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CARBON TETRABROMIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Carbon tetrabromide is an organic synthesis reactive agent.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C-Br4

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Acute exposure may result in upper respiratory tract irritation and injury to lungs, liver, and kidneys. Low level, chronic exposures usually produce primarily liver injury.
    B) When heated to decomposition, carbon tetrabromide emits toxic fumes of bromine.
    0.2.4) HEENT
    A) Carbon tetrabromide is a potent lacrimator even at low levels. The undiluted material may cause severe irritation and temporary corneal damage if splashed in the eyes.
    0.2.6) RESPIRATORY
    A) Based on animal studies, acute exposure may lead to upper respiratory tract irritation and lung injury.
    0.2.7) NEUROLOGIC
    A) High concentrations of vapor may cause anesthesia.
    0.2.9) HEPATIC
    A) Animal studies have indicated fatty degenerative changes in the liver after chronic exposures.
    0.2.10) GENITOURINARY
    A) Oliguria, aciduria, and kidney damage have been seen in acutely poisoned experimental animals.
    0.2.14) DERMATOLOGIC
    A) If confined closely to the skin, it may cause hyperemia and moderate edema.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the teratogenic potential of the agent or the potential for effects during pregnancy or lactation.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

    A) Although carbon tetrabromide may release bromine ions during metabolism, clinical bromism is not expected to occur.
    B) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    C) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    D) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Because of the irritant properties of this substance, EMESIS SHOULD NOT BE INDUCED.
    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) Obtain baseline, liver, and renal function studies.
    E) Maintain fluid and electrolyte status.
    F) Hemodialysis and peritoneal dialysis are probably not of any value. Forced diuresis is of no value.
    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.
    B) Obtain baseline, liver, and renal function studies.
    C) Maintain fluid and electrolyte status.
    D) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    E) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    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.
    B) Because of the potential for significant ocular damage after direct eye contact with the solid material, prolonged initial flushing and early ophthalmologic consultation are recommended.
    1) Permanent corneal damage has resulted from exposure to the solid material.
    C) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    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).
    2) Obtain baseline, liver, and renal function studies.
    3) Maintain fluid and electrolyte status.
    4) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Exposure to airborne concentrations of 0.1 to 0.5 ppm for 7 hours per day, 5 days per week for 6 months caused liver injury in rats.

Clinical Effects

Summary Of Exposure

    A) Acute exposure may result in upper respiratory tract irritation and injury to lungs, liver, and kidneys. Low level, chronic exposures usually produce primarily liver injury.
    B) When heated to decomposition, carbon tetrabromide emits toxic fumes of bromine.

Heent

    3.4.1) SUMMARY
    A) Carbon tetrabromide is a potent lacrimator even at low levels. The undiluted material may cause severe irritation and temporary corneal damage if splashed in the eyes.
    3.4.3) EYES
    A) Carbon tetrabromide is a potent lacrimator even at low levels. In rabbit's eyes, the undiluted material caused severe irritation and permanent corneal damage.
    1) When washed out fairly quickly, pain and irritation were present but corneal damage was temporary (Clayton & Clayton, 1982).

Respiratory

    3.6.1) SUMMARY
    A) Based on animal studies, acute exposure may lead to upper respiratory tract irritation and lung injury.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Based on animal studies, acute exposure may lead to upper respiratory tract irritation and lung injury, depending upon concentration and duration of exposure (Clayton & Clayton, 1982; (ACGIH, 1991).

Neurologic

    3.7.1) SUMMARY
    A) High concentrations of vapor may cause anesthesia.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) High concentrations of vapor (unspecified) are said to be anesthetic (ITI, 1975).

Hepatic

    3.9.1) SUMMARY
    A) Animal studies have indicated fatty degenerative changes in the liver after chronic exposures.
    3.9.2) CLINICAL EFFECTS
    A) STEATOSIS OF LIVER
    1) Based on animal studies, hepatic injury may be seen with high dose, acute exposures or chronic, low dose exposures (ACGIH, 1991).
    2) Rats exposed to 0.7 to 74 ppm, 4 hours/day for 4 months had metabolic changes in the liver. Another study indicated the minimum effect level to be 0.1 ppm. Higher concentrations produced fatty and degenerative changes in the liver (Clayton & Clayton, 1982).

Genitourinary

    3.10.1) SUMMARY
    A) Oliguria, aciduria, and kidney damage have been seen in acutely poisoned experimental animals.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) Injury to the kidney has been reported in animal studies (Hathaway et al, 1991).
    B) OLIGURIA
    1) A single intraperitoneal injection of carbon tetrabromide in rats caused oliguria, aciduria, and hypoosmolality (Agarwal et al, 1983).

Dermatologic

    3.14.1) SUMMARY
    A) If confined closely to the skin, it may cause hyperemia and moderate edema.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Contact of this chemical with rabbit skin caused slight irritation. If confined tightly against the skin, it caused hyperemia and moderate edema (Clayton & Clayton, 1982).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the teratogenic potential of the agent or the potential for effects 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.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    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 CAS558-13-4 (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
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) At the time of this review, no data were available to assess the mutagenic or genotoxic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Although carbon tetrabromide may release bromine ions during metabolism, clinical bromism is not expected to occur.
    B) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    C) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    D) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Although carbon tetrabromide may release bromine ions during metabolism, clinical bromism is not expected to occur.
    2) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    3) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    B) ACID/BASE
    1) BLOOD GASES
    a) Monitor arterial blood gases and/or pulse oximetry in patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Monitor the chest x-ray in patients with significant exposure.

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) It is unclear how closely the toxicity of carbon tetrabromide correlates with that of carbon tetrachloride. If severe liver toxicity results, such treatments as vitamin K, N-acetylcysteine, and pyridoxine might be useful. Refer to the carbon tetrachloride MEDITEXT(R) medical management for more information.

Monitoring

    A) Although carbon tetrabromide may release bromine ions during metabolism, clinical bromism is not expected to occur.
    B) This agent may cause hepatotoxicity. Monitor liver function tests in patients with significant exposure.
    C) This agent may cause nephrotoxicity. Monitor renal function tests and urinalysis in patients with significant exposure.
    D) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Because of the irritant properties of this substance, EMESIS SHOULD NOT BE INDUCED.
    B) 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.
    C) 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).
    6.5.3) TREATMENT
    A) MONITORING OF PATIENT
    1) Obtain baseline liver and renal function studies.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Maintain fluid and electrolyte status.
    C) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

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) MONITORING OF PATIENT
    1) Obtain baseline liver and renal function studies.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Maintain fluid and electrolyte status.
    C) IRRITATION SYMPTOM
    1) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    D) ACUTE LUNG INJURY
    1) Respiratory tract irritation, if severe, can progress to pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    3) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    4) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    5) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    6) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    7) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    8) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    E) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    F) 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).
    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) CORNEAL DAMAGE - Because of the potential for significant ocular damage after direct eye contact with the solid material, prolonged initial flushing and early ophthalmologic consultation are recommended. Permanent corneal damage has resulted from exposure to the solid material.
    2) SYSTEMIC TOXICITY - If systemic toxicity is suspected following eye exposure -
    a) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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) MONITORING OF PATIENT
    1) Obtain baseline liver and renal function studies.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Maintain fluid and electrolyte status.
    C) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EFFICACY
    1) Hemodialysis or peritoneal dialysis are probably not of any value.
    2) Forced diuresis is of no value.

Range Of Toxicity

Summary

    A) Exposure to airborne concentrations of 0.1 to 0.5 ppm for 7 hours per day, 5 days per week for 6 months caused liver injury in rats.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum lethal human dose to this agent has not been delineated.

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to this agent has not been delineated.
    B) ANIMAL DATA
    1) In rats, concentrations of 0.1 to 0.5 ppm for 7 hours/day, 5 days/week for 6 months caused liver injury. Concentrations of 0.07 ppm 4 hours/day for 4 months caused irritation of the eyes and respiratory tract (ACGIH, 1991a).
    2) In the eyes of rabbits, the undiluted material caused severe irritation and permanent corneal damage. When the material was promptly washed from the eyes, pain and irritation were noted but the corneal damage was temporary (Clayton & Clayton, 1981).
    3) Skin contact causes relatively slight irritation in rabbits (Clayton & Clayton, 1981).

Workplace Standards

    A) ACGIH TLV Values for CAS558-13-4 (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 tetrabromide
    a) TLV:
    1) TLV-TWA: 0.1 ppm
    2) TLV-STEL: 0.3 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): Liver dam; eye, URT, and skin irr
    d) Molecular Weight: 331.65
    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 CAS558-13-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Carbon tetrabromide
    2) REL:
    a) TWA: 0.1 ppm (1.4 mg/m(3))
    b) STEL: 0.3 ppm (4 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS558-13-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Carbon tetrabromide
    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 ; Listed as: Carbon tetrabromide
    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 CAS558-13-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Clayton & Clayton, 1981 RTECS, 1992 Sax & Lewis, 1989
    1) LD50- (SUBCUTANEOUS)MOUSE:
    a) 298 mg/kg
    2) LD50- (ORAL)RAT:
    a) 1800 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) In rat studies, carbon tetrabromide induced lipid peroxidation (as indicated by an increased release of thiobarbituric acid-reactive substances) in the liver, spleen, and testes. It was also shown to inhibit protein synthesis in the rat.
    1) The extent of lipid peroxidation and the ability to inhibit protein synthesis correlated with the LD50 level, suggesting these events may be involved in cell injury or death mediated by free radicals (Fraga et al, 1989; Fraga et al, 1987).

Physicochemical

Physical Characteristics

    A) At room temperature, pure carbon tetrabromide is a colorless, nonflammable solid; however, samples are generally yellow-brown in color (ACGIH, 1991a).

Ph

    1) No information found at the time of this review.

Molecular Weight

    A) 331.65

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.
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