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BORON TRIFLUORIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Boron trifluoride is a colorless, reactive gas used as a catalyst in chemical reactions, a fumigant and a magnesium solder flux (Finkel, 1983; Hathaway et al, 1996).

Specific Substances

    1) Boron Fluoride
    2) Borane, Trifluoro-
    3) Trifluoroboron
    4) Tribluoroborane
    5) CAS 7637-07-2
    6) BORON TRIFLUORIDE, COMPRESSED
    1.2.1) MOLECULAR FORMULA
    1) B-F3

Available Forms Sources

    A) FORMS
    1) It is formulated as a pure grade (99%), 10% in methanol, 99.5% boron trifluoride hydrate and 95% boron trifluoride dihydrate (HSDB, 2004).
    B) USES
    1) Boron trifluoride it is used primarily as an acid catalyst for esterification, nitrations, oxidations, reductions, and halogenations (HSDB, 2004).
    2) It is used as a catalyst for alkylation of aromatic compounds; as a catalyst in polymer production of phenolic and epoxy resins; as a catalyst in the synthesis on boron-containing organic compounds; and for the separation of boron isotopes in nuclear technology (Budavari, 1989; HSDB , 1992; ITI, 1988).
    3) It also is used as a fire retardant and anti-oxidant to protect molten magnesium in the magnesium industry, and as a flux for gas brazing magnesium and soldering silver (Budavari, 1996; HSDB, 2004; ITI, 1995).
    4) Boron trifluoride is most often encountered as an industrial catalyst, but is also used as a fumigant, in ionization chambers to count neutrons and in soldering and protecting magnesium (ITI, 1988).

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 trifluoride is a severe ocular and pulmonary system irritant. Dermal irritation and/or burns may occur.
    B) It reacts in moist air to form boric acid, hydrogen fluoride, fluoroboric acid, and other products. Thus the respiratory passage (which contains moist air) may produce these products which would be free to react with tissue.
    C) SYSTEMIC EFFECTS - BORON affects the central nervous system, leading to depressed blood pressure, persistent vomiting, and diarrhea.
    D) INHALATION EXPOSURE - Acute exposure to boron trifluoride gas has resulted in loss of consciousness and hypoxemia.
    E) DERMAL EXPOSURE - Boron trifluoride can burn the skin, and contact with the liquid may cause frostbite. It is absorbed through the skin.
    0.2.4) HEENT
    A) Teeth: Rats exposed to 15 to 100 ppm developed hypoplasia of the teeth and excessive fluoride deposition.
    B) Eye irritation may occur from exposure to this gas.
    C) Nose bleed and nasal dryness has been reported in humans.
    0.2.6) RESPIRATORY
    A) Acute inhalations have resulted in hypoxemia.
    B) Pulmonary irritation is expected with inhalation. Pneumonitis has been reported in animals. Long term effects in humans are unclear. Physical examination of exposed workers appear to show some decrease in pulmonary function without positive x-ray findings.
    0.2.7) NEUROLOGIC
    A) Acute exposure to boron trifluoride gas has resulted in rapid loss of consciousness.
    0.2.10) GENITOURINARY
    A) Renal tubular degeneration has been reported in fatally poisoned animals.
    0.2.12) FLUID-ELECTROLYTE
    A) Hypophosphatemia, hypocalcemic and elevated fluoride levels have developed in animal studies.
    0.2.14) DERMATOLOGIC
    A) Skin irritation is expected on contact. When soaked into a cotton ball and placed on the skin for 1 to 2 days, boron trifluoride left a HF type burn.

Laboratory Monitoring

    A) Obtain at least hourly serum electrolytes including serial total or ionized calcium, magnesium, and potassium levels. Total calcium may not reflect true hypocalcemia, but usually has a more rapid turnaround. Therapy should be directed toward signs and symptoms of toxicity. Serum fluoride level may be used to confirm HF exposure. Obtain ABGs and chest X-ray in symptomatic patients.
    B) Obtain serial ECGs looking for signs of hypocalcemia (prolonged QTc interval) and hyperkalemia (peaked T waves). Institute continuous cardiac monitoring.

Treatment Overview

    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) 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.
    C) OBSERVATION - Carefully observe patients with inhalation exposure for the development of abnormal systemic signs or symptoms and administer symptomatic treatment as necessary. Signs and symptoms of pulmonary edema may be delayed for 24 to 72 hours in some cases.
    D) INITIAL TREATMENT - Mild inhalational symptoms may be treated with 2.5% calcium gluconate nebulization.
    0.4.4) EYE EXPOSURE
    A) Irrigate promptly with crystalloid solution. Carefully evaluate for eye damage; exposure to dilute solutions may result in delayed signs and symptoms of ocular damage. The patient should be evaluated by an ophthalmologist following appropriate decontamination.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) There is no specific antidote. Treatment is directed at supporting respirations and limiting potential caustic damage.
    2) 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).
    3) Dermal absorption is unlikely; however, in the event dermal absorption is suspected, refer to the management on HYDROFLUORIC ACID for additional information.

Range Of Toxicity

    A) The minimum lethal exposure has not been established for humans.
    B) Levels of 12 ppm and below in a general work area have been reported without comment on adverse effects.
    C) Rats exposed to 17 mg/m(3) developed renal toxicity while those exposed to 6 mg/m(3) did not produce toxic symptoms.

Clinical Effects

Summary Of Exposure

    A) Boron trifluoride is a severe ocular and pulmonary system irritant. Dermal irritation and/or burns may occur.
    B) It reacts in moist air to form boric acid, hydrogen fluoride, fluoroboric acid, and other products. Thus the respiratory passage (which contains moist air) may produce these products which would be free to react with tissue.
    C) SYSTEMIC EFFECTS - BORON affects the central nervous system, leading to depressed blood pressure, persistent vomiting, and diarrhea.
    D) INHALATION EXPOSURE - Acute exposure to boron trifluoride gas has resulted in loss of consciousness and hypoxemia.
    E) DERMAL EXPOSURE - Boron trifluoride can burn the skin, and contact with the liquid may cause frostbite. It is absorbed through the skin.

Heent

    3.4.1) SUMMARY
    A) Teeth: Rats exposed to 15 to 100 ppm developed hypoplasia of the teeth and excessive fluoride deposition.
    B) Eye irritation may occur from exposure to this gas.
    C) Nose bleed and nasal dryness has been reported in humans.
    3.4.2) HEAD
    A) Rats exposed to 42 mg/m(3) (15 ppm) for 30 days developed hypoplasia of the teeth and at 100 ppm, fluoride deposition 25 times the normal rate. Dental fluorosis was seen in 3 other animal species repeatedly given 12.8, 7.7 or 3 ppm for periods ranging up to 6 months (Torkelson et al, 1961).
    3.4.3) EYES
    A) Boron trifluoride is a severe eye irritant (Hathaway et al, 1996). Rats exposed chronically developed excessive lacrimation (Rusch et al, 1986).
    3.4.5) NOSE
    A) EPISTAXIS and nasal dryness occurred in chronically exposed workers(HSDB, 2004).

Respiratory

    3.6.1) SUMMARY
    A) Acute inhalations have resulted in hypoxemia.
    B) Pulmonary irritation is expected with inhalation. Pneumonitis has been reported in animals. Long term effects in humans are unclear. Physical examination of exposed workers appear to show some decrease in pulmonary function without positive x-ray findings.
    3.6.2) CLINICAL EFFECTS
    A) HYPOXEMIA
    1) CASE REPORT - A man, his pregnant wife, and son were overcome by fumes of boron trifluoride after inadvertently knocking the valve from a cylinder of the gas. Lab findings included hypoxemia with minimal acidosis. Urinary fluoride levels were not elevated. Serum calcium levels were not depressed(Stewart & Waisberg, 1998).
    B) IRRITATION SYMPTOM
    1) Irritation of the pulmonary system is expected with inhalation (Harbison, 1998). Pneumonitis occurred in animals exposed to 42 mg/m(3) (15 ppm) for an unspecified period of time (Kasparov, 1974). Mice exposed to this concentration had a 19% mortality rate due to pulmonary damage.
    2) It reacts in moist air to form boric acid, hydrogen fluoride, fluoroboric acid, and other products (ACGIH, 2001). Thus respiratory passage (which contain moist air) may produce these products which would be free to react with tissue.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) IRRITATION
    a) In studies with rats and guinea pigs, acute and chronic exposures produced extensive respiratory tract irritation leading to eventual respiratory failure and kidney damage (Budavari, 1989; HSDB, 2004).

Neurologic

    3.7.1) SUMMARY
    A) Acute exposure to boron trifluoride gas has resulted in rapid loss of consciousness.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) CASE REPORT - A man, his pregnant wife, and son were overcome by boron trifluoride gas after inadvertently knocking the valve from a cylinder of the gas. The woman was unconscious for 36 hours and recovered slowly. Measured urinary fluoride levels were not elevated in any of the 3 patients and all recovered uneventfully (Stewart & Waisberg, 1998).

Genitourinary

    3.10.1) SUMMARY
    A) Renal tubular degeneration has been reported in fatally poisoned animals.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RENAL TUBULAR DISORDER
    a) Renal tubule degeneration occurred in animals exposed to 42 mg/m(3) (15 ppm) for an unspecified period of time (Kasparov, 1974).
    2) RENAL TUBULAR NECROSIS
    a) RATS - Necrosis and pyknosis of the proximal tubular epithelium were reported in rats exposed to 180 mg/m(3) (Kasparov, 1974).

Dermatologic

    3.14.1) SUMMARY
    A) Skin irritation is expected on contact. When soaked into a cotton ball and placed on the skin for 1 to 2 days, boron trifluoride left a HF type burn.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) Skin irritation is expected on contact . When soaked into a cotton ball and placed on the skin for 1 to 2 days, an acid-like burn, similar to, but less severe and not as penetrating as a hydrogen fluoride acid burn, resulted (Clayton & Clayton, 1982; Hathaway et al, 1996).
    B) FROSTBITE
    1) Contact with gas or liquified gas may cause frostbite(HSDB, 2004).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7637-07-2 (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) Obtain at least hourly serum electrolytes including serial total or ionized calcium, magnesium, and potassium levels. Total calcium may not reflect true hypocalcemia, but usually has a more rapid turnaround. Therapy should be directed toward signs and symptoms of toxicity. Serum fluoride level may be used to confirm HF exposure. Obtain ABGs and chest X-ray in symptomatic patients.
    B) Obtain serial ECGs looking for signs of hypocalcemia (prolonged QTc interval) and hyperkalemia (peaked T waves). Institute continuous cardiac monitoring.
    4.1.2) SERUM/BLOOD
    A) TOXICITY
    1) Toxic serum levels have not been established.
    2) Patients chronically exposed may have elevated fluoride levels or diminished phosphorous or calcium levels (Rusch et al, 1986).
    4.1.4) OTHER
    A) OTHER
    1) ECG
    a) Obtain serial ECGs, looking for signs of hypocalcemia (prolonged QTc interval) and hyperkalemia (peaked T waves). Institute continuous cardiac monitoring.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) A chest x-ray may be indicated in exposed individuals (Proctor et al, 1988).

Methods

    A) OTHER
    1) No methods for determining boron triflouride in biological specimens is available in normal hospital laboratories. Urinary fluoride levels can be measured.
    2) AIR - A method for determining boron trifluoride in air utilizes a collection by an impinger preceded by a filter followed by colorimetric analysis (NIOSH, 1977).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Obtain at least hourly serum electrolytes including serial total or ionized calcium, magnesium, and potassium levels. Total calcium may not reflect true hypocalcemia, but usually has a more rapid turnaround. Therapy should be directed toward signs and symptoms of toxicity. Serum fluoride level may be used to confirm HF exposure. Obtain ABGs and chest X-ray in symptomatic patients.
    B) Obtain serial ECGs looking for signs of hypocalcemia (prolonged QTc interval) and hyperkalemia (peaked T waves). Institute continuous cardiac monitoring.

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) OBSERVATION REGIMES
    1) If inhaled, observe in a medical facility for 72 hours for delayed onset of severe pulmonary edema (Proctor et al, 1988).
    B) MONITORING OF PATIENT
    1) Chest x-ray should be obtained.
    2) Should pulmonary complications occur, consider pulse oximetry, arterial blood gas analysis, administration of oxygen by mask or cannula, mechanical ventilation, and PEEP.
    3) Monitor serum calcium, magnesium and potassium.
    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) CALCIUM
    1) Administration of nebulized CALCIUM GLUCONATE 2.5 percent has been recommended (Trevino et al, 2001; Trevino et al, 1983).
    2) CASE SERIES - Lee et al (1992) report the use of calcium gluconate nebulization in 13 workers exposed to 150 to 200 parts per million HF gas for 2 minutes. Patients were treated quickly after exposure, and only minor upper respiratory tract irritation was noted. All patients tolerated the treatment without adverse effects. None developed delayed pulmonary edema or any permanent sequelae.
    3) CASE REPORT - Following a one minute exposure to fumes from an anhydrous HF spill in an enclosed area, a male worker experienced immediate upper airway irritation and dyspnea. Three nebulized calcium gluconate treatments were immediately administered with resolution of respiratory complaints. The authors suggested this treatment may have prevented pulmonary injury (Boyer et al, 2000).
    4) CASE SERIES - After 5 workers were exposed to inhalational HF fumes, they presented to the ED 4 hours later. Burning of the mouth and tongue were reported in 3 of the patients and one complained of nausea and abdominal cramps. All patients were administered a 2.5% calcium gluconate nebulized treatment. All symptoms resolved by the end of the treatment. The authors recommend calcium gluconate nebulization therapy for mild symptoms of HF inhalation (Trevino et al, 2001).

Eye Exposure

    6.8.1) DECONTAMINATION
    A) Irrigate promptly with crystalloid solution. Carefully evaluate for eye damage; exposure to dilute solutions may result in delayed signs and symptoms of ocular damage. The patient should be evaluated by an ophthalmologist following appropriate decontamination.

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).
    2) Due to its corrosivity and toxicity, safety showers must be provided for immediate, thorough flushing/washing where boron trifluoride will be handled (HSDB, 2004).
    6.9.2) TREATMENT
    A) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    4) Dermal absorption is unlikely; however, in the event that dermal absorption is suspected, refer to the HYDROFLUORIC ACID management for additional information.

Range Of Toxicity

Summary

    A) The minimum lethal exposure has not been established for humans.
    B) Levels of 12 ppm and below in a general work area have been reported without comment on adverse effects.
    C) Rats exposed to 17 mg/m(3) developed renal toxicity while those exposed to 6 mg/m(3) did not produce toxic symptoms.

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) HUMAN - Levels of 12 parts per million and below in a general work area have been reported, without comment of adverse effects (Clayton & Clayton, 1982).
    B) ANIMAL DATA
    1) Rats exposed to 17 milligrams/cubic meter of boron fluoride 16 hours/day, 5 days/week for 13 weeks, developed renal toxicity (Rusch et al, 1985).
    2) Rats exposed to 6 milligrams/cubic meter as above did not produce a toxic response other than elevated fluoride levels (Rusch et al, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS7637-07-2 (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) Boron trifluoride
    a) TLV:
    1) TLV-TWA:
    2) TLV-STEL:
    3) TLV-Ceiling: 1 ppm
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): LRT irr; pneumonitis
    d) Molecular Weight: 67.82
    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) Under Study
    1) Boron trifluoride
    a) TLV:
    1) TLV-TWA:
    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):
    d) Molecular Weight:
    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 CAS7637-07-2 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Boron trifluoride
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 1 ppm (3 mg/m(3))
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 25 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7637-07-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Boron trifluoride
    2) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Boron trifluoride
    3) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    4) 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
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Boron trifluoride
    6) MAK (DFG, 2002): Not Listed
    7) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7637-07-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Boron trifluoride
    2) Table Z-1 for Boron trifluoride:
    a) 8-hour TWA:
    1) ppm: 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: 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: (C) - An employee's exposure to this substance shall at no time exceed the exposure limit given.
    4) Skin Designation: No
    5) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: HSDB, 2004; RTECS, 2004; Lewis, 2000

Pharmacology Toxicology

Toxicologic Mechanism

    A) Boron trifluoride's primary toxic action is acidic irritation due to slow hydrolysis to form boric acid, hydrogen fluoride, fluoroboric acids, and other products (ACGIH, 1986).

Physicochemical

Physical Characteristics

    A) Boron trifluoride is a colorless gas with a pungent odor. It has also been described as having a pleasant, acidic odor at concentrations as low as 1.5 ppm; becoming an irritating and suffocating gas at higher concentrations(Clayton & Clayton, 1994; HSDB, 2004).

Ph

    A) Boron trifluoride is a strong Lewis acid (Budavari, 1996) .

Molecular Weight

    A) 67.81 (Budavari, 1996)

Other

    A) ODOR THRESHOLD
    1) The reported odor threshold was 4.50 mg/m(3); 3 ppm is also listed; neither serve as an adequate warning (Hathaway et al, 1996; HSDB, 2004).

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