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EC number: 234-373-8 | CAS number: 11129-15-0
- 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
Short-term toxicity to fish
Administrative data
Link to relevant study record(s)
Description of key information
The endpoint is covered by a weight of evidence approach including one short-term fish study for zirconium dioxide (Bazzon, 2000) and two short-term fish studies for calcium hydroxide (Egeler et al., 2007a; Locke et al., 2009). Zirconium dioxide did not cause any adverse effects in Brachydanio rerio up to and including the limit test concentration of 100 mg/L (nominal loading rate). For calcium oxide, two studies performed with calcium hydroxide were added to the dossier because calcium oxide is transformed to calcium hydroxide when in contact with water. Both calcium oxide and calcium hydroxide will initially increase the pH of the aqueous medium in which they are dissolved. The observed adverse effects in the two studies added to the dossier could be ascribed to this pH increase, with initial pH being > 10 in test solutions close to the reported median effect concentrations. However, since Eidam (2014, 2015) demonstrated that only a limited amount of calcium is released (in pure water) from calcium zirconium oxide, no drastic pH increase is to be expected from adding the substance to aqueous media. Therefore, taking into account all abovementioned information, calcium zirconium oxide can be concluded to be not toxic or harmful to fish.
Key value for chemical safety assessment
Additional information
1. Information on zirconium dioxide
The 96-h acute toxicity of zirconium dioxide to Brachydanio rerio was studied (Bazzon, 2000) under static conditions, according to OECD guideline 203. Fish were exposed to control and test chemical at a nominal concentration of 100 mg/L. Mortality/immobilization were monitored daily. No mortality was observed during the test, neither in the control group nor in the group exposed to the test item. The 96-h LC50 was thus > 100 mg/L.
2. Information on calcium oxide
For calcium oxide, data obtained from tests performed with calcium hydroxide were added to the dossier. The rationale behind this is that in the environment, CaO will result in Ca(OH)2 formation when in contact with water, according to the following (general) reaction:
CaO + H2O <--> Ca(OH)2
Two studies performed with Ca(OH)2 were added to the weight of evidence approach. The first study is a short-term toxicity study with the freshwater fish rainbow trout (Egeler et al., 2007a) which was executed according to OECD guideline 203. The biological findings (96-h LC50 = 50.6 mg Ca(OH)2/L) appeared to be closely related to the initial pH of the test solutions, which was > 10 at concentrations close to the LC50. The second study is a short-term toxicity study performed with the marine species Gasterosteus aculeatus (threespine stickleback) (Locke et al., 2009). Also in this study, a concentration-response relationship was established, yielding a 96-h LC50 of 457 mg Ca(OH)2/L. Here too, increased pH levels (> 10) were observed in test solutions where mortality occurred.
In the environment, lime substances rapidly dissociate or react with water. These reactions, together with the equivalent amount of hydroxyl ions set free when considering 100 mg of the lime compound (hypothetic example), are illustrated below:
Ca(OH)2 <--> Ca2+ + 2OH-
100 mg Ca(OH)2 or 1.35 mmol sets free 2.70 mmol OH-
CaO + H2O <--> Ca2+ + 2OH-
100 mg CaO or 1.78 mmol sets free 3.56 mmol OH-
From the dissociation in the aquatic environment, it is clear that the effect of calcium oxide or calcium hydroxide must be caused either by calcium or hydroxyl ions. Since calcium is abundantly present in the environment and since the 96-h LC50 reported by Egeler et al. (2007a) is within the same order of magnitude of its typical natural concentrations, it can be assumed that the adverse effects are mainly caused by the pH increase and not by calcium.
3. Conclusion on calcium zirconium oxide
Calcium zirconium oxide is zirconium dioxide with calcium partly replacing zirconium in the crystal lattice. Zirconium dioxide has been demonstrated not to cause any adverse effects in fish. Calcium oxide (as an individual substance) on the other hand is expected to be hydrolysed to calcium hydroxide, which will in its turn be subject to dissociation, releasing OH- ions and resulting in a pH increase. The observed effects in the short-term toxicity studies in fish were ascribed to this pH increase. Calcium as such is abundantly present in the environment and the lowest LC50 (reported by Egeler et al., 2007a) is within the same order of magnitude of its typical natural concentrations, therefore, there is no reason to assume that the observed toxicity is caused by calcium. Further, it was demonstrated by Eidam (2014, 2015) that only limited amounts of calcium are released (in pure water) from calcium zirconium oxide. Consequently, no dramatic pH increase is to be expected from the limited dissolution of calcium zirconium oxide in water and therefore the substance is considered to be not toxic or harmful to fish.
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