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EC number: 406-260-5 | CAS number: 58834-75-6 BTN; VPO CATALYST
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Endpoint summary
Administrative data
Link to relevant study record(s)
Description of key information
Short description of key information on bioaccumulation potential result:
Absorption via the oral and dermal routes is regarded as low. Absorption by the inhalation route is greater. Following absorption, vanadium is transported in the serum bound to transferrin and is distributed widely throughout the body. The highest amounts have been located in the bone, kidneys, liver, spleen and testes. Retention of vanadium has been reported, particularly in bone. Absorbed vanadium is predominantly excreted via urine. In humans initial clearance via urine is rapid, followed by a slower phase. About 60% of absorbed vanadium is excreted by the kidneys within 24 hours.
Key value for chemical safety assessment
- Bioaccumulation potential:
- low bioaccumulation potential
Additional information
Toxicokinetics
Absorption
In general, available data indicate that in both animals and humans, absorption of vanadium via the gastrointestinal tract is low.Vanadium in the vanadate (+5) state is absorbed about three to five times more effectively than in the vanadyl (+4) state (NTP,2008).Based on the poor absorption of vanadium from the GI tract, internal tissue concentrations and toxicity from oral exposure are expected to be low.Ingested vanadium is absorbed poorly by the gastrointestinal tract of humans. Only 0.1-1.0% of a 100 and 125 mg dose of diammonium oxytartarovanadate was absorbed gastrointestinally, and 60% of the absorbed dose was excreted by the kidneys within 24 hours (Curran et al, 1959). An oral dose of 0.3 mg/kg vanadium from vanadium pentoxide administered to rats resulted in only 2.6% being absorbed (Conklin et al, 1982). Wiegman et al studied the absorbtion and excretion of radioactive vanadium in rats. Vanadium was administered as sodium metavanadate by gavage (5μmol, corresponding to 0.255 mg vanadium). After 4 days, 18% of the dose was excreted in urine and 69% was recovered in the faeces. The remainder was retained in various organs and tissues. When A1(OH)3gel was given to the rats at the same time as vanadium administration, aluminum hydroxide decreased the absorbtion of vanadium, 8% of the administered radioactivity being recovered in the urine and 86% recovered in the faeces.One study reported by Azay et al on the bioavailability of vanadium from vanadium sulphate after oral gavage administration of 7.5 and 15 mg vanadium/kg to rats indicates higher absorption, estimated to be 16.8 and 12.5 %, as determined from area under the curve (AUC) data compared with intravenous administration.
Dermal exposure is also reported to result in poor absorption (Janssen et al., 1998; EFSA, 2004; IARC, 2006).
Absorption of vanadium in the lungs following inhalation exposure is higher and depends on particle size and the solubility of the vanadium compound (Janssen et al., 1998).Conklin et al. (1982) reported that 100% of an intratracheal dose of 0.3 mg/kg vanadium administered as radiolabeled vanadium pentoxide was absorbed by rats. Approximately 40% of the recovered radioactivity had been cleared from the lungs within 1 hour, and 90% had been cleared within 3 days. Clearance from the lung was primarily into blood, liver and bone, indicating rapid absorption. By post-treatment day 3, 40% of the radioactivity had been recovered in the urine. Similar results were obtained for vanadyl chloride.
Distribution
Following oral uptake in rats, vanadium is transported in the serum bound to transferrin and is distributed widely throughout the body. The highest amounts were located in the bone, kidneys, liver, spleen and testes. Retention of vanadium was reported, particularly in bone (WHO, 2000; NTP, 2002; EFSA, 2004). Limited data indicate that vanadium binds to transferrin in plasma in humans (NTP, 2002).
Excretion
Absorbed vanadium is predominantly excreted via urine. In rats and mice, vanadium is eliminated from plasma in three phases (plasma half times of 15 minutes, 14 hours and 8.5 days (EFSA, 2004)). In humans, initial clearance via urine is rapid, followed by a slower phase. About 60% of absorbed vanadium is excreted by the kidneys within 24 hours (NTP, 2002).
Azay, J., Bres, J., Krosniak, M., Tesseidre, P.-L., Cabanis, J.-C., Serrano, J.-J. and Cros, G.
Vanadium pharmacokinetics and oral bioavailability upon single-dose administration of vanadyl sulfate to rats.
Fundamental Clinical Pharmacology15(5): 313-324,2001
Conklin, A.W., C.S. Skinner, T.L. Felten and C.L. Sanders.
Clearance and distribution of intratracheally instilled vanadium-48 compounds in the rat.
Toxicol. Lett. 11(1-2): 199-204, 1982
Curran, G.L., D.L. Arzarnoff and R.E. Bohnger.
Effect of cholesterol synthesis inhibition in normocholesteremic young men.
J. Clin. Invest. 38: 1251-1261, 1959
EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the tolerable upper intake level of vanadium (Request N° EFSA-Q-2003-018); European Food Safety Authority, Parma, Italy. The EFSA Journal 33: 1-22 (2004)
IARC. Cobalt Sulfate, Gallium Arsenide, Indium Phospide and Vanadium Pentoxide. IARC Monographs on the evaluation of carcinogenic risks to humans Vol. 86: Summary of data reported and evaluation. International Agency for Research on Cancer,,, 2006.
Janssen PJCM,van, Engelen JGM van, Schielen PCJI, Wouters MFA.
Maximum permissible risk levels for human intake of soil contaminants: fourth series of compounds.
RIVM report No. 711701004; National Institute for Public Health and the Environment, Bilthoven, The Netherlands. 1998
NTP. Technical report on the toxicology and carcinogenesis studies of vanadium pentoxide (CAS no. 1314-62-1) in F344/N rats and B6C3F1 mice (inhalation studies).
National Toxicology Program, Technical Report Series No 507, NIH Publication no. 03-4441. Dept. of Health and Human Services,,. 2002
NTP test proposal.NTP Board of Scientific Counselors Meeting, June 11-12, 2008
Wiegman, T.B., H.D. Day and R.V. Patak.
Intestinal absorption and secretion of radioactive vanadium (48VO3-) in rats and effect of Al(OH)3.
J. Toxicol. Environ. Health. 10: 233-245, 1982
WHO. Air Quality Guidelines - Second Edition; Chapter 6.12: Vanadium.
World Health Organization, Regional Office for Europe, 2000
Discussion on bioaccumulation potential result:
Toxicokinetics
Absorption
In general, available data indicate that in both animals and humans, absorption of vanadium via the gastrointestinal tract is low.Vanadium in the vanadate (+5) state is absorbed about three to five times more effectively than in the vanadyl (+4) state (NTP,2008).Based on the poor absorption of vanadium from the GI tract, internal tissue concentrations and toxicity from oral exposure are expected to be low.Ingested vanadium is absorbed poorly by the gastrointestinal tract of humans. Only 0.1-1.0% of a 100 and 125 mg dose of diammonium oxytartarovanadate was absorbed gastrointestinally, and 60% of the absorbed dose was excreted by the kidneys within 24 hours (Curran et al, 1959). An oral dose of 0.3 mg/kg vanadium from vanadium pentoxide administered to rats resulted in only 2.6% being absorbed (Conklin et al, 1982). Wiegman et al studied the absorbtion and excretion of radioactive vanadium in rats. Vanadium was administered as sodium metavanadate by gavage (5μmol, corresponding to 0.255 mg vanadium). After 4 days, 18% of the dose was excreted in urine and 69% was recovered in the faeces. The remainder was retained in various organs and tissues. When A1(OH)3gel was given to the rats at the same time as vanadium administration, aluminum hydroxide decreased the absorbtion of vanadium, 8% of the administered radioactivity being recovered in the urine and 86% recovered in the faeces.One study reported by Azay et al on the bioavailability of vanadium from vanadium sulphate after oral gavage administration of 7.5 and 15 mg vanadium/kg to rats indicates higher absorption, estimated to be 16.8 and 12.5 %, as determined from area under the curve (AUC) data compared with intravenous administration.
Dermal exposure is also reported to result in poor absorption (Janssen et al., 1998; EFSA, 2004; IARC, 2006).
Absorption of vanadium in the lungs following inhalation exposure is higher and depends on particle size and the solubility of the vanadium compound (Janssen et al., 1998).Conklin et al. (1982) reported that 100% of an intratracheal dose of 0.3 mg/kg vanadium administered as radiolabeled vanadium pentoxide was absorbed by rats. Approximately 40% of the recovered radioactivity had been cleared from the lungs within 1 hour, and 90% had been cleared within 3 days. Clearance from the lung was primarily into blood, liver and bone, indicating rapid absorption. By post-treatment day 3, 40% of the radioactivity had been recovered in the urine. Similar results were obtained for vanadyl chloride.
Distribution
Following oral uptake in rats, vanadium is transported in the serum bound to transferrin and is distributed widely throughout the body. The highest amounts were located in the bone, kidneys, liver, spleen and testes. Retention of vanadium was reported, particularly in bone (WHO, 2000; NTP, 2002; EFSA, 2004). Limited data indicate that vanadium binds to transferrin in plasma in humans (NTP, 2002).
Excretion
Absorbed vanadium is predominantly excreted via urine. In rats and mice, vanadium is eliminated from plasma in three phases (plasma half times of 15 minutes, 14 hours and 8.5 days (EFSA, 2004)). In humans, initial clearance via urine is rapid, followed by a slower phase. About 60% of absorbed vanadium is excreted by the kidneys within 24 hours (NTP, 2002).
Azay, J., Bres, J., Krosniak, M., Tesseidre, P.-L., Cabanis, J.-C., Serrano, J.-J. and Cros, G.
Vanadium pharmacokinetics and oral bioavailability upon single-dose administration of vanadyl sulfate to rats.
Fundamental Clinical Pharmacology15(5): 313-324,2001
Conklin, A.W., C.S. Skinner, T.L. Felten and C.L. Sanders.
Clearance and distribution of intratracheally instilled vanadium-48 compounds in the rat.
Toxicol. Lett. 11(1-2): 199-204, 1982
Curran, G.L., D.L. Arzarnoff and R.E. Bohnger.
Effect of cholesterol synthesis inhibition in normocholesteremic young men.
J. Clin. Invest. 38: 1251-1261, 1959
EFSA. Opinion of the Scientific Panel on Dietetic Products, Nutrition and Allergies on a request from the Commission related to the tolerable upper intake level of vanadium (Request N° EFSA-Q-2003-018); European Food Safety Authority, Parma, Italy. The EFSA Journal 33: 1-22 (2004)
IARC. Cobalt Sulfate, Gallium Arsenide, Indium Phospide and Vanadium Pentoxide. IARC Monographs on the evaluation of carcinogenic risks to humans Vol. 86: Summary of data reported and evaluation. International Agency for Research on Cancer,,, 2006.
Janssen PJCM,van, Engelen JGM van, Schielen PCJI, Wouters MFA.
Maximum permissible risk levels for human intake of soil contaminants: fourth series of compounds.
RIVM report No. 711701004; National Institute for Public Health and the Environment, Bilthoven, The Netherlands. 1998
NTP. Technical report on the toxicology and carcinogenesis studies of vanadium pentoxide (CAS no. 1314-62-1) in F344/N rats and B6C3F1 mice (inhalation studies).
National Toxicology Program, Technical Report Series No 507, NIH Publication no. 03-4441. Dept. of Health and Human Services,. 2002
NTP test proposal.NTP Board of Scientific Counselors Meeting, June 11-12, 2008
Wiegman, T.B., H.D. Day and R.V. Patak.
Intestinal absorption and secretion of radioactive vanadium (48VO3-) in rats and effect of Al(OH)3.
J. Toxicol. Environ. Health. 10: 233-245, 1982
WHO. Air Quality Guidelines - Second Edition; Chapter 6.12: Vanadium.
World Health Organization, Regional Office for Europe,,, 2000
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