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BORON HYDRIDES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) A group of chemicals with diverse uses including chemical synthesis, fungicide, bactericide, high energy fuel and rubber synthesis, metal plating (Plunkett, 1976).
    B) These compounds are approximately 100-fold more toxic than borates.

Specific Substances

    A) DIBORANE
    1) Boroethane
    2) Diboron Hexahydride
    3) CAS 19287-45-7
    PENTABORANE
    1) Dihydropentaborane
    2) Dihydropentaborane (9)
    3) Pentaboron Undecahydride
    4) CAS 19624-22-7
    DECABORANE
    1) Decaboron Tetradecahydride
    2) CAS 17702-41-9
    SODIUM BOROHYDRIDE
    1) Sodium Tetrahydroborate
    2) CAS 16940-66-2

Available Forms Sources

    A) USES
    1) DIBORANE: Diborane is the starting material for the manufacture of various other borohydrides, as well as a fuel, a polymerization catalyst for ethylene, a reducing agent and doping agent in semiconductors. The major route of occupational exposure to diborane is inhalation (Hathaway et al, 1996).
    2) PENTABORANE: Potent reducing agent and synthetic fuel.
    3) DECABORANE: Decaborane is a solid fuel propellant, polymer synthesis agent, fuel additive, corrosion inhibitor, moth proofer, dye-stripper, fluxing agent and reducing agent.
    4) BOROHYDRIDE (SODIUM): A source of hydrogen and reducer of aldehydes, ketones and acid chlorides, a wood pulp bleacher and a blowing agent for plastic.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Boron hydrides are highly toxic by inhalation, skin absorption or ingestion. Pentaborane is considered more toxic than diborane.
    B) Inhalation of diborane may cause chest tightness, shortness of breath, coughing, nausea, shivering and drowsiness. Pentaborane and decaborane have primarily neurologic toxicity.
    C) ONSET - Signs and symptoms may develop immediately after diborane exposure or may be delayed 24 hours and persist 2 to 3 days.
    0.2.3) VITAL SIGNS
    A) Dyspnea and shallow respirations may occur.
    B) Temperature may be increased.
    C) Hypotension may occur.
    0.2.4) HEENT
    A) Boron hydrides have caused irreversible eye damage.
    0.2.5) CARDIOVASCULAR
    A) Mild hypertension was noted in a few human cases. No cardiac toxicity was noted in 137 human cases.
    B) Sinus tachycardia deteriorating to atrial fibrillation has occurred.
    0.2.6) RESPIRATORY
    A) These substances are respiratory irritants. One may see tightness in the chest, dyspnea, cough and wheezing for 3 to 5 days after an exposure. Diborane has the most activity on the lungs, pentaborane and decaborane have fewer respiratory symptoms.
    0.2.7) NEUROLOGIC
    A) Dizziness, weakness, CNS depression, and incoordination have been seen in patients exposed to industrial spills. Tremors leading to seizures and severe brain injury have been seen in high dose pentaborane intoxication.
    0.2.8) GASTROINTESTINAL
    A) Nausea is one of the first symptoms seen.
    0.2.9) HEPATIC
    A) Boron hydrides may cause fatty liver degeneration.
    0.2.11) ACID-BASE
    A) Acidosis may be seen, especially in relation to seizures.
    B) Metabolic acidosis without respiratory compensation may occur.
    0.2.15) MUSCULOSKELETAL
    A) Rhabdomyolysis may occur.
    0.2.18) PSYCHIATRIC
    A) Hallucinations have been reported in exposures to pentaborane.
    B) Posttraumatic stress disorder has been reported 4 to 12 weeks after exposure to pentaborane.
    0.2.20) REPRODUCTIVE
    A) Although toxic effects have been seen in experiments on animal spermatogenesis, similar effects have NOT been shown in humans exposed in industry.

Laboratory Monitoring

    A) Tissue pentaborane levels have not yet been established as useful. Liver and renal function tests may be indicated. Boron levels are elevated in blood and document exposures.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Ingestion of these products is unusual. Most exposures occur either by inhalation or dermally. Ingestions of diborane are extremely unlikely since it is a gas at room temperature. Pentaborane hydrolyzes in a few hours, and decaborane requires approximately 30 days for degradation in aqueous solutions, so decontamination may be of value with these 2 compounds.
    B) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    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) 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.
    E) Supportive care including oxygen, chlorpromazine, and meperidine has been recommended.
    F) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 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) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 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).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    G) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.3) INHALATION EXPOSURE
    A) RESCUE - Rescuers must have self-contained respiratory equipment and plastic gloves.
    B) 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.
    C) Use diazepam for seizure therapy.
    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) Remove all contaminated clothing. Dilute the area copiously with cool water. These substances may hydrolyze exothermically, so small amounts of water may result in thermal burns. A physician may need to examine the area if irritation or pain persists.

Range Of Toxicity

    A) TLV - decaborane 0.05 ppm; diborane 0.1 ppm, pentaborane 0.005 ppm.
    B) DIBORANE - 1000 PPM for 1 minute may be lethal.

Clinical Effects

Summary Of Exposure

    A) Boron hydrides are highly toxic by inhalation, skin absorption or ingestion. Pentaborane is considered more toxic than diborane.
    B) Inhalation of diborane may cause chest tightness, shortness of breath, coughing, nausea, shivering and drowsiness. Pentaborane and decaborane have primarily neurologic toxicity.
    C) ONSET - Signs and symptoms may develop immediately after diborane exposure or may be delayed 24 hours and persist 2 to 3 days.

Vital Signs

    3.3.1) SUMMARY
    A) Dyspnea and shallow respirations may occur.
    B) Temperature may be increased.
    C) Hypotension may occur.
    3.3.2) RESPIRATIONS
    A) Dyspnea, cough, wheezing or tachypnea may be noted after exposure to diborane.
    3.3.3) TEMPERATURE
    A) Hyperthermia has been reported in pentaborane exposures (Yarbrough et al, 1985-1986).
    3.3.4) BLOOD PRESSURE
    A) Hypotension may occur from exposures to pentaborane (Yarbrough et al, 1985-1986).

Heent

    3.4.1) SUMMARY
    A) Boron hydrides have caused irreversible eye damage.
    3.4.3) EYES
    A) CONJUNCTIVITIS - Keratoconjunctivitis may be seen (Plunkett, 1976). One mg of borohydride (sodium) instilled in rabbit eyes caused irreversible damage (Stokinger, 1982).
    B) CORNEA - Corneal opacification has been seen in experiments on mice (Stokinger, 1982).
    C) CORTICAL BLINDNESS was reported in a patient exposed to pentaborane. The patient experienced acidosis, seizures, and cardiac arrest. After regaining consciousness he sustained cortical blindness (Silverman et al, 1985).
    D) DIPLOPIA and difficulty in focusing have been reported in severe cases of diborane toxicity; however, symptoms disappeared when exposure was discontinued (HSDB , 2001).

Cardiovascular

    3.5.1) SUMMARY
    A) Mild hypertension was noted in a few human cases. No cardiac toxicity was noted in 137 human cases.
    B) Sinus tachycardia deteriorating to atrial fibrillation has occurred.
    3.5.2) CLINICAL EFFECTS
    A) HYPERTENSIVE EPISODE
    1) Mild hypertension was observed in dogs poisoned by diborane (Kunkel et al, 1956), and in a few human cases (Lowe & Freeman, 1957).
    B) TACHYARRHYTHMIA
    1) CASE REPORT - Sinus tachycardia deteriorating to atrial fibrillation was reported in a case of dermal exposure to pentaborane (Yarbrough et al, 1985-1986).
    C) LACK OF EFFECT
    1) CASE SERIES - Of 137 human cases reviewed by Lowe & Freeman (1957), no cardiac toxicity was noted.
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) BRADYCARDIA
    a) Bradycardia, as well as, a decrease in cardiac output has been noted in dogs (Lowe & Freeman, 1957).

Respiratory

    3.6.1) SUMMARY
    A) These substances are respiratory irritants. One may see tightness in the chest, dyspnea, cough and wheezing for 3 to 5 days after an exposure. Diborane has the most activity on the lungs, pentaborane and decaborane have fewer respiratory symptoms.
    3.6.2) CLINICAL EFFECTS
    A) PNEUMONITIS
    1) These substances are respiratory irritants (Plunkett, 1976). One may see tightness in the chest, dyspnea, cough and wheezing for 3 to 5 days after an exposure (Cordasco et al, 1962). Pneumonia is also possible. Diborane has the most activity on the lungs, pentaborane and decaborane have fewer respiratory tract symptoms (Finkel, 1983). Repetitive exposures may result in chronic respiratory distress (Stokinger, 1982).
    B) RESPIRATORY ACIDOSIS
    1) Respiratory acidosis has been seen in the early hospital course of patients exposed to pentaborane (Yarbrough et al, 1985-1986).
    C) METAL FEVER
    1) After acute exposure, symptoms similar to those of metal fume fever (tightness, heaviness and burning in chest, coughing, shortness of breath, pericardial pain, nausea, shivering & drowsiness) may occur. Symptoms may occur soon after exposure or may be delayed for up to 24 hours and persist for 2 to 3 days(HSDB , 2001). Refer to "METAL FUME FEVER" management for more information.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) PULMONARY EDEMA
    a) Animal tests demonstrate that diborane creates exothermic hydrolysis which leads to pulmonary irritation and edema (Schechter, 1958; Lowe & Freeman, 1957; Kunkel et al, 1956).
    2) RESPIRATORY DISORDER
    a) The lungs were the target of acute diborane inhalation in mice. Diffuse pan bronchiolitis-like lesions involving infiltration of inflammatory cells into the terminal bronchioles and alveoli, and pulmonary congestion, bleeding and/or edema, developed in the lungs of mice exposed to 15 ppm diborane for periods up to 8 hours (Uemura et al, 1995).

Neurologic

    3.7.1) SUMMARY
    A) Dizziness, weakness, CNS depression, and incoordination have been seen in patients exposed to industrial spills. Tremors leading to seizures and severe brain injury have been seen in high dose pentaborane intoxication.
    3.7.2) CLINICAL EFFECTS
    A) DIZZINESS
    1) Dizziness, often accompanied by weakness, is seen with industrial spill exposures (Rozendaal, 1951). Even low levels may produce this effect (Finkel, 1983).
    B) SEIZURE
    1) Muscle fasciculations and tremors leading to seizures have been seen with high dose severe pentaborane (Finkel, 1983) Yarbrough et al, 1985) and borohydride intoxication (Rozendaal, 1951).
    C) CENTRAL NERVOUS SYSTEM DEFICIT
    1) Drowsiness is often seen in those patients exposed accidentally. Coma may also be seen (Lowe & Freeman, 1957) Yarbrough et al, 1985).
    D) COORDINATION PROBLEM
    1) Studies indicate marked decreases in performance in monkeys injected with 2 to 4 mg of decaborane. Workers generally show performance deficits in the first 50 hours (Stokinger, 1982). Apathy, pain insensitivity and stupor were seen in animals chronically exposed to low doses of pentaborane (Levinskas, 1958). Performance decrements were noted on 5 of 11 neuropsychological tests administered to workers and rescue squad members with a mild exposure to pentaborane 2 months previously (Hart et al, 1984). Workers exposed are often confused, have difficulty concentrating and have memory loss (Rozendaal, 1951).
    E) RAISED INTRACRANIAL PRESSURE
    1) Intracranial hypertension has been reported in patients with seizures and coma after pentaborane exposure (Yarbrough et al, 1985).
    F) TOXIC ENCEPHALOPATHY
    1) CASE SERIES - Fourteen persons exposed to pentaborane were evaluated 4 to 12 weeks after exposure. Persistent psychiatric symptoms, neuropsychological deficits, EEG changes, elevated CNS neurotransmitter levels, and ventricular brain ratios (computed tomographic scan) revealed evidence of CNS damage (Silverman et al, 1985).
    G) TETRAPLEGIA
    1) CASE REPORT - Quadriplegia was reported in a patient exposed to pentaborane. The patient experienced acidosis, seizures, and cardiac arrest. After regaining consciousness, he sustained quadriplegia (Silverman et al, 1985).
    H) CEREBRAL EDEMA
    1) Cerebral edema has been reported in progression of CNS damage due to pentaborane exposure (Yarbrough et al, 1985-1986).
    I) OPISTHOTONUS
    1) CASE SERIES - Opisthotonic spasms occurred in 3 cases of pentaborane exposures. Serious symptoms may be delayed up to 40 hours (Yarbrough et al, 1985-1986).
    J) HEADACHE
    1) Headache has been noted after accidental spills, and low level exposures to pentaborane or decaborane (Lowe & Freeman, 1957; Finkel, 1983).
    K) TREMOR
    1) Tremors, diffuse fasciculations and muscle spasms have all been reported with severe decaborane or pentaborane intoxication (Cordasco et al, 1962; Rozendaal, 1951).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea is one of the first symptoms seen.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA
    1) Nausea is often one of the first symptoms seen after boron hydride intoxications (Lowe & Freeman, 1957; Plunkett, 1976).
    B) EXCESSIVE SALIVATION
    1) CASE SERIES - Ten percent of patients seen by Cordasco et al (1962) reported hypersalivation, nausea and anorexia.
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ANOREXIA
    a) Anorexia was seen in animals exposed to 0.2 ppm for 6 months (Levinskas, 1958).

Hepatic

    3.9.1) SUMMARY
    A) Boron hydrides may cause fatty liver degeneration.
    3.9.2) CLINICAL EFFECTS
    A) TOXIC HEPATITIS
    1) Boron hydrides may cause fatty degeneration of the liver (Krackow, 1953; Lowe & Freeman, 1957) Yarbrough et al, 1985).
    B) LIVER ENZYMES ABNORMAL
    1) Serum transaminase levels may be increased in acute exposures to pentaborane (Yarbrough et al, 1985-1986).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) NEPHRITIS
    1) These substances may cause kidney damage, but it is not a frequently reported effect (Lowe & Freeman, 1957; Rozendaal, 1951). Since highest concentrations are reached during excretion, kidneys are more seriously damaged than other organs (HSDB , 2001).
    B) MYOGLOBINURIA
    1) Myoglobinuria has been reported in pentaborane exposures (Yarbrough et al, 1985-1986).
    C) SEMEN EXAM: ABNORMAL
    1) CASE REPORT - Absence of mature spermatozoa in the testicles was observed at autopsy in a dermal exposure to pentaborane resulting in death (Yarbrough et al, 1985-1986).

Acid-Base

    3.11.1) SUMMARY
    A) Acidosis may be seen, especially in relation to seizures.
    B) Metabolic acidosis without respiratory compensation may occur.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) Acidosis appears to be related to lactic acid secondary to seizure activity (Yarbrough et al, 1985).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DISCOLORATION OF SKIN
    1) Exposure to vapor may lead to reddening of the skin.

Musculoskeletal

    3.15.1) SUMMARY
    A) Rhabdomyolysis may occur.
    3.15.2) CLINICAL EFFECTS
    A) RHABDOMYOLYSIS
    1) CPK values over 3000 have been reported (Yarborough et al, 1985).

Reproductive

    3.20.1) SUMMARY
    A) Although toxic effects have been seen in experiments on animal spermatogenesis, similar effects have NOT been shown in humans exposed in industry.
    3.20.2) TERATOGENICITY
    A) SEMEN ABNORMAL
    1) Although toxic effects have been seen in experiments on animal spermatogenesis, similar effects have NOT been shown in humans exposed in industry (Lee et al, 1978).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS19287-45-7 (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
    B) IARC Carcinogenicity Ratings for CAS19624-22-7 (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
    C) IARC Carcinogenicity Ratings for CAS17702-41-9 (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

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Tissue pentaborane levels have not yet been established as useful. Liver and renal function tests may be indicated. Boron levels are elevated in blood and document exposures.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) The usefulness of pentaborane levels in tissues have not been established (Stokinger, 1982). Since some early studies found liver abnormalities, liver function tests may be indicated.
    2) NEUROTRANSMITTER METABOLITE VALUES - May be measured. Increased levels of homovanillic acid and 5-hydroxyindoleacetic acid may be increased following exposures to pentaborane (Silverman et al, 1985).
    4.1.4) OTHER
    A) OTHER
    1) CEREBROSPINAL FLUID
    a) Increased levels of homovanillic acid, 5-hydroxyindoleacetic acid, and 3-methoxy-4-hydroxyphenolglycol may be seen following exposures to pentaborane (Silverman et al, 1985).

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Numerous methods are available for detection of boron. In body tissues and fluids, spectrographic methods are generally employed (Alexander et al, 1951).
    2) Serum boron levels may be obtained by direct coupled Argon plasma emission spectrophotometry (Yarbrough et al, 1985-1986).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients with known mild inhalation exposure should be followed to detect psychiatric abnormalities (Silverman, 1985).

Monitoring

    A) Tissue pentaborane levels have not yet been established as useful. Liver and renal function tests may be indicated. Boron levels are elevated in blood and document exposures.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED -
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) ACTIVATED CHARCOAL -
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    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).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) 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).
    C) GASTRIC LAVAGE
    1) Ingestion of these products is unusual. Most exposures occur either by inhalation or dermally. Ingestions of diborane are extremely unlikely since it is a gas at room temperature. Pentaborane hydrolyzes in a few hours, and decaborane requires approximately 30 days for degradation in aqueous solutions, so decontamination may be of value with these 2 compounds.
    2) 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.
    3) 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.
    4) 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.
    5) 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).
    6) 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) SUPPORT
    1) Treatment is symptomatic and supportive provide oxygen therapy as indicated. Give chlorpromazine or meperidine as necessary (Stokinger, 1982).
    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, 2009; 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) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) 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)
    3) 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).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) 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).
    7) 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).
    D) MONITORING OF PATIENT
    1) Monitor kidney and liver functions.
    E) EXPERIMENTAL THERAPY
    1) Borane hydrides have a marked reducing potential, so methylene blue, a readily available oxidizing agent, was injected into rabbits for 2 days after a lethal dose of decaborane was administered. Methylene blue appeared to prevent brain and heart norepinephrine depletion and prolonged life (Merrit Jr, 1965). Human trials are lacking.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Rescuers must be protected from inhalation by self-contained breathing apparatuses and from dermal contact by gloves.
    B) 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.
    C) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    D) 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) Treatment is symptomatic and supportive evalute respiratory function and provide oxygen. Give chlorpromazine or meperidine as indicated (Stokinger, 1982).
    2) Monitor kidney and liver functions.
    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, 2009; 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) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) 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)
    3) 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).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) 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).
    7) 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).
    D) 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) These substances may be absorbed through the skin. Patients exposed dermally should dilute the area copiously with cool water. These substances may hydrolyze exothermically, so using small amounts of water may result in thermal burns. Dermal irritation may occur after exposure to gaseous boron hydride.
    B) OTHER
    1) A 3% aqueous ammonia solution has been used to complex the borane to facilitate removal from the skin following dermal exposure (Yarbrough et al, 1985-1986).
    6.9.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) A physician may need to examine the exposed area if irritation or pain persists after the area is washed.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) TLV - decaborane 0.05 ppm; diborane 0.1 ppm, pentaborane 0.005 ppm.
    B) DIBORANE - 1000 PPM for 1 minute may be lethal.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) No marked signs of decaborane poisoning were observed in rats following single oral dosages of 20 to 31.6 mg/kg. At amounts of 40 to 63 mg/kg signs included listlessness, limp and flaccid states, dyspnea, ataxia and convulsive tremors, which persisted for 14 hours (Svirbely, 1955).
    2) BOROHYDRIDE (SODIUM) - Six of ten animals died after dermal application of 400 mg of boron hydride. Results are not consistent and may depend on moisture being on the skin for absorption (Stokinger, 1982).
    3) DIBORANE - 1000 PPM for 1 minute may be lethal (HSDB , 2001).

Maximum Tolerated Exposure

    A) ROUTE OF EXPOSURE
    1) PENTABORANE can be detected by smell without causing symptoms. Inhaling only a little more than a detectable amount may lead to intoxication.
    2) DIBORANE - Mild symptoms may occur with inhalation of 25 PPM for 5 minutes (HSDB , 2001).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) DIBORANE - 1000 PPM for 1 minute may be lethal. Mild symptoms may occur with inhalation of 25 PPM for 5 minutes (HSDB , 2001).

Workplace Standards

    A) ACGIH TLV Values for CAS19287-45-7 (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) Diborane
    a) TLV:
    1) TLV-TWA: 0.1 ppm
    2) TLV-STEL:
    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): URT irr; headache
    d) Molecular Weight: 27.69
    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) ACGIH TLV Values for CAS19624-22-7 (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) Pentaborane
    a) TLV:
    1) TLV-TWA: 0.005 ppm
    2) TLV-STEL: 0.015 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): CNS convul; CNS impair
    d) Molecular Weight: 63.17
    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:

    C) ACGIH TLV Values for CAS17702-41-9 (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) Decaborane
    a) TLV:
    1) TLV-TWA: 0.05 ppm
    2) TLV-STEL: 0.15 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Skin
    3) Definitions:
    a) 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): CNS convul; cognitive decrement
    d) Molecular Weight: 122.31
    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:

    D) NIOSH REL and IDLH Values for CAS19287-45-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Diborane
    2) REL:
    a) TWA: 0.1 ppm (0.1 mg/m(3))
    b) STEL:
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 15 ppm
    b) Note(s): Not Listed

    E) NIOSH REL and IDLH Values for CAS19624-22-7 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Pentaborane
    2) REL:
    a) TWA: 0.005 ppm (0.01 mg/m(3))
    b) STEL: 0.015 ppm (0.03 mg/m(3))
    c) Ceiling:
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 1 ppm
    b) Note(s): Not Listed

    F) NIOSH REL and IDLH Values for CAS17702-41-9 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Decaborane
    2) REL:
    a) TWA: 0.3 mg/m(3) (0.05 ppm)
    b) STEL: 0.9 mg/m(3) (0.15 ppm)
    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: 15 mg/m3
    b) Note(s): Not Listed

    G) Carcinogenicity Ratings for CAS19287-45-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Diborane
    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: Diborane
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    H) Carcinogenicity Ratings for CAS19624-22-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Pentaborane
    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: Pentaborane
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    I) Carcinogenicity Ratings for CAS17702-41-9 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Decaborane
    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: Decaborane
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    J) OSHA PEL Values for CAS19287-45-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Diborane
    2) Table Z-1 for Diborane:
    a) 8-hour TWA:
    1) ppm: 0.1
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.1
    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

    K) OSHA PEL Values for CAS19624-22-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Pentaborane
    2) Table Z-1 for Pentaborane:
    a) 8-hour TWA:
    1) ppm: 0.005
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.01
    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

    L) OSHA PEL Values for CAS17702-41-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Decaborane
    2) Table Z-1 for Decaborane:
    a) 8-hour TWA:
    1) ppm: 0.05
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.3
    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: Yes
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) DECABORANE
    1) LD50- (INHALATION)MOUSE:
    a) 25.7 ppm for 48H (Stockinger, 1982)
    2) LD50- (ORAL)MOUSE:
    a) 40.9 mg/kg (Stockinger, 1982)
    3) LD50- (INHALATION)RAT:
    a) 95 ppm for 48H (Stockinger, 1982)
    4) LD50- (ORAL)RAT:
    a) 64.3 mg/kg (Stockinger, 1982)
    B) DIBORANE
    C) PENTABORANE
    1) LD50- (INHALATION)MOUSE:
    a) 170 ppm for 2M (Weeks et al, 1964)

Pharmacology Toxicology

Toxicologic Mechanism

    A) DECABORANE - lowers levels of norepinephrine, dopamine and serotonin in rat brain. An intermediate formed in the nonenzymatic hydrolysis of decaborane is an inhibitor of 3 decarboxylases and 1 transaminase which require pyridoxal phosphate for activation. Decaborane inhibits pyridoxal phosphate requiring enzymes (Naeger & Liebman, 1972).
    B) PENTABORANE - and decaborane have been shown in animal experiments to selectively react with nervous tissue and probably deplete the CNS of monoamine neurotransmitters (Silverman et al, 1985).
    C) DERMAL REACTIONS - exothermic reactions with boron hydrides and water may cause heat injury with the rate of reaction being sufficiently rapid to dehydrate tissues. Pentaborane reaction with water is the slowest of the boron hydrides (Yarbrough et al, 1985-1986).

Physicochemical

Physical Characteristics

    A) DIBORANE: Nauseating odor, detectable in man at 2-4 mg/m(3); colorless gas.
    B) PENTABORANE: Pungent odor, detectable at 2.5 mg/m(3); colorless liquid.
    C) DECABORANE: Detectable at 0.3 mg/m(3); white crystalline substance.

Molecular Weight

    A) DECABORANE: 122.31
    B) DIBORANE: 27.67
    C) PENTABORANE: 63.17

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