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EC number: 237-898-0 | CAS number: 14059-33-7
- 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
Description of key information
Three inhalation studies and one oral study are available. Rats were exposed in a 28 day study
(similar to OECD guideline 412) to 2, 8, and 80 mg/m3 of the test
substance and observed for up to 12 month post exposure. A 90 day study
(according to OECD guideline 413) with rats and 0.1, 0.7 and 4 mg/m3
yielded the NOAEC. A non-guideline two-week study with exposure to 1.2
and 0.11 mg/L of uncoated BiVO4, 1.3 and 0.15 mg/L silica coated BiVO4
or silica coated TiO2 (1.9 mg/L) with a post-exposure time of up to 12
months. In a second experiment, rats were exposed to 1.2 mg/L BiVO4 for
two weeks and observed for 6 months until scheduled sacrifice. All
studies revealed that the target organ is the lung, systemic toxicity
was not observed.
In addition, rats were exposed by gavage to 40, 200, 100 mg/kg bw/day
for 28 days with a protocol similar to OECD guideline 407. Again,
systemic toxicity was not observed but females of the highest dose group
revealed necrosis of the glandular stomach. This local effect used to
set the NOAEL of this study at 200 mg/kg bw/day.
Key value for chemical safety assessment
Repeated dose toxicity: via oral route - systemic effects
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed
- Dose descriptor:
- NOAEL
- 200 mg/kg bw/day
- Study duration:
- subacute
- Species:
- rat
Repeated dose toxicity: inhalation - systemic effects
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- NOAEC
- 0.1 mg/m³
- Study duration:
- subchronic
- Species:
- rat
Repeated dose toxicity: inhalation - local effects
Endpoint conclusion
- Endpoint conclusion:
- no study available
Repeated dose toxicity: dermal - systemic effects
Endpoint conclusion
- Endpoint conclusion:
- no study available
Repeated dose toxicity: dermal - local effects
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
A comparative study that exposed rats (20/group) for two weeks to either 1.9 mg/L silica coated TiO2 or 0.1 mg/L and 1.2 mg/L uncoated bismuth vanadate revealed that lung lesions caused by either substance were reduced (bismuth vanadate) or no longer evident (TiO2) following a 12 month post exposure period. The mass median aerodynamic diameter for both substances was 0.05 -0.35 µm which is indicative of a considerable amount of nano-material (< 100 nm) present in the test substances. The normal architecture of the lung was almost restored after 12 months post exposure for coated TiO2. Exposure to uncoated bismuth vanadate resulted in a number of lung lesions comparable to those seen in the 28 day and 90 day study (see below). The lesions (especially alveolar proteinosis) caused by bismuth vanadate were reduced after 12 months post exposure and large portions of the lung regained normal alveolar architecture. At 0.1 mg/L uncoated bismuth vanadate, even foamy dust cells and alveolar proteinosis had disappeared at the 12 month sacrifice.
During a 28 day study, rats (5/sex/dose) were exposed to 2, 8, and 80 mg/m3. Deposition and clearance of the test substance from the lungs was concentration dependent, which is thought to be due to alterations in the function of the respiratory system caused by the test substance. The test substance did not translocate to the liver or the brain and low amounts of bismuth were found in the kidney only at the highest dose; vanadium was also detected in the kidney at the highest dose, albeit only around the limit of detection. The target organ was the lung, systemic toxicity which can be attributed to the test material was not observed. Increased absolute and relative lung weights occurred in all dose groups concentration dependently. Alveolar proteinosis and multifocal re-epithelialization of the pulmonary alveoli was observed in all treatment groups with increasing incidence at higher concentrations. Proliferation of alveolar macrophages was observed in all treatment groups. During the 12 month post-exposure observation period, re-epithelialization (hyperplasia of type II pneumocytes) following damage of type I pneumocytes was accompanied by alveolar proteinosis and most pronounced 6 months after cessation of exposure. Alveolar proteinosis recessed entirely at 2 mg/m3 during the post-exposure observation period. Other lesions showed distinct signs of regeneration or repair. Pulmonary fibrosis was not detected. The NOEC under the conditions of this study is below 2 mg/m3.
A 90 day study was conducted with rats (10/sex/dose) at doses of 0.1, 0.7 and 4 mg/m3. At the mid and high concentration, a significant increase in the relative and absolute lung weights, alveolar proteinosis, hyperplasia of type II pneumocytes, collagenization and cholesterol crystals (in some animals) was observed. One female of the high dose group exhibited focal squamous cell metaplasia. Systemic toxicity was not observed in either the 0.7 or the 4 mg/m3 dose groups. Animals of the 0.1 mg/m3 dose group showed no changes of toxicological significance in either the lung or systemically. This concentration is therefore considered the NOAEC under the conditions of the study.
Bioavailability of the vanadium ion was not observed in any of the repeated dose inhalation studies as all measurements in the different tissue types were either below or at the limit of detection. This in contrast to measurements that were performed in the course of inhalation studies with soluble vanadium compounds, especially vanadium pentoxide which translocates to a number of tissues upon inhalation exposure including kidney, bone and spleen. However, the low bioavailability of the bismuth vanadate is in agreement with the dissolution of bismuth vanadate in comparison with vanadium pentoxide which was done according to the OECD 29 protocol (see water solubility). The test revealed that the concentration of bismuth and vanadium were at or below the limit of detection at pH 5.5 and 6.5 and only slightly above the limit of detection at pH 8.5. By contrast, the solubility of vanadium pentoxide was a factor of 700-5000 higher, depending on the pH used. In addition, no significant toxicity was observed in the acute oral study and the i.p. micronucleus test with bismuth vanadate which contrasts studies with soluble vanadates that revealed considerable toxicity following single oral or i.p. administration.
The target organ after inhalation exposure with bismuth vanadate pigment was the lung as the pigment lead to considerable impairment of the functionality of the respiratory system which is reflected by a lower clearance rate and higher deposition in a dose dependent manner. In both the subacute and the subchronic studies, the test substance initiated an inflammatory response with concomitant repair of the damaged tissue. It cannot be excluded that these effects are not inherent to the substance but are due to the particle size generated for the studies. In both the 28 day and the 90 day study, the mass median aerodynamic diameter was below 1.3 µm and as low as 0.5 µm (high dose of the 28 day study) which indicates that a considerable amount of the pigment was present as fine or even super-fine dust. During the two week exposure of the comparative repeated dose study, a considerable amount of the test substance was in the range of nano particles. Because the number of particles is proportional to their size at a given lung burden, even at a comparatively low lung burden of 1.7 mg/lung in the 90 day study, the number of particles may have exceeded the capacity of the lung clearance mechanism which in turn was responsible for the effects seen. Nevertheless, a NOAEC for local effects on the lung was determined during the 90 day study at 0.1 mg/m3 while systemic toxicity was not observed in any repeated dose inhalation study. This concentration apparently led to a deposition of a number of particles that did not disturb the lung’s clearance system.
During a 28 day study that included a 14 day recovery period, rats (6/sex/dose) were exposed orally to 40, 200 or 1000 mg/kg bw./day by gavage. Systemic toxicity was not observed but 1/6 female animals of the high dose group showed necrosis of the glandular stomach at the 28 day necropsy and 3/6 female animals had the same finding at the end of the 14 day recovery period. This finding was not observed in male animals after 28 days; the male animals of the recovery group were not examined. This local effect is thought to be related to the test material and was used to set the NOEL at the mid dose of 200 mg/kg bw/day.
Repeated dose toxicity: inhalation - systemic effects (target
organ) respiratory: lung
Justification for classification or non-classification
The test material causes local effects in the lung following inhalation exposure. This inflamatory response is, at least in part, reversible and reminescent of effects caused by inert particles (accumulation of macrophages). The small particle sizes used in the repeated dose studies make it likely that despite a relatively low lung burden of 1.7 mg/lung in the 90 day study, a high number of particles were present in the lung of the animals. At the same time, systemic toxicity was not observed in any of the inhalation repated dose studies which is in line with the low acute oral (see acute toxicity oral) and intraperitoneal (see genetic toxicity in vivo) toxicity and extremely low solubility of the test material. Therefore, despite the low NOAEL of 0.1 mg/m3, it is proposed to classify the substance with Xn, R48/20 according to 67/548/EEC and STOT repeated exposure, Cat. 2 according to UN GHS criteria.
The local effects observed in the rat stomach do not warrant a classification.
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