Vanadic acid, ammonium salt

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use "alcohol" foam, dry chemical, or carbon dioxide. /Vanadium compound, N.O.S./

Containers of vanadium shall be kept tightly closed at all times when not in use. Containers shall be stored in a safe manner to minimize accidental breakage, spillage, or contact with moisture. Combustible materials, such as finely ground vanadium carbide, vanadium aluminum alloys, vanadium metal, or ferrovanadium should be kept away from heat, sparks, or flames. /Vanadium compounds/

Divalent and trivalent vanadium compounds are reducing agents and require storage under an inert atmosphere to avoid oxidation. /Divalent and trivalent vanadium compounds/

Environmental considerations: Water spill: Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates. /Vanadium compound, N.O.S./

Environmental considerations: Land spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with plastic sheet to prevent dissolving in rain or fire fighting water. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. /Vanadium compound, N.O.S./

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Waste material contaminated with vanadium shall be disposed of in a manner not hazardous to employees. The disposal method must conform with applicable local, state, and federal regulations and must not constitute a hazard to the surrounding population or environment. /Vanadium/

The following wastewater treatment technologies have been investigated for vanadium: Concentration process: chemical precipitation. /Vanadium/

Personnel protection: Avoid breathing dusts, and fumes from burning material. Keep upwind. ... Avoid bodily contact with the material. ... Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water. /Vanadium compound, N.O.S./

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. /Vanadium compound, N.O.S./

SRP: Contaminated protective clothing should be segregated in a manner such that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. The completeness of the cleaning procedures should be considered before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at the end of shift, but should remain at employee's place of work for cleaning.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

For more Preventive Measures (Complete) data for VANADIC ACID, AMMONIUM SALT (7 total), please visit the HSDB record page.

The employer shall use engineering controls if needed to keep the concentration of airborne vanadium at or below the limits specified and shall provide protective clothing and equipment resistant to the penetration of vanadium when necessary to prevent gross skin and eye contact with liquid vanadium solutions. Protective equipment suitable for emergency use shall be located at clearly identified stations outside the work area. /Vanadium/

Wear appropriate personal protective clothing to prevent skin contact. /Vanadium dust/

Wear appropriate eye protection to prevent eye contact. /Vanadium dust/

Respirator Recommendations: Up to 0.5 mg/cu m (as V): /Vanadium dust; Vanadium fume/[Table#5679]

For more Personal Protective Equipment (PPE) (Complete) data for VANADIC ACID, AMMONIUM SALT (9 total), please visit the HSDB record page.

EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.

IDENTIFICATION AND USE: Ammonium vanadate is an orange powder. It is used as a spray color revealing device in analytical toxicology of drugs. HUMAN EXPOSURE AND TOXICITY: There are no data available. ANIMAL STUDIES: Ammonium vanadate (10 or 20 mg/L) in drinking water had no influence on tumor development of large-bowel neoplasms in mice treated with 1,2-dimethylhydrazine (DMH) given by subcutaneous injection for 20 weeks. Although thymidine incorporation was increased, ammonium vanadate did not have any effect on the incidence or type of tumor induced by DMH. Rats fed 15 mg vanadium/kg as ammonium vanadate for 2 months showed increased ventricular pressure and pulmonary hypertension, but no changes in systemic circulation. When ammonium vanadate was administered orally to rats and mice in doses of 0.005-1 mg vanadium/kg for 21 days (higher levels) to 6 months (lower levels), a dose of 0.05 mg vanadium/kg was found to be the threshold for functional disturbances in the conditioned reflex activity in both rats and mice. ECOTOXICITY STUDIES: A concentration of 0.02 mg/L ammonium vanadate interfered with the cell division of the fresh-water algae Chlorella pyrenoidosa, whereas 0.25 mg/L was lethal.

Vanadium damages alveolar macrophages by decreasing the macrophage membrane integrity, thus impairing the cells' phagocytotic ability and viability. The pentavalent form of vanadium, vanadate, is a potent inhibitor of the Ca+-ATPase and Na+,K+-ATPase of plasma membranes, which decreases intracellular ATP concentration. Vanadium is also believed to induce the production of reactive oxygen species. This may damage DNA and also cause oxidative stress, which can damage the reproductive system. Vanadium also inhibits protein tyrosine phosphatases, producing insulin-like effects. (L837, A247, A248, A249, A250, A251)

/AQUATIC SPECIES/ A concentration of 0.02 mg/L, as ammonium vanadate, interfered with the cell division of the fresh-water algae Chlorella pyrenoidosa, whereas 0.25 mg/L was lethal.

/AQUATIC SPECIES/ This paper deals with the underlying biochemical mechanism of the cytotoxicity of vanadium (as ammonium monovanadate) in a warm water teleost, Clarias batrachus (Linn). Lipid peroxidation, a well-known biochemical marker for cell injury, was found to be significantly enhanced in fish liver, kidney, and brain after 12 hr and maximally induced after 72 hr exposure of this compound (10 mg/L). When the fish were exposed to 5, 10, 15, and 20 mg/L of vanadium compound for 72 hr, lipid peroxidation in these three organs were elevated dose-dependently but the degree of increase varied between organs. The induction of both enzymatic (paraquat-NADPH) and nonenzymatic (ascorbate-Fe2+) in vitro lipid peroxidation was enhanced by this vanadium salt when added in micromolar concentrations (42 or 85 uM) to the liver, kidney, and brain microsomal preparations. Both in vivo and in vitro studies revealed that kidney tissue was most severely affected with acute vanadium intoxication, followed by liver and brain.

Biological monitoring of vanadium in serum, blood, and urine has been used to monitor vanadium levels in the general population or in occupationally exposed workers. Vanadium levels in these matrices have not, however, been shown to correlate with vanadium levels in the air and as such are of limited usefulness as quantitative biomarkers of exposure. /Vanadium compounds/

Because of cases of bronchial asthma and bronchitis in worker population exposed to vanadium compounds, periodic testing of pulmonary function is recommended. /Vanadium compounds/

The assessment of vanadium exposure can be accomplished through measurement of vanadium. This test may be useful for assessing /exposure/ to larger than normal amounts of vanadium, but there was no information found in the literature showing a correlation of these levels with environmental levels or onset of clinical effects. Blood Reference Ranges: Normal - less than 1 ug/L; Exposed - not established; Toxic - not established. Serum or Plasma Reference Ranges: Normal - less than 0.24 ug/L; Exposed - not established; Toxic - not established. Urine Reference Ranges: Normal - 0.06 to 0.87 ug/L; Exposed - Workers exposed to average 8 hr air concentrations of 6.0 to 6.4 mg/cu m had urine vanadium levels between 2.6 to 4.6 ug/L in specimens that were collected at the start of the next work day. BAT for vanadium pentoxide (sampling time for long term exposures: after several shifts, measured as vanadium): 70 ug/g creatinine; Toxic - In a study involving controlled human exposure to vanadium pentoxide, where levels caused development of mild respiratory effects, the peak urine vanadium level was 130 ug/L at 3 days after exposure. /Vanadium/

Pulmonary Function Tests: The tests that have been found to be practical for population monitoring include: spirometry and expiratory flow-volume curves; determination of lung volumes; diffusing capacity for carbon monoxide; single-breath nitrogen washout; inhalation challenge tests; serial measurements of peak expiratory flow; exercise testing. /Vanadium/

Differentiating vanadium pulmonary toxicity from infection or allergy of the respiratory tract is difficult in that presenting signs and symptoms are similar. A specific vanadium exposure history must be elicited from affected individuals. Examination may reveal a patient with clear watery discharge from the eyes and nose. Mucosal surfaces may be erythematous. Auscultation of lung fields will reveal rhonchi or wheezing. /Vanadium compounds/

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Rats fed 15 mg vanadium/kg as ammonium vanadate for 2 months showed increased ventricular pressure and pulmonary hypertension, but no changes in systemic circulation ...

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ In studies where ... ammonium vanadate /was/ administered orally to rats and mice in doses of 0.005-1 mg vanadium/kg for 21 days (higher levels) to 6 months (lower levels), a dose of 0.05 mg vanadium/kg was found to be the threshold for functional disturbances in the conditioned reflex activity in both rats and mice.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Ammonium vanadate (10 or 20 mg/L) in drinking water had no influence on tumor development of large-bowel neoplasms in mice treated with 1,2-dimethylhydrazine (DMH) given by subcutaneous injection for 20 weeks. Although thymidine incorporation was increased, ammonium vanadate did not have any effect on the incidence or type of tumor induced by DMH.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/

For advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) or lorazepan (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

Section 8(a) of TSCA requires manufacturers of this chemical substance to report preliminary assessment information concerned with production, exposure, and use to EPA as cited in the preamble in 51 FR 41329. Effective date: 7/11/03; Reporting date: 9/9/03.

(AZ) ARIZONA 7 ug/L /Vanadium/

(FL) FLORIDA 49 ug/L /Vanadium/

(MN) MINNESOTA 50 ug/L /Vanadium/

(WI) WISCONSIN 30 ug/L /Vanadium/

(CA) CALIFORNIA 50 ug/L /Vanadium/