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VANADIUM PENTOXIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Vanadium pentoxide is a pentavalent vanadium compound. It is one of the most toxic vanadium compounds (ACGIH, 1992).

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) O5-V2

Available Forms Sources

    A) FORMS
    1) Airborne vanadium pentoxide can exist as fume or dust (ACGIH, 1992; RTECS , 1991).
    a) The fume of vanadium pentoxide is believed to be more toxic than the dust because its smaller particle size makes it respirable (ACGIH, 1992; Hathaway et al, 1996).
    2) It can be obtained in the following industrial grades (98-99% purity): commercial air dried, commercial fused, chemical purity air dried, and chemical purity fused (HSDB, 2001).
    B) SOURCES
    1) Vanadium pentoxide is prepared by heating ammonium metavanadate (Budavari, 1996).
    2) It can be obtained from alkali or acid extraction from vanadium minerals and from concentrated ferrophosphorus slag by roasting with sodium chloride, leaching with water, purifying via solvent extraction, precipitation, and heating (Lewis, 1997).
    3) Exposure to vanadium oxide dust and fume can occur in smelting and refining and also from oil-fired furnace flues, where vanadium pentoxide may constitute as much as 50% of the soot by weight (ILO , 1998).
    C) USES
    1) Vanadium pentoxide is used in textile dyes, inks, pesticides, ceramic tile coloring agent, sanitary ware colorant, photographic developer, and coating for welding electrodes (ACGIH, 2001; (Hathaway et al, 1996; ILO , 1998) OHM, TADS, 2001).
    2) It is used as a depolarizer and UV inhibitor in glass (OHM/TADS, 2001).
    3) It is used as a ferrovanadium alloy ingredient in automotive steels and in jet engines and airframes (ACGIH, 1991).
    4) It is used as a catalyst in oxidation reactions involving sulfur oxide, oxides of nitrogen, phthalic acid, maleic acid, adipic acid, acrylic acid, and oxalic acid (ACGIH, 1991) HSDB, 2001; (ILO , 1998).
    5) Additional uses include (HSDB, 2001):
    a) Lowering the melting point of enamel frits for the coating of aluminum, substrates.
    b) Inhibiting corrosion in carbon dioxide scrubbing solution of the Benfield and related processes for the production of hydrogen from hydrocarbons.
    c) Serving as a cathode in primary and secondary (rechargeable) lithium batteries.
    d) Functioning as a catalyst in automobile catalytic converters.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Inhalation of dust or fume is the most common form of poisoning. Vanadium pentoxide may be irritating to the eyes, skin and mucous membranes. Signs and symptoms of exposure may include conjunctivitis, rhinitis, cough, dyspnea, wheezing, tracheitis, hemoptysis, epistaxis, bronchitis, bronchospasm, pulmonary edema, and a greenish-black discoloration of the tongue. Pulmonary function may be diminished with chronic exposure, but pneumoconiosis does not develop.
    B) Other effects may include skin rashes, chest pain or palpitations, nervousness, headache, vertigo, palor, hematuria, and albuminuria. Nausea, vomiting, and abdominal pain may develop following ingestion. Anemia may occur. Liver and kidney injury have been noted in experimental animals.
    0.2.4) HEENT
    A) Conjunctivitis, corneal vascularization, irritation of the nose and throat, a greenish-black tongue, and a higher incidence of diseased teeth are associated with exposure to vanadium pentoxide.
    0.2.5) CARDIOVASCULAR
    A) Chest pain and extrasystoles were observed.
    0.2.6) RESPIRATORY
    A) Pulmonary edema/pneumonia, chronic bronchitis/asthma, and reduced pulmonary function have been noted as effects of vanadium pentoxide.
    0.2.7) NEUROLOGIC
    A) Neurologic disorders, including nervous depression, psychiatric disturbances, and tremors have been seen in connection with exposure to vanadium pentoxide.
    0.2.8) GASTROINTESTINAL
    A) Nausea and vomiting were observed.
    0.2.9) HEPATIC
    A) Hepatotoxicity, including fatty changes, partial cell necrosis, and decreased cellular respiration, have been seen in connection with vanadium pentoxide exposure.
    0.2.10) GENITOURINARY
    A) Nephrotoxicity and hematuria have been noted.
    0.2.13) HEMATOLOGIC
    A) Anemia is a possible effect.
    0.2.14) DERMATOLOGIC
    A) Papular eruptions may appear on the face, hands, or dorsa of the feet. Contact dermatitis has been reported.
    0.2.17) METABOLISM
    A) The metabolic significance of vanadium is uncertain.
    0.2.18) PSYCHIATRIC
    A) There have been unconfirmed reports of psychiatric effects of exposure to vanadium pentoxide.
    0.2.19) IMMUNOLOGIC
    A) Sensitization may be an effect.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no reproductive studies were found for vanadium pentoxide in humans.
    B) ANIMAL STUDIES - Vanadium pentoxide has been shown to be teratogenic in the hamster and mouse.
    0.2.22) OTHER
    A) Chronic respiratory disease appears to be a predisposing medical condition for susceptibility to vanadium pentoxide toxicity.

Laboratory Monitoring

    A) Vanadium levels in plasma or urine increase with exposure.
    B) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    C) 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) 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.
    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.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    0.4.4) 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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

Range Of Toxicity

    A) Inhalation exposure to an airborne concentration of 0.116 mg/m(3) produced no effect, while exposure to an airborne concentration of 1 mg/m(3) for 8 hours caused respiratory tract and eye irritation and bronchoconstriction.

Clinical Effects

Summary Of Exposure

    A) Inhalation of dust or fume is the most common form of poisoning. Vanadium pentoxide may be irritating to the eyes, skin and mucous membranes. Signs and symptoms of exposure may include conjunctivitis, rhinitis, cough, dyspnea, wheezing, tracheitis, hemoptysis, epistaxis, bronchitis, bronchospasm, pulmonary edema, and a greenish-black discoloration of the tongue. Pulmonary function may be diminished with chronic exposure, but pneumoconiosis does not develop.
    B) Other effects may include skin rashes, chest pain or palpitations, nervousness, headache, vertigo, palor, hematuria, and albuminuria. Nausea, vomiting, and abdominal pain may develop following ingestion. Anemia may occur. Liver and kidney injury have been noted in experimental animals.

Heent

    3.4.1) SUMMARY
    A) Conjunctivitis, corneal vascularization, irritation of the nose and throat, a greenish-black tongue, and a higher incidence of diseased teeth are associated with exposure to vanadium pentoxide.
    3.4.2) HEAD
    A) DENTAL - A higher incidence of diseased teeth, gingivitis, and pyorrhea was found in vanadium ore exposed workers, as opposed to controls (Vintinner et al, 1955).
    3.4.3) EYES
    A) CONJUNCTIVITIS - Vanadium pentoxide dust or fume may irritate the eyes and cause profuse lacrimation and a burning sensation of the conjunctiva (Sittig, 1985).
    1) A higher airborne concentration of vanadium pentoxide is required to cause eye irritation than is needed to cause respiratory tract irritation (Grant, 1986).
    B) CORNEAL VASCULARIZATION - Increased vascularization of the cornea was significantly more frequent in workers exposed to active-ore than in controls (Vintinner et al, 1955).
    3.4.5) NOSE
    A) IRRITATION - Vanadium pentoxide dust or fume may irritate the upper respiratory tract, causing serous or hemorrhagic rhinitis (Sittig, 1985).
    1) Sores in the nares, dryness or smarting of the nose, and nasal obstruction in the absence of rhinitis have occurred with occupational exposure (Sjoberg, 1951).
    3.4.6) THROAT
    A) IRRITATION - Vanadium pentoxide dust or fume may cause sore throat, cough, tracheitis, metallic taste, and expectoration (Sittig, 1985; Hathaway et al, 1991).
    B) GREENISH-BLACK TONGUE - The hallmark of vanadium poisoning is a greenish-black discoloration of the tongue (Gosselin et al, 1984).
    1) This discoloration has occurred within hours of acute exposure, and in extreme cases may also affect the skin (Musk & Tees, 1982).

Cardiovascular

    3.5.1) SUMMARY
    A) Chest pain and extrasystoles were observed.
    3.5.2) CLINICAL EFFECTS
    A) CHEST PAIN
    1) Vanadium pentoxide has caused chest pain and palpitations (Sittig, 1985; Budavari, 1996).
    B) ECTOPIC BEATS
    1) Electrocardiograms after exertion revealed a higher than expected incidence of extrasystoles, but it was unclear that this was due to vanadium pentoxide exposure (Sjoberg, 1951).

Respiratory

    3.6.1) SUMMARY
    A) Pulmonary edema/pneumonia, chronic bronchitis/asthma, and reduced pulmonary function have been noted as effects of vanadium pentoxide.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Vanadium pentoxide dust and fume are respiratory tract irritants and can cause serous or hemorrhagic rhinitis, hacking cough, bronchitis, and expectoration (Sittig, 1985).
    a) TOLERANCE may develop to the irritant effects of vanadium compounds (Clayton & Clayton, 1994).
    B) ACUTE LUNG INJURY
    1) Exposure to high concentrations of the dust or fume may produce pulmonary edema and fatal pneumonia (Sittig, 1985).
    C) BRONCHITIS
    1) Even acute exposure may cause persistent bronchitis and an asthma-like condition with fine rales and wheezing, beginning by the end of the first exposure.
    2) Bronchospasm may persist for 48 hours after exposure and rales for up to a week. Cough may persist for two weeks following acute exposure and for years after chronic exposure (Sittig, 1985; Musk & Tees, 1982; Hathaway et al, 1991).
    3) So-called "Boilermakers' Bronchitis" was seen in at least 74 of 100 boilermakers exposed to high levels of vanadium pentoxide fume. Symptoms were productive cough, sore throat, dyspnea upon exertion, chest pain or discomfort, wheezing, mild hypoxemia, and reduced expiratory flow rates, but chest X-rays were normal (Levy et al, 1984).
    4) Increased bronchial responsiveness to methacholine challenge in the absence of overt bronchial symptoms was seen in a group of 11 vanadium pentoxide-exposed workers (Pistelli et al, 1991).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Cynomolgus monkeys exposed to airborne concentrations of 0.5 and 5 mg/m(3) of vanadium pentoxide had central and peripheral airflow limitation, but no detectable changes in parenchymal function. Large increases in the numbers of polymorphonuclear leukocytes were seen in the bronchoalveolar lavage fluid (Knecht et al, 1985).
    2) PULMONARY HEMORRHAGE
    a) Rabbits exposed to airborne concentrations of vanadium pentoxide varying between 0.01 and 0.1 mg/m(3) for 8 months developed moderate hyperemia and minor hemorrhages in the lungs (Sjoberg, 1950).

Neurologic

    3.7.1) SUMMARY
    A) Neurologic disorders, including nervous depression, psychiatric disturbances, and tremors have been seen in connection with exposure to vanadium pentoxide.
    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) Acute exposure to vanadium in mining has produced anorexia, headache, tinnitus, blurring of vision, and nervous disturbances (O'Donoghue, 1985).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Functional disturbances in conditioned reflexes were produced when vanadium was given orally to rats and mice (O'Donoghue, 1985).
    2) PARALYSIS
    a) Paralysis of hind limbs, depression of the respiratory center, and convulsions precede death from vanadium poisoning in experimental animals (Friberg et al, 1986).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea and vomiting were observed.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA
    1) Vanadium pentoxide will cause nausea if ingested (CHRIS, 1996).
    B) NAUSEA, VOMITING AND DIARRHEA
    1) Nausea, vomiting, and diarrhea have been mentioned as symptoms of acute exposure (ITI, 1985).

Hepatic

    3.9.1) SUMMARY
    A) Hepatotoxicity, including fatty changes, partial cell necrosis, and decreased cellular respiration, have been seen in connection with vanadium pentoxide exposure.
    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Fatty changes, partial cell necrosis, and decreased liver cell respiration were seen in livers of rats and rabbits exposed to vanadium pentoxide by inhalation at airborne concentrations of 10 to 70 mg/kg for 9 to 12 months; serum albumin was also decreased (Roshchin, 1968; (Sjoberg, 1950).
    1) These effects have not been reported in exposed humans.

Genitourinary

    3.10.1) SUMMARY
    A) Nephrotoxicity and hematuria have been noted.
    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) Derangement of kidney function has been mentioned in a review of effects of inhalation of vanadium dust (Gosselin et al, 1984); however this has not been confirmed in independent occupational studies.
    B) BLOOD IN URINE
    1) Albuminuria and hematuria have been mentioned as symptoms (ITI, 1985), but these have not been commonly seen with occupational exposure.
    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Fatty changes in the convoluted and straight tubules of the kidney were seen in rabbits exposed to vanadium pentoxide by inhalation (Sjoberg, 1950).

Hematologic

    3.13.1) SUMMARY
    A) Anemia is a possible effect.
    3.13.2) CLINICAL EFFECTS
    A) ANEMIA
    1) Anemia has been mentioned in reviews of effects of inhalation of vanadium dust (Gosselin et al, 1984; ITI, 1985); however this has not been confirmed in independent occupational studies.

Dermatologic

    3.14.1) SUMMARY
    A) Papular eruptions may appear on the face, hands, or dorsa of the feet. Contact dermatitis has been reported.
    3.14.2) CLINICAL EFFECTS
    A) ERUPTION
    1) Vanadium pentoxide may cause a papular skin rash or an eczematous rash with intense itching and sometimes with generalized urticaria (Budavari, 1996; Sittig, 1985).
    a) Papular eruptions may appear on the face, hands, or dorsa of the feet (Sjoberg, 1951).
    B) CHEMICAL BURN
    1) Prolonged skin contact may cause burns (HSDB , 1996).

Immunologic

    3.19.1) SUMMARY
    A) Sensitization may be an effect.
    3.19.2) CLINICAL EFFECTS
    A) ACUTE ALLERGIC REACTION
    1) Development of eczematous skin lesions and an asthma-like respiratory response from exposure to vanadium pentoxide suggest that it might be a sensitizer (Friberg et al, 1986).
    2) Soluble vanadium salts such as VOSO4 are sensitizers in guinea pigs (Friberg et al, 1986). Rare cases of humans reacting in patch tests have been reported (Sjoberg, 1950; Motolese et al, 1993).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no reproductive studies were found for vanadium pentoxide in humans.
    B) ANIMAL STUDIES - Vanadium pentoxide has been shown to be teratogenic in the hamster and mouse.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) VANADIUM PENTOXIDE -
    a) Vanadium pentoxide caused musculoskeletal abnormalities in mouse fetuses when given at the high dose of 10,900 mg/kg intravenously to pregnant females 8 days after conception (RTECS , 1996; Wide, 1984).
    b) Vanadium pentoxide produced skeletal abnormalities in hamster fetuses when injected into the pregnant dams (Carlton, 1982).
    c) Vanadium pentoxide was not teratogenic in NIH mice when given by intraperitoneal injection at various times during gestation. It did induce increased resorptions and delayed ossification (Zhang et al, 1991a).
    2) RELATED COMPOUNDS
    a) Sodium metavanadate (a pentavalent vanadium compound similar to vanadium pentoxide) had no effect on fertility when given orally to male and female rats at doses up to 20 mg/kg/day. It did increase resorptions and dead fetuses, but not significantly (Domingo, 1986).
    b) Sodium orthovanadate was embryotoxic at the preimplantation stage when injected into pregnant rats (Roschin & Dazimov, 1980).
    c) Vanadium may concentrate in the fetuses of mice (Soremark, 1962), but another study found that it preferentially concentrated in the placenta (Friberg et al, 1986).
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the possible effects of vanadium pentoxide exposure during pregnancy in humans.
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) RELATED COMPOUNDS
    1) Sodium metavanadate depressed growth of rat pups when nursing mothers were given a dose of 5 mg/kg/day orally (Domingo, 1986).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS1314-62-1 (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) IARC Classification
    a) Listed as: Vandium pentoxide
    b) Carcinogen Rating: 2B
    1) The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    3.21.4) ANIMAL STUDIES
    A) CARCINOGEN
    1) In one animal study, alveolar/bronchiolar neoplasms were observed in male rats exposed to 0.5 and 2 mg/m(3) of vanadium pentoxide (by whole-body inhalation for 2 years) at incidences exceeding the National Toxicology Program historical control ranges. In female rats exposed to 0.5 mg/m(3), a marginal increase in alveolar/bronchiolar neoplasms was also noted. In exposed male and female rats, increases in chronic inflammation, interstitial fibrosis, alveolar and bronchiolar hyperplasia/metaplasia, and squamous metaplasia were noted. In exposed mice (1, 2, or 4 mg/m(3) of vanadium pentoxide), there were increases in chronic inflammation, interstitial fibrosis, and alveolar and bronchiolar epithelial hyperplasia. Vanadium pentoxide acted as a pulmonary carcinogen in male rats and male and female mice. These effects occurred at or only slightly above the permissible human occupational exposure limit of 0.5 mg/m(3) (Ress et al, 2003).
    B) LACK OF EFFECT
    1) Vanadium pentoxide was not carcinogenic when given to rabbits at a dose of 100 ppm in the diet for 68 days (Sax, 1988).

Genotoxicity

    A) MICRONUCLEI were induced in Chinese hamster V79 cells in culture, but sister chromatid exchanges and mutations were not (Zhong et al, 1994).
    B) Vanadium pentoxide was inactive for inducing chromosome aberrations or sister chromatid exchanges in human lymphocytes, but did increase the frequency of polyploid cells and DNA satellites (Roldan & Altamirano, 1990).
    C) DNA repair was noted in B. subtilis after exposure to vanadium pentoxide (RTECS , 1996).
    D) Vanadium pentoxide induced DNA single strand breaks in whole human lymphocytes, as detected by the single-cell gel electrophoresis assay (Comet Assay) (Rojas et al, 1996).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Vanadium levels in plasma or urine increase with exposure.
    B) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    C) 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) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Vanadium levels in urine may be useful as an index of exposure (Sittig, 1985). Levels of vanadium were elevated in urine but not in blood of two workers with high-level exposures, compared with unexposed workers (Kawai et al, 1989).
    B) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Medical surveillance for persons exposed to vanadium pentoxide should include pre-employment and periodic physical examinations with emphasis on the eyes, skin, and lungs (Sittig, 1985).
    1) Tests for pulmonary function should include FVC and FEV (1 sec) (Hathaway et al, 1991).
    b) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    c) Diagnostic tests should include electrocardiogram and sputum gram stain and culture (Hathaway et al, 1991).
    2) PULMONARY FUNCTION TESTS
    a) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Medical surveillance should include a chest x-ray (Hathaway et al, 1991).
    a) However, no significant differences in chest x-rays were seen between men with long-term exposure to vanadium and matched controls (Kiviluoto, 1980).
    2) If respiratory tract irritation is present, monitor chest x-ray.

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Vanadium pentoxide dust and fume may be collected on a filter and worked up with sodium hydroxide followed by atomic absorption analysis (Sittig, 1985).
    2) Vanadium can be measured in serum using atomic absorption spectrometry (Baselt, 1982).
    3) Vanadium levels may be measured in urine using atomic absorption spectrometry (Baselt, 1982).
    B) OTHER
    1) Vanadium can be measured in urine by radiochemical neutron activation analysis (Kucera et al, 1994).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

Monitoring

    A) Vanadium levels in plasma or urine increase with exposure.
    B) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    C) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.

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) MONITORING OF PATIENT
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    2) Monitoring urine vanadium levels may be useful as an index of exposure.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) If significant fluid losses occur because of vomiting or diarrhea, fluid and electrolyte status monitoring and replacement therapy could be required.
    C) OBSERVATION REGIMES
    1) Carefully observe patients with ingestion exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    2) Patients symptomatic following exposure should be observed in a controlled setting until all signs and symptoms have fully resolved.

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) IRRITATION SYMPTOM
    1) Respiratory tract irritation, if severe, can progress to noncardiogenic pulmonary edema which may be delayed in onset up to 24 to 72 hours after exposure in some cases.
    2) There are no controlled studies indicating that early administration of corticosteroids can prevent the development of noncardiogenic pulmonary edema in patients with inhalation exposure to respiratory irritant substances, and long-term use may cause adverse effects (Boysen & Modell, 1989).
    a) However, based on anecdotal experience, some clinicians do recommend early administration of corticosteroids (such as methylprednisolone 1 gram intravenously as a single dose) in an attempt to prevent the later development of pulmonary edema.
    1) Anecdotal experience with dimethyl sulfate inhalation showed possible benefit of methylprednisolone in the TREATMENT of noncardiogenic pulmonary edema (Ip et al, 1989).
    3) Anecdotal experience also indicated that systemic corticosteroids may have possible efficacy in the TREATMENT of drug-induced noncardiogenic pulmonary edema (Zitnik & Cooper, 1990; Stentoft, 1990; Chudnofsky & Otten, 1989) or noncardiogenic pulmonary edema developing after cardiopulmonary bypass (Maggart & Stewart, 1987).
    4) It is not clear from the published literature that administration of systemic corticosteroids early following inhalation exposure to respiratory irritant substances can PREVENT the development of noncardiogenic pulmonary edema. The decision to administer or withhold corticosteroids in this setting must currently be made on clinical grounds.
    C) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    D) MONITORING OF PATIENT
    1) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    2) Monitoring pulmonary function tests may be advisable in patients with either chronic inhalation exposure or significant acute exposure.
    3) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    4) Monitoring urine vanadium levels may be useful as an index of exposure.
    E) OBSERVATION REGIMES
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    F) CONDUCTION DISORDER OF THE HEART
    1) Cardiac monitoring should be done for patients with chest pain or palpitations. If ventricular arrhythmias are present, antiarrhythmic therapy could be required.
    G) LIDOCAINE
    1) LIDOCAINE/DOSE
    a) ADULT: 1 to 1.5 milligrams/kilogram via intravenous push. For refractory VT/VF an additional bolus of 0.5 to 0.75 milligram/kilogram can be given at 5 to 10 minute intervals to a maximum dose of 3 milligrams/kilogram (Neumar et al, 2010). Only bolus therapy is recommended during cardiac arrest.
    1) Once circulation has been restored begin a maintenance infusion of 1 to 4 milligrams per minute. If dysrhythmias recur during infusion repeat 0.5 milligram/kilogram bolus and increase the infusion rate incrementally (maximal infusion rate is 4 milligrams/minute) (Neumar et al, 2010).
    b) CHILD: 1 milligram/kilogram initial bolus IV/IO; followed by a continuous infusion of 20 to 50 micrograms/kilogram/minute (de Caen et al, 2015).
    2) LIDOCAINE/MAJOR ADVERSE REACTIONS
    a) Paresthesias; muscle twitching; confusion; slurred speech; seizures; respiratory depression or arrest; bradycardia; coma. May cause significant AV block or worsen pre-existing block. Prophylactic pacemaker may be required in the face of bifascicular, second degree, or third degree heart block (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010).
    3) LIDOCAINE/MONITORING PARAMETERS
    a) Monitor ECG continuously; plasma concentrations as indicated (Prod Info Lidocaine HCl intravenous injection solution, 2006).
    H) FOLLOW-UP VISIT
    1) If the possibility of chronic pulmonary complications or sequelae exists after exposure, long-term follow-up should be provided.
    I) 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).
    6.9.2) TREATMENT
    A) BURN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EFFICACY
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this agent.

Abstracts

Case Reports

    A) ROUTE OF EXPOSURE
    1) INHALATION
    a) Five volunteers exposed to an airborne concentration of 0.25 mg/m(3) for 8 hours developed productive cough by the following morning (Zenz & Berg, 1967).
    b) Two volunteers exposed to an airborne concentration of 0.1 mg/m(3) for 8 hours had no symptoms immediately after exposures, but developed considerable mucous production within 24 hours (Zenz & Berg, 1967).
    c) So-called "Boilermakers' Bronchitis" was seen in at least 74 of 100 boilermakers exposed to high levels of vanadium pentoxide fume. They experienced productive cough, sore throat, dyspnea upon exertion, chest pain or discomfort, wheezing, mild hypoxemia, and reduced expiratory flow rates, but chest X-rays were normal (Levy et al, 1984).
    d) Reduction in FVC and FEV were found in 17 boiler cleaners exposed to an airborne time-weighted average of 78 mcg/m(3) of vanadium (as 15 percent of total respirable dust). These reductions were reversible (Lees, 1980).
    2) ROUTE-OTHER
    a) Two volunteers exposed to 1 mg/m(3) for 8 hours had coughing which lasted for 8 days. Cough, rales, and wheezing developed after a subsequent exposure, but pulmonary function tests were normal (Zenz & Berg, 1967).
    b) Eighteen men occupationally exposed to heavy concentrations of pure vanadium pentoxide had burning eyes, sore throat, and dry cough by the end of the first day of exposure. Repeated exposure produced rales and incessant coughing.
    1) After two weeks of exposure, all employees had conjunctivitis, nasopharyngitis, hacking cough, fine rales, and wheezing. Repeated exposure increased the intensity of symptoms (Zenz et al, 1962).
    c) No radiologic evidence of pneumoconiosis or emphysema was seen in 36 workers eight years after vanadium pentoxide exposure. However, six of these workers still had bronchitis and asthma-like rhonchi with bouts of dyspnea (Hathaway et al, 1991; Kiviluoto, 1980).

Range Of Toxicity

Summary

    A) Inhalation exposure to an airborne concentration of 0.116 mg/m(3) produced no effect, while exposure to an airborne concentration of 1 mg/m(3) for 8 hours caused respiratory tract and eye irritation and bronchoconstriction.

Minimum Lethal Exposure

    A) ADULT
    1) "Probable oral lethal dose for humans is between 5 and 50 mg/kg" (Sittig, 1991).
    B) ANIMAL STUDIES
    1) Vanadium pentoxide is more toxic than other vanadium forms (although vanadium is poisonous to all species studied in all but very small doses irregardless of the route of administration) (ACGIH, 1991).
    2) RABBIT - The lethal dose by intravenous administration to rabbit is reported to be about 1.5 mg of vanadium pentoxide per kilogram of body weight (ACGIH, 1991).
    3) RAT - Deaths were reported in rats exposed to 70 mg/m(3) of vanadium pentoxide fume for over 2 hours. The lethal concentration of vanadium pentoxide dust was 700 to 800 mg/m(3) for 1 hour (ACGIH, 1991; Bingham et al, 2001).

Maximum Tolerated Exposure

    A) ADULT
    1) "Occupational vanadium poisoning has been associated with its mining and milling and from cleaning gas turbine heat exchanges or oil-fired boilers". Evaluation of occupational exposures to vanadium pentoxide is confounded by the concomitant potential exposures to vanadium trioxide, an intermediate in the reduction of vanadium pentoxide to metallic vanadium (ACGIH, 1991).
    a) Workers who were exposed to vanadium pentoxide dust at concentrations in excess of 0.5 mg/m(3) for a period of up to 2 weeks developed acute respiratory symptoms and demonstrable vanadium levels in urine. The signs and symptoms persisted fro nearly 2 weeks after removal from exposure (Baselt, 1997; Baselt, 2000).
    b) "Controlled human exposure to vanadium pentoxide at a concentration of 0.1 mg/m(3) for 8 hours produced mucous formation in the lungs and cough that subsided within 3 days, while a concentration of 0.25 mg/m(3) caused a loose cough that persisted for 7-10 days" (Baselt, 1997; Baselt, 2000).
    2) The lowest published toxic airborne concentration was 346 mg/m(3), producing cough, dyspnea, and excessive sputum (RTECS , 2001).
    3) Russian studies determined that 0.116 mg/m(3) was the no-effect concentration and 0.27 mg/m(3) the EC50 for irritant effects in humans (IRPTC, 1984).
    4) From older studies when vanadium compounds were used therapeutically, daily divided doses of 24 to 80 mg (as V) were tolerated by humans (Clayton & Clayton, 1994).
    5) The level which is immediately dangerous to life or heath is listed as 35 mg/m(3) by NIOSH (HSDB, 2001).
    B) ANIMAL STUDIES
    1) RABBIT - After 10 months of inhalation exposure at 10 to 30 mg/m(3), rabbits exhibited symptoms of bronchitis, pneumonia, weight loss, and bloody diarrhoea (Bingham et al, 2001).
    2) RABBIT - After 8 months of inhlation exposure at 20 to 40 mg/m(3) for 1 hour a day, rabbits exhibited symptoms of conhunctivitis, chronic rhinitis, tracheitis, emphysema, pathces of lung atelectasis, bronchopneumonia, and some pyelonephritis (Bingham et al, 2001).
    3) RAT - Acute intoxications were reported in rats exposed to 10 mg/m(3) of vanadium pentoxide fume for 2 hours and those exposed to 80 mg.m(3) of vanadium pentoxide dust for 1 hour (ACGIH, 1991).
    4) RAT - Intoxications from subchronic inhalation exposures to vanadium pentoxide were also reported when white rats were exposed to 3 to 5 mg/m(3) of vanadium pentoxide fume every other day (2 hours a day) for 3 months and when white rats were exposed to 10 to 30 mg/m(3) of vanadium pentoxide dust every other day (1 hour a day) for 4 months (ACGIH, 1991; Bingham et al, 2001).
    5) RAT - Mininmum effective concentration of vanadium pentoxide fume for rat has been reported to be 10 mg/m(3) by inhalation route (Bingham et al, 2001).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) 90 percent of blood vanadium is in the plasma. Normal levels are 0.4 to 2.8 mcg/L in plasma and 2 to 4 mcg/L in serum.
    b) Levels in serum of vanadium workers ranged from 11 to 20 mcg/L (Baselt, 1982).

Workplace Standards

    A) ACGIH TLV Values for CAS1314-62-1 (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) Vanadium pentoxide, as V
    a) TLV:
    1) TLV-TWA: 0.05 mg/m(3)
    2) TLV-STEL:
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: A3
    2) Codes: I
    3) Definitions:
    a) A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    b) I: Inhalable fraction; see Appendix C, paragraph A (of TLV booklet).
    c) TLV Basis - Critical Effect(s): URT and LRT irr
    d) Molecular Weight: 181.88
    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 CAS1314-62-1 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Vanadium dust
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 0.05 mg V/m(3) [15-minute]
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s): [*Note: The REL applies to all vanadium compounds except Vanadium metal and Vanadium carbide (see Ferrovanadium dust).],
    3) Listed as: Vanadium fume
    4) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 0.05 mg V/m(3) [15-minute]
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    5) IDLH: Not Listed

    C) Carcinogenicity Ratings for CAS1314-62-1 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Vanadium pentoxide, as V
    a) A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
    2) EPA (U.S. Environmental Protection Agency, 2011): Information reviewed but value not estimated. Refer to Full IRIS Summary. ; Listed as: Vanadium pentoxide
    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): 2B ; Listed as: Vandium pentoxide
    a) 2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Vanadium dust
    5) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Vanadium fume
    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 CAS1314-62-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Vandium, Respirable dust (as V2-O5)
    2) Table Z-1 for Vandium, Respirable dust (as V2-O5):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.5
    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
    3) Listed as: Vandium, Fume (as V2-O5)
    4) Table Z-1 for Vandium, Fume (as V2-O5):
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3: 0.1
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value: (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: ACGIH, 1991 Bingham et al, 2001 CHRIS, 2001 ) ITI, 1995 OHM/TADS, 2001; RTECS, 2001
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 23 mg/kg
    2) LD50- (ORAL)MOUSE:
    a) 5 mg/kg
    b) 23 mg/kg (ACGIH, 1991; CHRIS, 2001)
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 10 mg/kg
    4) LD50- (INTRAPERITONEAL)RAT:
    a) 12 mg/kg
    5) LD50- (INTRATRACHEAL)RAT:
    a) 6 mg/kg
    6) LD50- (ORAL)RAT:
    a) 10 mg/kg -- caused coma
    7) LD50- (SUBCUTANEOUS)RAT:
    a) 14 mg/kg -- caused coma
    8) TCLo- (INHALATION)HUMAN:
    a) 0.1 mg/m(3) for 8H (OHM/TADS, 2001)
    b) 1 mg/m(3) for 8H -- caused coughing, bronchiolar constriction, and conjunctive irritation
    c) 346 mg/m(3) -- induced coughing, dyspnea, and sputum
    9) TCLo- (INHALATION)RAT:
    a) 2 mg/m(3) for 1H/13W-intermittent -- altered classical behavioral conditioning
    b) 60 mcg/m(3) for 4H/22W- intermittent -- caused fatty liver degeneration and induced changes in serum composition and dehydrogenases
    c) 100 mcg/m(3) for 24H/24D- continuous -- affected brain, body weight, and phosphatases

Pharmacology Toxicology

Toxicologic Mechanism

    A) Just as in the environment, vanadium pentoxide appears to catalyze oxidations in the body (Friberg et al, 1986; Clayton & Clayton, 1994).
    1) Vanadium may increase the oxidation rate of fatty acids of liver phospholipids and may inhibit phospholipid synthesis (Clayton & Clayton, 1994).
    B) Vanadium inhibits a number of enzyme reactions (Clayton & Clayton, 1994).
    1) Vanadate is a potent inhibitor of sodium-potassium ATPase, calcium-ATPase, adenylate kinase, ribonuclease, phosphofructokinase and glucose-6-phosphatase in vitro (Friberg et al, 1986). These effects have not been demonstrated in vivo.
    2) Vanadium compounds may inhibit the biosynthesis of cholesterol. Vanadium workers tend to have lower plasma cholesterol levels (Sittig, 1985; Clayton & Clayton, 1994).
    a) The mechanism for reduction of cholesterol is inhibition of conversion of hydroxymethylglutaric to methylcrotonic acid and prevention of utilization of mevalonic acid (Clayton & Clayton, 1994).
    3) Vanadium may inhibit the activity of cholinesterase (Sittig, 1985).
    C) Vanadium has reduced the level of cystine in fingernails of workers. This may be the earliest detectable subclinical effect (Clayton & Clayton, 1994).
    1) Vanadium may lower the level of sulfhydryl groups in the liver (Clayton & Clayton, 1994).
    D) Vanadium has reduced levels of Coenzyme Q in mitochondria (Friberg et al, 1986).
    E) Vanadium has stimulated monoamine oxidase, an enzyme involved in the oxidation of serotonin, but may inhibit the oxidation of serotonin at high levels (Friberg et al, 1986).
    F) Vanadium pentoxide reduced viability of pulmonary macrophages, and this is believed to be critical to its ability to cause respiratory irritation (Clayton & Clayton, 1994).

Physicochemical

Physical Characteristics

    A) Vanadium pentoxide is an odorless, noncombustible solid (AAR, 2000; (Sittig, 1991).
    B) It has been described as a yellow-orange powder (Sittig, 1991), or dark gray flakes (Sittig, 1991), or yellow to rust brown orthorhombic crystals (Budavari, 1996).

Molecular Weight

    A) 181.88

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 49 CFR 172.101: Department of Transportation - Table of Hazardous Materials. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 11, 2005.
    5) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    6) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    7) 65 FR 39264: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
    8) 65 FR 77866: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
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