to mating -- affected the prostate, Cowper's gland, accessory glands, seminal vesicle; sperm genetic material, morphology, count, and motility (RTECS, 2004)

Pharmacology Toxicology

Toxicologic Mechanism

    A) REACTIVE GROUPS - Carbon disulfide reacts with numerous nucleophilic functional groups, including amino-, mercapto- hydroxyl- and others. The reaction results in the production of agents capable of chelating various metal ions. Enzyme inactivation and cell injury result (Davidson & Feinleib, 1972).
    B) PARKINSONISM -
    1) Inhibition of dopamine beta-hydroxylase, with exposed cells subsequently susceptible to the potentially damaging effects of superoxide, is a proposed mechanism for carbon disulfide-induced basal ganglia damage (Bleecker, 1988).
    2) Formation of covalent adducts with pyridoxamine, with derangement of vitamin B6 metabolism, has also been suggested to be responsible for the toxic effects of carbon disulfide(Vasak & Kopecky, 1967).

Physicochemical

Physical Characteristics

    A) Carbon disulfide exists as a mobile, colorless to light-yellow liquid with a sweet, pleasing, etheral odor (pure form) (ACGIH, 1991; Budavari, 2000).
    1) Reagent and commercial grades of this compound are foul smelling (disagreeable rotten egg odor) (Budavari, 2000; NFPA, 1997; NIOSH , 2001).
    B) Carbon disulfide is a toxic, highly refractile, extremely flammable liquid (Lewis, 2000; Sittig, 1991).

Molecular Weight

    A) 76.15

References

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