MOBILE VIEW  | 

GALLIUM TRICHLORIDE

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Gallium trichloride is the trichloride salt of trivalent gallium prepared by the action of either hydrogen chloride or chlorine on the metal (Budavari, 1996). Gallium compounds are used in the manufacture of electronic instruments, semiconductors, alloys, and lubricants (ITI, 1995; (Plunkett, 1976). Gallium metal is not used commercially (ITI, 1995).

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) Cl3-Ga

Available Forms Sources

    A) FORMS
    1) Gallium trichloride is the trichloride salt of trivalent gallium prepared by the action of either hydrogen chloride or chlorine on the metal (Budavari, 1996).
    B) USES
    1) Gallium compounds are used in the manufacture of electronic instruments, semiconductors, alloys, and lubricants (ITI, 1995; (Plunkett, 1976). Gallium metal is not used commercially (ITI, 1995).

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Human gallium trichloride poisonings are rare. A single patient exposed to fumes of the similar compound, gallium trifluoride, developed a petechial rash and radial nerve palsy. A college student working in a laboratory who had an acute dermal exposure and chronic inhalation and dermal exposure to gallium chloride-containing complexes developed allergic hypersensitivity dermatitis, and approximately one-month later developed systemic effects including dizziness, shortness of breath, supraventricular tachycardia, palpitations, tremors and severe headache. She gradually improved, but long term follow-up was not reported.
    B) Experimental animals have developed lung consolidation when exposed to gallium trichloride vapor. Renal injury similar to that produced by mercury was noted in experimental animals given various gallium salts, but gallium trifluoride may lack hemato- and renal toxicity.
    0.2.4) HEENT
    A) MUCOSAL IRRITATION: Liberated chlorine vapors can cause irritation of the nose and throat.
    0.2.6) RESPIRATORY
    A) RESPIRATORY TRACT IRRITATION: Chlorine vapors released from gallium trichloride can cause wheezing, coughing, dyspnea, a sense of suffocation, burning chest pain, and, in more severe cases, cyanosis, laryngeal edema, respiratory arrest, or delayed pulmonary edema.
    0.2.7) NEUROLOGIC
    A) Peripheral neuropathy has been observed in a single patient with exposure to the similar compound, gallium trifluoride.
    0.2.8) GASTROINTESTINAL
    A) Anorexia, nausea, and vomiting might occur.
    0.2.10) GENITOURINARY
    A) Various gallium salts produce renal failure in experimental animals, but gallium trichloride may lack this effect.
    0.2.11) ACID-BASE
    A) Acidosis may occur.
    0.2.12) FLUID-ELECTROLYTE
    A) Decreased serum sodium and potassium levels may occur.
    0.2.13) HEMATOLOGIC
    A) While administration of some gallium salts to experimental animals has caused hematotoxicity, gallium trichloride may lack this effect.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Laboratory Monitoring

    A) Monitor complete blood count, platelet count, serum electrolytes, renal function tests, and urinalysis in patients with significant exposure.
    B) Monitor arterial blood gases or pulse oximetry and chest x-ray in patients with significant inhalation exposure.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) 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.
    C) Treat vomiting symptomatically. Replace fluids and electrolytes if indicated.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) The minimum lethal human exposure to gallium trichloride has not been established. ADULT: A young adult with chronic inhalation and dermal contact with gallium chloride-containing complexes developed allergic hypersensitivity dermatitis after a splash exposure to her face, and approximately one-month later developed systemic effects including shortness of breath, supraventricular tachycardia, palpitations, tremors and severe headache. She gradually improved, but long-term follow-up was not reported. ANIMAL DATA: Rats fed gallium trichloride for 26 weeks at doses of 10 to 1000 ppm developed no toxicity. Rats inhaling nebulized solutions of gallium trichloride at concentrations of 25 to 125 mg/m(3) for 0.5 to 4 hours developed lung consolidation.

Summary Of Exposure

    A) Human gallium trichloride poisonings are rare. A single patient exposed to fumes of the similar compound, gallium trifluoride, developed a petechial rash and radial nerve palsy. A college student working in a laboratory who had an acute dermal exposure and chronic inhalation and dermal exposure to gallium chloride-containing complexes developed allergic hypersensitivity dermatitis, and approximately one-month later developed systemic effects including dizziness, shortness of breath, supraventricular tachycardia, palpitations, tremors and severe headache. She gradually improved, but long term follow-up was not reported.
    B) Experimental animals have developed lung consolidation when exposed to gallium trichloride vapor. Renal injury similar to that produced by mercury was noted in experimental animals given various gallium salts, but gallium trifluoride may lack hemato- and renal toxicity.

Heent

    3.4.1) SUMMARY
    A) MUCOSAL IRRITATION: Liberated chlorine vapors can cause irritation of the nose and throat.
    3.4.3) EYES
    A) PHOTOPHOBIA and blindness were found in rats administered lethal doses of various gallium salts (Grant, 1993). Rabbits, dogs, and goats did not develop these effects (Grant, 1993). No human cases of photophobia or blindness have been reported following exposure to gallium salts.
    B) A gallium trichloride ammonia-neutralized gelatinous suspension was not injurious to rabbit eyes (Grant, 1993).
    3.4.5) NOSE
    A) MUCOSAL IRRITATION: Although not reported in human exposures, chlorine liberated during thermal decomposition of gallium trichloride (Lewis, 1996) would be expected to cause irritation of the mucosa of the nose and throat.
    3.4.6) THROAT
    A) MUCOSAL IRRITATION: Although not reported in human exposures, chlorine liberated during thermal decomposition of gallium trichloride (Lewis, 1996) would be expected to cause irritation of the mucosa of the nose and throat.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) SUPRAVENTRICULAR TACHYCARDIA
    1) WITH POISONING/EXPOSURE
    a) A 20-year-old college student working in a laboratory and washing out a flask that contained remnants of gallium chloride-containing complexes when some splashed in her left eye resulting in allergic hypersensitivity dermatitis. Initially, she noticed only dermatologic events. Two weeks after the initial event, the patient noticed systemic effects including dizziness, shortness of breath, increased heart rate, and severe headaches. After a complete exam, it was concluded she may have had ongoing dermal and inhalation exposure. She developed episodes of tachycardia and an erratic pulse rates from 65 to 156 beats/min. She was started on atenolol to treat supraventricular tachycardia and was gradually improving. Long-term follow-up was not reported (Ivanoff et al, 2012).

Respiratory

    3.6.1) SUMMARY
    A) RESPIRATORY TRACT IRRITATION: Chlorine vapors released from gallium trichloride can cause wheezing, coughing, dyspnea, a sense of suffocation, burning chest pain, and, in more severe cases, cyanosis, laryngeal edema, respiratory arrest, or delayed pulmonary edema.
    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) Chlorine liberated from gallium trichloride during thermal decomposition (Lewis, 1996) could produce wheezing, coughing, dyspnea, burning chest pain, or a sense of suffocation (Hedges & Morrissey, 1979).
    B) APNEA
    1) Chlorine liberated from gallium trichloride during thermal decomposition (Lewis, 1996) could produce laryngeal spasm, cyanosis, or respiratory arrest in more serious cases (Lawson, 1981; Hedges & Morrissey, 1979).
    C) ACUTE LUNG INJURY
    1) Chlorine liberated from gallium trichloride during thermal decomposition (Lewis, 1996) could produce noncardiogenic pulmonary edema that may be delayed in onset for about 24 hours (Kaufman & Burkons, 1971).

Neurologic

    3.7.1) SUMMARY
    A) Peripheral neuropathy has been observed in a single patient with exposure to the similar compound, gallium trifluoride.
    3.7.2) CLINICAL EFFECTS
    A) SECONDARY PERIPHERAL NEUROPATHY
    1) A single patient who inhaled fumes of the similar compound, gallium trifluoride, developed mild radial nerve palsy with pain and weakness which resolved over about 3 months (Clayton & Clayton, 1994). This effect has not been reported with gallium trichloride exposure.
    B) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Severe headaches were reported in a college study working with gallium halides with chalcogenide complexes in a synthetic chemical research lab following suspected acute-on-chronic inhalation and dermal contact. Initially, she noticed only dermatologic events. Two weeks after the initial event, the patient developed systemic effects including dizziness, shortness of breath, increased heart rate, and severe headaches. She had ongoing symptoms that appeared to gradually improve; however, long-term follow-up was not reported (Ivanoff et al, 2012).
    C) TREMOR
    1) WITH POISONING/EXPOSURE
    a) Tremor in the lower extremities was reported in a college student working with gallium halides with chalcogenide complexes in a synthetic chemical research lab following suspected acute-on-chronic inhalation and dermal contact. She had episodes of sporadic tremors in the one or both legs that lasted between 15 to 30 minutes occurring daily or once or twice a week. One month later she was improving, but continued to complain of tremors. Long-term follow-up was not reported (Ivanoff et al, 2012).

Gastrointestinal

    3.8.1) SUMMARY
    A) Anorexia, nausea, and vomiting might occur.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) Anorexia, nausea, and vomiting have been noted in humans given a mixture of gallium-72 and stable gallium (Clayton & Clayton, 1994). These effects have not been reported in humans exposed specifically to gallium trichloride.
    2) Nausea was reported in a college study working with gallium halides with chalcogenide complexes in a synthetic chemical research lab following suspected acute-on-chronic inhalation and dermal contact. Initially, she noticed only dermatologic events. Two weeks after the initial event, the patient developed systemic effects including dizziness, nausea, shortness of breath, increased heart rate, and severe headaches. She had ongoing symptoms that appeared to gradually improve; however, long-term follow-up was not reported (Ivanoff et al, 2012).

Genitourinary

    3.10.1) SUMMARY
    A) Various gallium salts produce renal failure in experimental animals, but gallium trichloride may lack this effect.
    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) While administration of some gallium salts to experimental animals has resulted in renal toxicity, gallium trichloride may lack this effect (Domingo & Corbella, 1991). Nephrotoxicity has not been reported in humans exposed to gallium metal or gallium salts including gallium trichloride.

Acid-Base

    3.11.1) SUMMARY
    A) Acidosis may occur.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) In rabbits administered gallium citrate, uncompensated acidosis was observed (Clayton & Clayton, 1982).

Hematologic

    3.13.1) SUMMARY
    A) While administration of some gallium salts to experimental animals has caused hematotoxicity, gallium trichloride may lack this effect.
    3.13.2) CLINICAL EFFECTS
    A) MYELOSUPPRESSION
    1) While administration of some gallium salts to experimental animals has caused hematotoxicity, gallium trichloride may lack this effect (Domingo & Corbella, 1991).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) A 20-year-old college student working in a laboratory was washing out a flask that contained remnants of gallium chloride-containing complexes and some splashed in her left eye resulting in allergic hypersensitivity dermatitis. Initially, no burning or stinging occurred, so no first aid measures were done. Two days after the event, she reported darkening and bruising of the skin under her eyes followed by some swelling of the skin and tongue, which was followed by erythema and swelling. Two weeks after the initial event, the patient noticed systemic effects including dizziness, shortness of breath, increased heart rate, and severe headaches. Eczema-like lesions developed on the back of her ears and a petechial rash on her arm also developed. Her dermatologic symptoms gradually improved once she was removed from the setting (Ivanoff et al, 2012).

Reproductive

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

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS13450-90-3 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic or mutagenic potential of this agent.

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor complete blood count, platelet count, serum electrolytes, renal function tests, and urinalysis in patients with significant exposure.
    B) Monitor arterial blood gases or pulse oximetry and chest x-ray in patients with significant inhalation exposure.
    4.1.2) SERUM/BLOOD
    A) HEMATOLOGIC
    1) Monitor complete blood count including platelet count.
    B) BLOOD/SERUM CHEMISTRY
    1) Obtain serum electrolytes, and renal function tests in patients with significant exposure.
    C) ACID/BASE
    1) Patients with inhalation exposure to chlorine liberated from gallium trichloride during thermal decomposition (Lewis, 1996) should have baseline arterial blood gases or pulse oximetry.
    4.1.3) URINE
    A) URINALYSIS
    1) Monitor urinalysis in patients with significant exposure.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Patients with inhalation exposure to chlorine liberated from gallium trichloride during thermal decomposition (Lewis, 1996) should have a baseline chest x-ray.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Measurement of gallium levels is of unknown value in assessing patients with gallium trichloride exposure.

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor complete blood count, platelet count, serum electrolytes, renal function tests, and urinalysis in patients with significant exposure.
    B) Monitor arterial blood gases or pulse oximetry and chest x-ray in patients with significant inhalation exposure.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    B) ACTIVATED CHARCOAL/CATHARTIC
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Vomiting should be treated symptomatically. Replacement of fluids and electrolytes should be done if indicated.
    B) MONITORING OF PATIENT
    1) Monitor complete blood count, platelet count, serum electrolytes, and urinalysis.
    C) GENERAL TREATMENT
    1) DIMERCAPROL/AMMONIUM CHLORIDE - NOT RECOMMENDED for the treatment of gallium trichloride poisoning.

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) OXYGEN
    1) Administer 100% supplemental humidified oxygen with assisted ventilation if required.
    B) MONITORING OF PATIENT
    1) Monitor arterial blood gases or pulse oximetry and chest x-ray in patients with significant inhalation exposure or respiratory tract irritation.
    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) 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).

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) HEMODIALYSIS/HEMOPERFUSION - Neither hemodialysis nor hemoperfusion have been evaluated for removal of gallium trichloride.

Summary

    A) The minimum lethal human exposure to gallium trichloride has not been established. ADULT: A young adult with chronic inhalation and dermal contact with gallium chloride-containing complexes developed allergic hypersensitivity dermatitis after a splash exposure to her face, and approximately one-month later developed systemic effects including shortness of breath, supraventricular tachycardia, palpitations, tremors and severe headache. She gradually improved, but long-term follow-up was not reported. ANIMAL DATA: Rats fed gallium trichloride for 26 weeks at doses of 10 to 1000 ppm developed no toxicity. Rats inhaling nebulized solutions of gallium trichloride at concentrations of 25 to 125 mg/m(3) for 0.5 to 4 hours developed lung consolidation.

Minimum Lethal Exposure

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

Maximum Tolerated Exposure

    A) SUMMARY
    1) A college student working in a laboratory with chronic inhalation and dermal contact with gallium chloride-containing complexes developed allergic hypersensitivity dermatitis after a splash exposure to her face, and approximately one-month later developed systemic effects including dizziness, shortness of breath, supraventricular tachycardia, palpitations, tremors and severe headache. She gradually improved, but long-term follow-up was not reported (Ivanoff et al, 2012).
    2) The only human toxicity from gallium salts reported was in a woman exposed to gallium trifluoride fumes, but the airborne concentration was not noted (Clayton & Clayton, 1994).
    B) ANIMAL DATA
    1) Rats fed gallium trichloride for 26 weeks at doses of 10 to 1000 ppm developed no toxicity (Clayton & Clayton, 1994).
    2) Rats inhaling nebulized solutions of gallium trichloride at concentrations of 25 to 125 mg/m(3) for 0.5 to 4 hours developed lung consolidation, but not more than when sodium chloride solutions acidified to the same degree were administered (Clayton & Clayton, 1994).

Workplace Standards

    A) ACGIH TLV Values for CAS13450-90-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS13450-90-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS13450-90-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS13450-90-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1999
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 36975 mcg/kg
    2) LD50- (SUBCUTANEOUS)RAT:
    a) 306 mg/kg

Toxicologic Mechanism

    A) Gallium trichloride can liberate chlorine vapors under certain conditions, such as when heated to decomposition (Lewis, 1996). Such vapors would be predicted to produce direct conjunctival and respiratory tract mucous membrane irritation.

Physical Characteristics

    A) Gallium trichloride is a colorless, needle-like solid (Lewis, 1996; (Budavari, 1996).

Molecular Weight

    A) 176.07 (Lewis, 1996)

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
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