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DITHIOBIURET

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Dithiobiuret is a thiourea compound.

Specific Substances

    1) Dithiobiuret
    2) Biuret, 2,4-dithio-
    3) DTB
    4) Imidodicarbonimidothioic diamide
    5) Thioimidodicarbonic diamide
    6) Urea, 2-thio-1-(thiocarbamoyl)-
    7) USAF B-44
    8) USAF EK-P-6281
    9) RCRA WASTE NUMBER: P049
    10) NIOSH/RTECS EC 1575000
    11) Molecular Formula: C2-H5-N3-S2
    12) CAS 541-53-7
    13) References: RTECS, 1989; EPA, 1985
    1.2.1) MOLECULAR FORMULA
    1) C2-H5-N3-S2

Available Forms Sources

    A) SOURCES
    1) Dithiobiuret is produced by the reaction of hydrogen sulfide with dicyandiamide (Lewis, 1993).
    B) USES
    1) Dithiobiuret is used a rubber accelerator, a plasticizer, and an intermediate in the manufacture of pesticides and synthetic resins (Lewis, 1993; EPA, 1985).
    a) It can also be used to delay the wilting of flowers (Budavari, 1996).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Cases of human poisoning with this agent have apparently not been reported. Dithiobiuret is a highly toxic material that can cause respiratory depression and respiratory failure in experimental animals.
    B) Studies in experimental animals have found weight loss, diuresis and dehydration, excessive lacrimation, watery diarrhea, and development of muscular weakness or flaccid paralysis from impairment of neuromuscular transmission without accompanying CNS depression.
    C) Dithiobiuret concentrates in the thyroid in rats, and depressed serum levels of thyroid hormones develop over a six-day exposure period.
    0.2.4) HEENT
    A) Lacrimation has been described in exposed experimental animals. This effect has not been reported in exposed humans.
    0.2.6) RESPIRATORY
    A) Respiratory failure has been described in exposed experimental animals. This effect has not been described in exposed humans.
    0.2.7) NEUROLOGIC
    A) Peripheral axonopathy may occur. CNS depression does not appear to accompany skeletal muscle flaccid paralysis. Acute exposure improved memory in rats.
    1) Peripheral axonopathy occurs in exposed experimental animals. CNS depression does not appear to accompany skeletal muscle flaccid paralysis. This effect has not been described in exposed humans.
    0.2.8) GASTROINTESTINAL
    A) Watery diarrhea occurs in experimental animals and leads to fluid losses and dehydration.
    0.2.12) FLUID-ELECTROLYTE
    A) Fluid losses with dehydration and weight loss were noted in exposed experimental animals.
    0.2.15) MUSCULOSKELETAL
    A) Due to the impairment of neuromuscular transmission, muscular weakness or flaccid paralysis occurred in exposed experimental animals.
    0.2.16) ENDOCRINE
    A) Hypothyroidism was observed in experimental animals. This effect has not been reported in exposed humans.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Laboratory Monitoring

    A) Monitor arterial blood gases and thyroid function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Because of possible respiratory depression, DO NOT induce emesis.
    B) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    C) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    D) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    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) Experimental animals have died or developed serious poisoning at doses of 1 to 25 mg/kg/day for 6 to 10 days.

Clinical Effects

Summary Of Exposure

    A) Cases of human poisoning with this agent have apparently not been reported. Dithiobiuret is a highly toxic material that can cause respiratory depression and respiratory failure in experimental animals.
    B) Studies in experimental animals have found weight loss, diuresis and dehydration, excessive lacrimation, watery diarrhea, and development of muscular weakness or flaccid paralysis from impairment of neuromuscular transmission without accompanying CNS depression.
    C) Dithiobiuret concentrates in the thyroid in rats, and depressed serum levels of thyroid hormones develop over a six-day exposure period.

Heent

    3.4.1) SUMMARY
    A) Lacrimation has been described in exposed experimental animals. This effect has not been reported in exposed humans.
    3.4.3) EYES
    A) LACRIMATION - Excessive lacrimation has been described in exposed experimental animals (Atchison & Peterson, 1981). This effect has not been reported in exposed humans.

Respiratory

    3.6.1) SUMMARY
    A) Respiratory failure has been described in exposed experimental animals. This effect has not been described in exposed humans.
    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) Exposed experimental animals have developed respiratory failure, presumably from diaphragmatic muscular flaccid paralysis (EPA, 1985). CNS depression does not appear to accompany skeletal muscle flaccid paralysis (Atchison & Peterson, 1981).

Neurologic

    3.7.1) SUMMARY
    A) Peripheral axonopathy may occur. CNS depression does not appear to accompany skeletal muscle flaccid paralysis. Acute exposure improved memory in rats.
    1) Peripheral axonopathy occurs in exposed experimental animals. CNS depression does not appear to accompany skeletal muscle flaccid paralysis. This effect has not been described in exposed humans.
    3.7.2) CLINICAL EFFECTS
    A) SECONDARY PERIPHERAL NEUROPATHY
    1) PERIPHERAL AXONOPATHY - Dithiobiuret interferes with neuromuscular transmission, resulting in skeletal muscle weakness or ascending flaccid paralysis after 5 to 6 days of treatment (Williams et al, 1987; Williams et al, 1986; Atchison & Peterson, 1981; Spitsbergen & Atchison, 1990). The peripheral nerve lesions do not occur proximal to the intramuscular nerves (Williams et al, 1987).
    B) UNEXPECTED THERAPEUTIC EFFECT
    1) MEMORY IMPROVEMENT - Dithiobiuret produced long-lasting facilitation of cognition in rats at doses too low to induce peripheral neuropathy (Bushnell & Oshiro, 1996).
    C) LACK OF EFFECT
    1) CNS depression does not appear to accompany skeletal muscle flaccid paralysis (Atchison & Peterson, 1981).

Gastrointestinal

    3.8.1) SUMMARY
    A) Watery diarrhea occurs in experimental animals and leads to fluid losses and dehydration.
    3.8.2) CLINICAL EFFECTS
    A) DIARRHEA
    1) Watery diarrhea occurs in experimental animals and leads to fluid losses and dehydration (Williams et al, 1987; Atchison & Peterson, 1981).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Watery diarrhea occurs and can lead to fluid losses and dehydration (Williams et al, 1987; Atchison & Peterson, 1981).

Musculoskeletal

    3.15.1) SUMMARY
    A) Due to the impairment of neuromuscular transmission, muscular weakness or flaccid paralysis occurred in exposed experimental animals.
    3.15.2) CLINICAL EFFECTS
    A) PARALYSIS
    1) Muscular weakness or flaccid paralysis occur in exposed experimental animals from impairment of neuromuscular transmission (Williams et al, 1987; Weiler et al, 1986; Atchison & Peterson, 1981).
    3.15.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Muscular weakness or flaccid paralysis occur in exposed experimental animals from impairment of neuromuscular transmission (Williams et al, 1987; Weiler et al, 1986; Atchison & Peterson, 1981).

Endocrine

    3.16.1) SUMMARY
    A) Hypothyroidism was observed in experimental animals. This effect has not been reported in exposed humans.
    3.16.2) CLINICAL EFFECTS
    A) HYPOTHYROIDISM
    1) Dithiobiuret accumulates in the thyroid gland at levels substantially greater than those found in the plasma, and serum thyroid hormones levels were depressed in rats treated with dithiobiuret for a six-day period (Williams et al, 1987; Porter et al, 1983). This effect has not been reported in exposed humans.
    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Dithiobiuret accumulates in the thyroid gland at levels substantially greater than those found in the plasma, and serum thyroid hormones levels were depressed in rats treated with dithiobiuret for a six-day period (Williams et al, 1987; Porter et al, 1983). This effect has not been reported in exposed humans.

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS541-53-7 (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
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor arterial blood gases and thyroid function tests.
    4.1.2) SERUM/BLOOD
    A) ACID/BASE
    1) Arterial blood gases should be monitored to assess adequacy of oxygenation if respiratory insufficiency is suspected.
    B) ENDOCRINE
    1) Monitor serum thyroid hormone levels in patients with significant, particularly chronic, exposure to this agent.
    4.1.3) URINE
    A) OTHER
    1) Urine output should be carefully recorded and balanced against fluid intake to assess for possible dehydration.
    4.1.4) OTHER
    A) OTHER
    1) ELECTROPHYSIOLOGICAL TESTING
    a) Neurophysiologic studies could be useful to assess the degree of impairment of neuromuscular transmission in patients with muscle weakness or flaccid paralysis.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory insufficiency occurs with generalized muscular weakness, the chest x-ray should be monitored to detect atelectasis or aspiration.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) Monitor arterial blood gases and thyroid function tests.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Because of possible respiratory depression, DO NOT induce emesis.
    B) ACTIVATED CHARCOAL/CATHARTIC
    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).
    C) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    6.5.3) TREATMENT
    A) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Significant fluid losses resulting in weight loss and dehydration have occurred in exposed experimental animals.
    2) Monitor urine output, fluid intake, fluid losses through diarrhea, and serum electrolytes.
    3) Replace fluid and electrolyte losses as required to prevent fluid-electrolyte imbalances.
    B) AIRWAY MANAGEMENT
    1) Monitor adequacy of respirations and oxygenation.
    2) If diaphragmatic weakness or paralysis occurs, endotracheal intubation and assisted ventilation may be required.
    C) SUPPORT
    1) FLACCID PARALYSIS
    a) NURSING CARE - Nursing care to prevent development of pressure necrosis and aspiration of gastric contents may be required if generalized flaccid paralysis develops.
    D) EXPERIMENTAL THERAPY
    1) A variety of potential antagonists (D-penicillamine, diethyldithiocarbamate, cysteamine, 2,2-pyridyl, and disulfiram) have been used to partially reverse dithiobiuret muscle paralysis in rats (Williams et al, 1986). None of these agents have been used in cases of human poisoning.
    2) D-penicillamine was one of the agents that completely reversed paralysis in rats (Williams et al, 1986), and a trial of this agent could be considered for use in seriously poisoned humans. No dosing recommendations for this indication have been made, but a dosing regimen similar to that used for chelation of heavy metals could be adopted if this experimental therapy is considered. Obtaining informed consent from the patient or responsible party would be advisable before undertaking this experimental therapy which is NOT a US FDA labelled indication.
    a) ADULTS AND CHILDREN - 25 milligrams per kilogram orally every six hours up to a maximum of 250 milligrams per dose or 1 gram per 24 hours.
    b) The dose may be doubled to a maximum of 500 milligrams per dose or 2 grams per 24 hours in serious cases.
    c) DO NOT ADMINISTER D-PENICILLAMINE TO PENICILLIN ALLERGIC PATIENTS - Cross sensitivity and anaphylactic reactions may occur.
    d) Treatment with D-penicillamine should not be continued for more than 10 days per course of therapy to prevent loss of essential trace metals.
    e) D-penicillamine therapy did NOT reverse the excessive diuresis and resultant dehydration in rats.
    E) HYPOTHYROIDISM
    1) Monitor thyroid function tests in patients with exposure.
    2) Thyroid hormone replacement could be necessary if signs and symptoms of hypothyroidism develop.
    F) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    2) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

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.
    6.7.2) TREATMENT
    A) GENERAL TREATMENT
    1) No cases of poisoning by the inhalation exposure route have been described in humans.
    2) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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) GENERAL TREATMENT
    1) No cases of poisoning by the percutaneous exposure route have been described in either humans or experimental animals.
    2) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EFFICACY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Range Of Toxicity

Summary

    A) Experimental animals have died or developed serious poisoning at doses of 1 to 25 mg/kg/day for 6 to 10 days.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.
    B) ANIMAL DATA
    1) Some deaths were noted in experimental animals given between 1 and 25 mg/kg daily for 6 days (Atchison & Peterson, 1981).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) ANIMAL DATA
    1) Some experimental animals have survived a 10-day course of between 1 and 25 mg/kg daily, although serious poisoning developed (Atchison & Peterson, 1981).

Workplace Standards

    A) ACGIH TLV Values for CAS541-53-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS541-53-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS541-53-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    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
    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 CAS541-53-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1996 Lewis, 1992)
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 50 mg/kg
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 29 mg/kg
    3) LD50- (ORAL)RAT:
    a) 5 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Dithiobiuret inhibited motor but not sensory neurological function in rats (Crofton et al, 1991). Exposure for up to 48 days produced a central-peripheral distal axonopathy (Sahenk, 1990).
    B) Dithiobiuret's mechanism of impairment of neuromuscular transmission does not seem to be directed specifically at acetylcholine (ACh) synthesis, but is rather an interference with the processes that either incorporate ACh into presynaptic vesicles or release ACh from these vesicles (Weiler et al, 1986).
    C) The development of a distal axonopathy caused by dithiobiuret does not appear to be mediated by an inhibition of glycolysis (LoPachin et al, 1984). Peripheral nerve inhibition and resultant muscular weakness are not accompanied by CNS depression (Atchison & Peterson, 1981).

Physicochemical

Physical Characteristics

    A) Dithiobiuret is a colorless crystalline solid; crystals are monoclinic or triclinic (Budavari, 1996; EPA, 1985; Lewis, 1993).

Ph

    A) 5.8 (saturated aqueous solution at 30 degrees C) (Budavari, 1996)

Molecular Weight

    A) 135.20 (Budavari, 1996)
    B) 135.22 (RTECS , 1996)

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    9) 66 FR 21940: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2001.
    10) 67 FR 7164: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2002.
    11) 68 FR 42710: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2003.
    12) 69 FR 54144: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2004.
    13) AIHA: 2006 Emergency Response Planning Guidelines and Workplace Environmental Exposure Level Guides Handbook, American Industrial Hygiene Association, Fairfax, VA, 2006.
    14) American Conference of Governmental Industrial Hygienists : ACGIH 2010 Threshold Limit Values (TLVs(R)) for Chemical Substances and Physical Agents and Biological Exposure Indices (BEIs(R)), American Conference of Governmental Industrial Hygienists, Cincinnati, OH, 2010.
    15) Atchison WD & Peterson RE: Potential neuromuscular toxicity of 2,4-dithiobiuret in the rat. Toxicol Appl Pharmacol 1981; 57:63-68.
    16) Budavari S: The Merck Index, 12th ed, Merck & Co, Inc, Whitehouse Station, NJ, 1996, pp 571.
    17) Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 1999; 34(2):205-212.
    18) Bushnell PJ & Oshiro WM: 2,4-dithiobiure in rats - cognitive facilitation after acute injection precedes motor impairment after repeated daily injections. Psychopharmacol 1996; 123:267-279.
    19) Caravati EM, Knight HH, & Linscott MS: Esophageal laceration and charcoal mediastinum complicating gastric lavage. J Emerg Med 2001; 20:273-276.
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