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EC number: 215-127-9 | CAS number: 1304-28-5
- 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
Key value for chemical safety assessment
Additional information
Studies specifically assessing effects of barium oxide on in vitro genetic toxicity are not available. However, data from the analogue substance barium chloride dihydrate (CAS 10326-27-9) were used. Barium oxide reacts with water to form the corresponding hydroxide being irritating or corrosive to skin and eyes. Barium chloride dihydrate and barium oxide share the barium ione as cation which may be toxophore of the registered compound barium oxide. For details on comparability of barium oxide and barium chloride dihydrate, please refer to the weight-of-evidence justification.
It is well documented that corrosivity itself does not induce genetic toxicity. Due to the cytotoxic properties of corrosive substances, cell death precedes any gene mutation or clastogenic effect. Therefore, the corrosive properties of barium oxide can be considered negative in terms of genetic toxicity.
Barium chloride dihydrate (100 to 10,000 µg/plate) did not induce gene mutations in any of five strains (TA100, TA1535, TA1537, TA97, and TA98) of S. typhimurium when tested in a preincubation protocol with and without Arodor 1254-induced male Sprague-Dawley rat or Syrian hamster liver S9 (NTP 1994).
The mutagenicity of barium chloride dihydrate (62.5 – 1000 µg/mL) was tested in mammalian cells in L5178Y mouse lymphoma cells similar to OECD TG 476 (NTP 1994). In the absence of metabolic activation, no increased incidence of TFT resistance was detected. If the cells were incubated with barium chloride dihydrate in the presence of S9 extract (see above), a statistically significant increase in mutations was observed. However, the biological significance of this finding is questionable since the number of mutant colonies in trial 1 (+S9) did not exceed the number of mutant colonies in the negative control of trial 2 (-S9). In order to assess the biological relevance of the data at hand, comparison with historical control data is required. Further, the cell viability was below 30% in all concentrations that resulted in increased mutant frequencies in trial 2 (+S9). Therefore, the results of this test are considered unreliable and the study is disregarded for mutagenicity assessment.
A second study assessing the mutagenicity of barium chloride dihydrate was conducted in 2010 according to OECD testing guideline 476 and under GLP (Lloyd 2010). The test substance was added for 3 hours with and without S9 mix or 24 hours without S9 mix in doses of 0-1400 µg/mL. This study was considered more appropriate for assessment of mutagenicity than the NTP study described above, since lack of cytotoxicity (concurrent with testing up to precipitating doses) together with adequate responses to control substances rendered it a more reliable study with robust data. No dose-dependent increase in mutant frequencies was observed in the first experiment, and 3 hours treatment without S9 mix was also negative in the second experiment. In the conditions of 3 hours treatment with S9 mix and 24 hours treatment without metabolic activation, the repetition led to a significant linear trend. However, since the maximum mutant frequency did not exceed the mean negative control values + global evaluation factor (GEF), the result was considered not biologically relevant and it is concluded that barium chloride dihydrate was not mutagenic in the mouse lymphoma assay under the experimental conditions tested.
The clastogenicity of barium chloride dihydrate was tested on the one hand in a chromosomal aberration assay and on the other hand in a sister chromatid exchange assay. The chromosomal aberration assay was performed similar to OECD TG 473, and concentrations of 50 – 5000 µg/mL were tested in two separate trials. Barium chloride dihydrate did not lead to an increased incidence of chromosomal aberrations, independent of metabolic activation. The sister chromatid exchange assay was performed similar to OECD TG 479 at concentrations of 50 – 3000 µg/mL in two separate trials with and without metabolic activation. Barium chloride dihydrate did not induce sister chromatid exchanges under the conditions tested.
Conclusion:
Based on the observations with BaCl2*2H2O (common dissociation product Ba2+), barium is not mutagenic in bacteria cells or mammalian cells and not clastogenic in mammalian cells.
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
BaO has two main routes of toxicity - corrosivity upon contact with water and barium toxicity after dissociation in water. It is well documented that corrosivity itself does not induce genetic toxicity.The mutagenic and clastogenic effects of barium were tested with barium chloride and showed no mutagenic or clastogenic potential in the Ames test, mouse lymphoma assay, chromosomal aberration assay, and sister chromatid exchange assay. A reliable mammalian cell mutagenesis assay generated negative results, and clastogenicity was not observed under the condistions tested. The present data on genetic toxicity do not fulfill the criteria laid down in regulation (EU) 1272/2008 and therefore, a non-classification is warranted.
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