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VANADIUM COMPOUNDS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Vanadium is ubiquitous in the environment. It is concentrated in fatty and oily foods, such as milk, food oils, and also in seafood, cereals, and vegetables. Drinking water may contain trace amounts (HSBD, 1999).
    B) These compounds are used as a catalysts in reactions involving the oxidation of sulfur dioxide, oxides of nitrogen and others. They are also found in fuel oils, yellow glass, special steels, and photographic developers.
    1) IMPLANTS: Dental and orthopedic implants may contain vanadium.

Specific Substances

    A) CONSTITUENTS OF THE GROUP
    1) Vanadium Metal
    2) Vanadium pentoxide
    3) Vanadium trioxide
    4) Vanadium tetraoxide
    5) Vanadium carbide
    6) Vanadium oxydichloride
    7) Vanadium oxytrichloride
    8) Vanadium sulfate
    9) Ammonium metavanadate
    10) Sodium metavandate
    11) Organo vanadium compounds
    12) Vanadin-tris (acetyl-acetonate)
    13) Vanadin-oxy-bis (acetyl-acetonate)
    14) Vanadyl ethylate
    15) Vanadyl n-propylate
    16) Vanadyl isopropylate
    17) Vanadyl n-butylate
    18) Vanadyl isobutylate
    19) Vanadic acid anydride
    20) Vanadium dust and fume
    21) Vanadium oxide (V203)
    22) Vanadium pentoxid (German)
    23) Vanadium pentoxyde (Dutch)

Available Forms Sources

    A) SOURCES
    1) Vanadium is ubiquitous in the environment. It is concentrated in fatty and oily foods, such as milk, food oils, and also in seafood, cereals, and vegetables. Drinking water may contain trace amounts (HSBD, 1999).
    B) USES
    1) Vanadium is used as a target material for x-rays (HSBD, 1999).
    2) CATALYST: Vanadium compounds are used in reactions of sulfur dioxide, oxides of nitrogen, synthetic rubber, and others.
    3) Vanadium compounds are used in the manufacture of yellow glass.
    4) These agents are constituent of fuel oils, photographic developers, special steels, coating for welding electrodes, paint, dyes, and insecticides.
    5) At the end of the 19th century, vanadium compounds were popular for treatment of tuberculosis, diabetes, syphilis, and chlorosis. Doses usually range from 1 to 8 mg. They are no longer used.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) GENERAL: Vanadium metal has low toxicity; pentavalent forms and vanadates are the most toxic. Vanadium salt toxicity is high parenterally, low orally, and intermediate via inhalation.
    B) INHALATION: If inhaled (as dust) the primary symptoms are respiratory. Symptoms may persist up to 2 weeks after exposure, but few if any systemic symptoms have been seen and the prognosis is favorable. The smaller the particle size the greater the pulmonary toxicity. Therefore the fumes are more toxic than the dust.
    1) RESPIRATORY TRACT IRRITATION: Atrophic rhinitis, pharyngitis, chronic bronchitis, and diffuse pulmonary fibrosis have been associated with inhalational exposure to vanadium.
    0.2.4) HEENT
    A) Dry mouth, rhinitis, epistaxis, tracheitis, metallic taste, green tongue, and irritated eyes have been reported in workers exposed to vanadium compound dust.
    0.2.5) CARDIOVASCULAR
    A) One of the primary effects of vanadium is peripheral vasoconstriction of lungs, spleen, kidneys, and intestines. Effects are local.
    B) Dysrhythmias and bradycardia may occur after prolonged exposure.
    0.2.6) RESPIRATORY
    A) Pulmonary irritation leading to pulmonary edema is a possible effect with high concentrations. Occupational asthma has been reported.
    B) Atrophic rhinitis, pharyngitis, chronic bronchitis, and diffuse pulmonary fibrosis have been associated with inhalational exposure to vanadium. Vanadate is toxic to alveolar macrophages and may therefore impair pulmonary resistance to infection.
    0.2.7) NEUROLOGIC
    A) CNS depression may occur, usually with fatal doses.
    B) Sensorimotor hemiparesis and aphasia developed shortly after ingestion of ammonium metavanadate.
    C) CNS MANIFESTATIONS include tremors, headaches, tinnitus, and changes in mental status. Vanadium-associated neuropathy may be more common in chronic hemodialysis patients.
    0.2.8) GASTROINTESTINAL
    A) Abdominal cramping, diarrhea, black stools, and green tongue developed in volunteers given ammonium vanadyl tartrate.
    0.2.14) DERMATOLOGIC
    A) Dermatitis, and green discoloration of the skin, may be seen with exposure to vanadium compounds.

Laboratory Monitoring

    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    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) CHELATION - The level at which chelation is necessary is uncertain, especially since systemic symptoms have been rare even in the presence of an excessive body burden. Two chelators have been investigated for vanadium; EDTA and BAL.
    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) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    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) Men exposed to vanadium from cleaning fuel-fired furnaces developed urine levels ranging from 38 to 1,300 mcg/L with primarily respiratory symptoms. Volunteers exposed to 0.25 mg/m(3) for 8 hours developed mild respiratory symptoms.
    B) Industrial exposures to vanadium pentoxide of 2 to 104 mg/m(3) have resulted in mild to moderate respiratory effects, but no systemic effects.

Clinical Effects

Summary Of Exposure

    A) GENERAL: Vanadium metal has low toxicity; pentavalent forms and vanadates are the most toxic. Vanadium salt toxicity is high parenterally, low orally, and intermediate via inhalation.
    B) INHALATION: If inhaled (as dust) the primary symptoms are respiratory. Symptoms may persist up to 2 weeks after exposure, but few if any systemic symptoms have been seen and the prognosis is favorable. The smaller the particle size the greater the pulmonary toxicity. Therefore the fumes are more toxic than the dust.
    1) RESPIRATORY TRACT IRRITATION: Atrophic rhinitis, pharyngitis, chronic bronchitis, and diffuse pulmonary fibrosis have been associated with inhalational exposure to vanadium.

Heent

    3.4.1) SUMMARY
    A) Dry mouth, rhinitis, epistaxis, tracheitis, metallic taste, green tongue, and irritated eyes have been reported in workers exposed to vanadium compound dust.
    3.4.3) EYES
    A) CONJUNCTIVITIS was reported after exposure of workers to concentrations of 0.5 to 2.2 mg/m(3) of vanadium pentoxide (ACGIH, 1986).
    3.4.5) NOSE
    A) RHINITIS may develop after only a few days exposure or even after a single exposure to vanadium pentoxide (Musk & Tees, 1982).
    B) EPISTAXIS has been a reported sign (Harbison, 1998).
    3.4.6) THROAT
    A) IRRITATION: Throat irritation and metallic taste developed in workers exposed to an average of 0.25 mg of vanadium pentoxide (there was also ammonium metavanadate present) (ACGIH, 1986).
    B) GREEN TONGUE ANDS LIPS are a common sign seen after inhalation or ingestion of vanadium compounds (Boulassel et al, 2011; Musk & Tees, 1982).
    C) DRY MOUTH has been seen after inhalation of ammonium vanadate (Musk & Tees, 1982).

Cardiovascular

    3.5.1) SUMMARY
    A) One of the primary effects of vanadium is peripheral vasoconstriction of lungs, spleen, kidneys, and intestines. Effects are local.
    B) Dysrhythmias and bradycardia may occur after prolonged exposure.
    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Dysrhythmias and bradycardia may occur after prolonged exposure (Dafnis & Sabatini, 1994).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) VASOSPASM
    a) One of the primary effects of vanadium is peripheral vasoconstriction of lungs, spleen, kidneys, and intestines. The effects are local in origin. Since this effect may be reversed by epinephrine, there may be both a neurologic as well as a muscular effect (Clayton & Clayton, 1994).

Respiratory

    3.6.1) SUMMARY
    A) Pulmonary irritation leading to pulmonary edema is a possible effect with high concentrations. Occupational asthma has been reported.
    B) Atrophic rhinitis, pharyngitis, chronic bronchitis, and diffuse pulmonary fibrosis have been associated with inhalational exposure to vanadium. Vanadate is toxic to alveolar macrophages and may therefore impair pulmonary resistance to infection.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE RESPIRATORY FAILURE
    1) WITH POISONING/EXPOSURE
    a) AMMONIUM VANADATE
    1) A 24-year-old woman developed acute respiratory distress the night after presenting to an emergency department (ED) with gastrointestinal distress, acute renal failure, and severe hypoglycemia approximately 12 hours after intentionally ingesting an unknown amount of ammonium vanadate. She remained stable for part of the day with systemic treatment and O2 at 2L/min, but later resuscitation attempts in response to respiratory distress were unsuccessful and the patient died the following morning. Postmortem examination revealed widespread asphyxia syndrome of the viscera and erosive gastritis (Boulassel et al, 2011).
    B) ACUTE LUNG INJURY
    1) No specific lung lesions have been identified but tracheitis, bronchitis, pulmonary edema, bronchial pneumonia and emphysema have all been described (ACGIH, 1986).
    C) BRONCHOSPASM
    1) Occupational asthma has been reported in relation to vanadium compounds (Musk & Tees, 1982).
    D) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Atrophic rhinitis, pharyngitis, chronic bronchitis, and diffuse pulmonary fibrosis have been associated with inhalational exposure to vanadium. Vanadate is toxic to alveolar macrophages and may therefore impair pulmonary resistance to infection (Dafnis & Sabatini, 1994).
    b) If inhaled (as dust) the primary symptoms are respiratory. Symptoms may persist up to 2 weeks after exposure, but few if any systemic symptoms have been seen and the prognosis is favorable (Baselt, 1995). The smaller the particle size the greater the pulmonary toxicity. Therefore the fumes are more toxic than the dust (Hathaway et al, 1996).
    E) BRONCHITIS
    1) WITH POISONING/EXPOSURE
    a) Tracheitis has been described after inhalation of vanadium pentoxide (ACGIH, 1986).

Neurologic

    3.7.1) SUMMARY
    A) CNS depression may occur, usually with fatal doses.
    B) Sensorimotor hemiparesis and aphasia developed shortly after ingestion of ammonium metavanadate.
    C) CNS MANIFESTATIONS include tremors, headaches, tinnitus, and changes in mental status. Vanadium-associated neuropathy may be more common in chronic hemodialysis patients.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) CNS depression is seen, but usually only when fatal doses have been administered (Clayton & Clayton, 1994).
    B) HEADACHE
    1) Headache has been reported after inhalation of ammonium vanadate (Musk & Tees, 1982).
    C) CEREBROVASCULAR ACCIDENT
    1) WITH POISONING/EXPOSURE
    a) Sensorimotor hemiparesis and aphasia developed in a 22-year-old woman several hours after ingestion of 10 to 15 g of ammonium metavanadate. A lesion in left parietal cortex was visualized by MRI and SPECT with Tc-99m-HMPAO (Schlake et al, 1994).
    D) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) CNS manifestations include tremors, headaches, tinnitus, and changes in mental status (Dafnis & Sabatini, 1994). Neurological disorders associated with high body vanadium load may be more common in chronic hemodialysis patients (Hosokawa & Yoshida, 1993).

Gastrointestinal

    3.8.1) SUMMARY
    A) Abdominal cramping, diarrhea, black stools, and green tongue developed in volunteers given ammonium vanadyl tartrate.
    3.8.2) CLINICAL EFFECTS
    A) GASTROENTERITIS
    1) WITH THERAPEUTIC USE
    a) Abdominal cramping, diarrhea, black stools and a green tongue developed in volunteers given 50 to 125 mg of ammonium vanadyl tartrate for periods of up to 6 weeks (Baselt, 1995).
    2) WITH POISONING/EXPOSURE
    a) AMMONIUM VANADATE
    1) CASE REPORT: A 24-year-old woman presented to the emergency department with abdominal pain, nausea and vomiting, and diarrhea approximately 12 hours after intentionally ingesting an unknown amount of ammonium vanadate. Upon examination, epigastric tenderness was noted. Lab analysis revealed severe hypoglycemia, acute renal failure, and elevated liver enzymes. The patient remained stable after admission with symptomatic treatment including IV glucose; however, she developed acute respiratory distress the night of admission and died the following morning after several resuscitation attempts. Postmortem examination revealed widespread asphyxia syndrome of the viscera and erosive gastritis (Boulassel et al, 2011).
    b) AMMONIUM METAVANADATE
    1) CASE REPORT: A 22-year-old woman developed nausea, vomiting and diarrhea 2 hours after ingesting 10 to 15 g of ammonium metavanadate. Endoscopy revealed erosive gastritis (Schlake et al, 1994).

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) LIVER ENZYMES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) AMMONIUM VANADATE
    1) CASE REPORT: A 24-year-old woman presented to the emergency department with gastrointestinal distress, acute renal failure, and severe hypoglycemia 12 hours after intentionally ingesting an unknown amount of ammonium vanadate. Laboratory analysis revealed elevated liver enzymes with an ALT of 114 International Units/L (normal: 10 to 45 International Units/L). The patient remained stable after admission with symptomatic treatment including IV glucose; however, she developed acute respiratory distress the night of admission and died the following morning after several resuscitation attempts (Boulassel et al, 2011).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ALBUMINURIA
    1) WITH POISONING/EXPOSURE
    a) AMMONIUM METAVANADATE
    1) CASE REPORT: A 22-year-old woman who ingested 10 to 15 g of ammonium metavanadate developed slight proteinuria, erythrocyturia and leukocyturia which resolved spontaneously (Schlake et al, 1994).
    B) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) AMMONIUM VANADATE
    1) CASE REPORT: A 24-year-old woman presented to the emergency department in acute renal failure with a glomerular filtration rate estimated at 21 mL/min and a creatinine of 265 micromol/L (normal 49 to 90 micromol/L) approximately 12 hours after intentionally ingesting an unknown amount of ammonium vanadate. Severe hypoglycemia, gastrointestinal distress, epigastric pain and elevated liver enzymes were also noted. The patient remained stable after admission with symptomatic treatment including IV glucose; however, she developed acute respiratory distress the night of admission and died the following morning after several resuscitation attempts (Boulassel et al, 2011).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) THROMBOCYTOPENIC DISORDER
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 22-year-old woman who ingested 10 to 15 g of ammonium metavanadate developed mild thrombocytopenia (platelets 73,000/microliter) and decreased PT (32% of normal) (Schlake et al, 1994).
    B) MYELOSUPPRESSION
    1) WITH POISONING/EXPOSURE
    a) Anemia, neutropenia, and basophilic granulation of leukocytes have been reported with human exposure to vanadium. In vitro tests have demonstrated vanadium's ability to lyse vitamin E-deficient erythrocytes (Hamada, 1994; Dafnis & Sabatini, 1994).

Dermatologic

    3.14.1) SUMMARY
    A) Dermatitis, and green discoloration of the skin, may be seen with exposure to vanadium compounds.
    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) Dermatitis developed in workers exposed to an average of 0.25 mg/m(3) of vanadium pentoxide (ACGIH, 1986).
    B) DISCOLORATION OF SKIN
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: One worker developed green discoloration of the fingers underneath his industrial gloves and green scrotum and upper legs through his pants, after shoveling ammonium vanadate (Musk & Tees, 1982).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) DISORDER OF BONE
    1) WITH THERAPEUTIC USE
    a) In some (5/22) chronic hemodialysis patients with osteofibrosis, the serum vanadium level was found to be elevated (32 +/- 5.4 ng/mL). Three of these 5 patients recovered following vitamin D3 treatment; their postrecovery serum vanadium level was 18.6 +/- 2.6 ng/mL (Hosokawa & Yoshida, 1993).
    3.15.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) BONE DISORDER
    a) In animal studies, Talvitie & Wagner (1954) reported that large vanadium accumulations in bone tissue were associated with bone disease.

Endocrine

    3.16.2) CLINICAL EFFECTS
    A) HYPOGLYCEMIA
    1) WITH POISONING/EXPOSURE
    a) AMMONIUM VANADATE
    1) CASE REPORT: A 24-year-old woman presented to the emergency department with severe hypoglycemia (glucose 0.2 g/L), gastrointestinal distress, and acute renal failure approximately 12 hours after intentionally ingesting an unknown amount of ammonium vanadate. She remained stable after admission with symptomatic treatment including IV glucose; however, she developed acute respiratory distress the night of admission and died the following morning after several resuscitation attempts (Boulassel et al, 2011).
    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LYMPHADENOPATHY
    a) LYMPH FLOW INCREASES have been reported in animal studies (Clayton & Clayton, 1994).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7440-62-2 (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
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) Vanadium has not been found to be carcinogenic in humans; it is not clastogenic and is only weakly mutagenic. It does, however, affect the distribution of chromosomes during mitosis (Leonard & Gerber, 1994).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Normal blood concentrations (90% of which is in the plasma) ranges from 0.4 to 2.8 mcg/liter, but serum concentrations may range from 2 to 4 mcg/liter (Baselt, 1995).
    2) Workers exposed to vanadium have blood concentrations averaging 1.8 mcg/liter (range 0.6 to 3.8) and serum concentrations averaging 11 mcg/liter.
    3) CHRONIC HEMODIALYSIS patients often have high blood levels of vanadium due to impaired renal excretion; studies have found average levels of 14.5 to 23.9 ng/mL (Hosokawa & Yoshida, 1993; Romero, 1994).
    4.1.3) URINE
    A) URINARY LEVELS
    1) "Normal" urine levels are less than 8 mcg/24 hours of the metal (Baselt, 1982). The current body burden considered "safe" in the United States is 0.5 mg/liter (Clayton & Clayton, 1994).

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) URINE - Colorimetry may be used for urine determinations, and air sampling (HSBD, 1999).
    2) BLOOD/SERUM - Because of greater sensitivity and specificity, atomic absorption spectrophotometry is preferred (Baselt, 1995).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) 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) 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).
    6.5.3) TREATMENT
    A) 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).
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Vomiting and diarrhea are usually not extensive, however, if the patient is losing significant fluids, monitor electrolytes.
    C) CHELATION THERAPY
    1) DEFEROXAMINE
    a) In the only known case of acute vanadium poisoning, deferoxamine mesylate given orally at 500 milligrams per day as a single dose, along with ascorbic acid, and plasmapheresis. Recovery was complete within a few days after ingestion of 10 to 15 grams ammonium metavanadate (Schlake et al, 1994).
    2) The level at which chelation is necessary is uncertain, especially since systemic symptoms have been rare even in the presence of an excessive body burden. Several chelators have been investigated for vanadium, with differing results.
    3) The most effective chelators in mice, in terms of protection against lethality and reduction of clinical signs and symptoms, were EDTA, glutathione, succinic acid, and DTPA. However, these agents did not increase urinary or fecal excretions (Domingo et al, 1990).
    4) CALCIUM EDTA
    a) EDTA was given intraperitoneally at 100 milligrams/kilogram 2 to 4 hours after poisoning dogs. It was effective in reversing the lethal effect. No studies have been done on humans.
    5) DIMERCAPROL/BAL
    a) Animal studies indicate that 125 milligrams/kilogram of BAL intravenously gave better results than calcium sodium EDTA (Harbison, 1998), but this was primarily a reversal of the blood pressure effects, and has been questioned by other authors (Clayton & Clayton, 1994).
    b) If the patient is symptomatic, cannot take penicillamine orally or has a documented penicillin allergy, administer BAL: 3 to 5 milligrams/kilogram/dose every 4 hours by deep intramuscular injection the first 2 days; 2.5 to 3 milligrams/kilogram/dose intramuscularly every 6 hours for 2 days; then 2.5 to 3 milligrams/kilogram/dose every 12 hours for a week intramuscularly. Adverse reaction such as urticaria may respond to diphenhydramine. Persistent hyperpyrexia is common in children getting BAL. Hypertension is possible - monitor.
    D) ASCORBIC ACID
    1) Ascorbic acid at a high oral dose of 1.5 grams TID was used in a case of intentional ingestion of 10 to 15 grams ammonium metavanadate. The ascorbic acid reduces V(5+) to the less toxic V(3+) valence state (Schlake et al, 1994).
    2) 125 milligrams/kilogram given intraperitoneally 20 minutes BEFORE a lethal injection gave complete protection from the lethal effects. The usefulness of this treatment in actual poisonings is obviously very limited (Clayton & Clayton, 1994).
    3) Ascorbic acid was effective in increasing urinary excretion of vanadium in mice (Domingo et al, 1990).
    E) PLASMAPHERESIS
    1) Daily plasmapheresis (2100 to 2300 milliliters plasma exchange for three days) was used after daily doses of ascorbic acid and deferoxamine in a case of intentional ingestion of 10 to 15 grams ammonium metavanadate (Schlake et al, 1994).

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) BRONCHOSPASM
    1) If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
    B) 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).
    C) 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) SUMMARY
    1) Vanadium is 90% protein bound, and therefore not likely to be dialyzable. However, vanadium removal has been documented in patients receiving chronic hemodialysis therapy (Tsukamoto et al, 1990; (Dafnis & Sabatini, 1994; Hosokawa & Yoshida, 1993).

Abstracts

Case Reports

    A) ADULT
    1) AMMONIUM VANADATE
    a) A 24-year-old woman presented to the emergency department with abdominal pain, nausea and vomiting, and diarrhea approximately 12 hours after intentionally ingesting an unknown amount of ammonium vanadate. Upon examination, vital signs were stable, SpO2 was below 99% with O2 at 2 L/min, and epigastric tenderness was noted. Lab analysis revealed severe hypoglycemia (glucose 0.2 g/L), acute renal failure (glomerular filtration rate 21 mL/min; creatinine 265 micromol/L (normal 49 to 90 micromol/L)), and ALT of 114 International Units (IU)/L (normal: 10 to 45 IU/L). Screening for drugs of abuse was negative. She received symptomatic treatment including IV glucose. The night of admission, she developed acute respiratory distress and died the following morning after several resuscitation attempts. Postmortem examination revealed asphyxia syndrome of the viscera and erosive gastritis (Boulassel et al, 2011).
    2) AMMONIUM METAVANADATE
    a) A 22-year-old woman intentionally ingested 10 to 15 g of ammonium metavanadate and developed nausea, vomiting, and diarrhea 2 hours after exposure, followed by right-sided brachiofacial paresis one hour later. Right hemihypesthesias, sensorimotor paresis of the right leg, and amnestic and sensorimotor aphasia followed. ECG, chest X-ray and abdominal sonography were normal, as were laboratory values except for decreased prothrombin time and reduced platelet count. Structural lesions were seen in the cortex and subcortex by T2-weighted MRI. Localized hypoperfusion was seen with SPECT. Focal delta activity in the left parieto temporal region was seen on EEG. The patient was treated with IV deferoxamine mesylate (500 mg/day), oral ascorbic acid (1.5 g 3 times daily), plasmapheresis, and decadron phosphate (8 mg 3 times daily) for prevention of pulmonary edema (Schlake et al, 1994).

Range Of Toxicity

Summary

    A) Men exposed to vanadium from cleaning fuel-fired furnaces developed urine levels ranging from 38 to 1,300 mcg/L with primarily respiratory symptoms. Volunteers exposed to 0.25 mg/m(3) for 8 hours developed mild respiratory symptoms.
    B) Industrial exposures to vanadium pentoxide of 2 to 104 mg/m(3) have resulted in mild to moderate respiratory effects, but no systemic effects.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) Vanadium is a trace element in biologic systems. Very little is known about its essential functions (see pharmacology and toxicology). The estimated average daily dietary intake is approximately 20 micrograms (Baselt, 1995).

Minimum Lethal Exposure

    A) SPECIFIC SUBSTANCE
    1) VANADIUM PENTOXIDE -
    a) ANIMALS - 25 parts per million in the diet of rats produced early signs of poisoning and 70 milligrams/cubic meter is fatal to animals in a few hours (ACGIH, 1986).
    b) HUMANS - Workers regularly exposed to concentrations of 0.2 to 0.5 milligram/cubic meter have a higher incidence of respiratory signs than controls. Volunteers exposed to 0.1 milligram/cubic meter developed delayed cough and increased mucous (ACGIH, 1986).

Maximum Tolerated Exposure

    A) SPECIFIC SUBSTANCE
    1) VANADIUM PENTOXIDE -
    a) HUMAN - Industrial exposures to concentrations of 2 to 104 milligrams/cubic meter have resulted in mild to moderate respiratory effects but no systemic poisonings. In another study, intermittant exposure to 99 milligrams/cubic meter produced no symptoms (ACGIH, 1986).
    b) VANADIUM ALCOHOLATES (ethylene through isobutylate) are considered extreme mucous membrane irritants, most likely due to hydrolysis with wet mucous membranes (Clayton & Clayton, 1994).
    c) A "fatal" dose has been estimated at 60 to 120 milligrams of presumably the salt forms of vanadium, but doses of 24 to 80 milligrams/day have been tolerated in man (Clayton & Clayton, 1994).
    d) Oral toxicity varies by diet (Clayton & Clayton, 1994).

Serum Plasma Blood Concentrations

    7.5.1) THERAPEUTIC CONCENTRATIONS
    A) THERAPEUTIC CONCENTRATION LEVELS
    1) GENERAL
    a) Normal blood concentrations (90% of which is in the plasma) ranges from 0.4 to 2.8 mcg/L but serum concentrations may range from 2 to 4 mcg/L (Baselt, 1995). Other studies have reported normal serum concentrations can range from 0.26 to 1.3 ng/mL, with an average of 0.4 ng/mL (Hosokawa & Yoshida, 1990).
    b) The average serum concentration in chronic non-dialyzed uremic patients is 12 ng/mL (Hosokawa & Yoshida, 1990).
    c) Chronic hemodialysis patients often have high blood levels of vanadium due to impaired renal excretion; studies have found average levels of 14.5 to 23.9 ng/mL (Hosokawa & Yoshida, 1990; Romero, 1994). The average serum concentration in chronic hemodialysis patients is 18 ng/mL (Hosokawa & Yoshida, 1990).
    d) Normal urine levels are less than 8 mcg/24 hours. The body burden considered safe is 0.5 mg/L.
    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) CONCENTRATION LEVEL
    a) URINE
    1) Volunteers exposed to 0.25 mg/cubic meter for 8 hours developed mild respiratory symptoms only and a peaked urinary concentration of 130 mcg/L 3 days after exposure. Vanadium was NOT detected 7 days after exposure.
    2) Men exposed to vanadium from cleaning fuel oil fired furnaces developed urine levels ranging from 38 to 1300 mcg/L with primarily respiratory symptoms (Baselt, 1995; Harbison, 1998).
    3) BODY BURDEN: The current body burden considered safe is 0.5 mg/L (Harbison, 1998).
    b) SERUM
    1) AMMONIUM VANADATE/POSTMORTEM: Postmortem blood analysis of a 24-year-old woman who ingested an unknown amount of ammonium vanadate revealed a vanadium concentration of 6.22 mg/L (normal: less than 1 mcg/L) (Boulassel et al, 2011).

Workplace Standards

    A) ACGIH TLV Values for CAS7440-62-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7440-62-2 (National Institute for Occupational Safety and Health, 2007):
    1) IDLH:
    a) IDLH: 35 mg V/m3
    b) Note(s): Not Listed
    2) IDLH:
    a) IDLH: 35 mg V/m3
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7440-62-2 :
    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 CAS7440-62-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) VANADIUM METAL
    1) LD50- (ORAL)RAT:
    a) 130 mg/kg
    B) VANADIUM PENTOXIDE
    C) VANADIUM TRICHLORIDE
    1) LD50- (ORAL)RAT:
    a) 23 mg/kg

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Vanadium alters sulfur metabolism of the body at levels causing no detectable vanadium toxicity. The cystine content of fingernails is reduced in workers exposed to vanadium chronically (Finkel, 1983).
    B) Vanadium also reduces plasma cholesterol by inhibition of conversion of hydroxymethylglutaric to methylcrotonic acid and thus prevents the utilization of mevalonic acid in cholesterol synthesis (Clayton & Clayton, 1994). Trace amounts also increase oxidation of fatty acids of liver phospholipids.
    C) Other physiologic effects involve inhibition of sulfhydryl-dependant succinic dehydrogenase of the liver (but not the kidney), retardation of coenzyme A synthesis, catalyzing the oxidation of pressor amines (suggesting that vanadium is the metal activator for MAO's) and inhibition of isolated sodium, potassium, ATP-ase (Clayton & Clayton, 1994; Akera et al, 1983).

Toxicologic Mechanism

    A) IRRITANT EFFECTS
    1) The strong respiratory irritant effect may lie with vanadium's ability to reduce cell (alveolar macrophages) viability, therefore reducing pulmonary defenses. Cytotoxicity in vitro was related to solubility, with vanadium pentoxide greater than vanadium trioxide greater than vanadium dioxide.
    B) Vanadium also mobilizes iron and changes the distribution of chromium, copper, manganese, and zinc (Clayton & Clayton, 1982).
    C) CARDIAC EFFECTS: Vanadium exhibits digitalis-like effects on heart muscle, including positive inotropic effects, diuresis, and natriuresis (Hosokawa & Yoshida, 1990).
    D) ANIMAL STUDIES: Both H+ and Na+ potassium ATPase activity in the renal collecting duct and distal tubules is inhibited in experimental animals given repeated oral and parenteral doses of vanadates (Boscolo et al, 1994; Dafnis & Sabatini, 1994).
    1) Other metabolic effects in chronically dosed experimental animals include increased urinary excretion of potassium; decreased urinary excretion of calcium; increased plasma renin and kallikrein activities; and decreased plasma aldosterone (Boscolo et al, 1994).

Physicochemical

Physical Characteristics

    A) VANADIUM METAL: A grey or white, soft metallic powder, fused hard lump, or cubic crystal (Budavari, 1996)
    B) VANADIUM PENTOXIDE: A yellow to rust-brown, noncombustible crystalline compound.
    C) VANADIUM CARBONYL: Blue-green pyrophoric crystals.
    D) VANADIUM PENTAFLUORIDE: Liquid.
    E) VANADIUM TRIOXIDE: A black powder which on exposure to air is gradually converted into indigo-blue crystals of V2O4.
    F) VANADIUM TRISULFATE: A lemon-yellow powder.
    G) VANADIUM TRISULFIDE: A greenish-black powder.
    H) VANADYL DICHLORIDE: Green very deliquescent tabular crystals.
    I) VANDYL SULFATE: A blue crystalline powder.
    J) VANDYL TRICHLORIDE: A yellow liquid, emitting red fumes upon exposure to moist air.

Molecular Weight

    A) VANADIUM: 50.92
    B) VANADIUM PENTOXIDE: 181.88
    C) VANADIUM TRIOXIDE: 149.88
    D) VANADIUM TETRAOXIDE: 82.94
    E) VANADIUM CARBIDE: 62.95
    F) VANADIUM OXYDICHLORIDE: 137.85
    G) VANADIUM OXYTRICHLORIDE: 173.3
    H) VANADYL SULFATE: 163
    I) AMMONIUM METAVANADATE: 116.98
    J) SODIUM METAVANDATE: 121.93
    K) VANADYL-TRIS(ACETYL-ACETONATE): 348.3
    L) VANADYL-OXY-BIS(ACETYL-ACETONATE): 265.2
    M) VANADYL ETHYLATE: 201.9
    N) VANADYL N-PROPYLATE: 244.2
    O) VANADYL ISOPROPYLATE: 244.2
    P) VANADYL N-BUTYLATE: 286.3

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