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EC number: 914-309-1 | CAS number: -
- 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
Although physico-chemical data tend to indicate that PBN1 mixture is a non-reactive inert substance and that its size and structure can not allow its absorption by skin or airway, a worst case approach has been chosen by considering the data for nickel chloride and nickel fluoride contained at a content of 4.5 and 9.5% respectively in PBN1 mixture.
Nickel was tested under a soluble form (nickel sulphate hexahydrate) in rats following oral administration for 2 years and in rats and mice following inhalation for 16 days, 13 weeks or 2 years. Oral administration mainly resulted in decreased survival rates (females) and reduced body weight gain (both genders) at the LOAEL. Inhalation exposure mainly resulted in local respiratory effects, with lung inflammation and fibrosis at all concentration levels.
Key value for chemical safety assessment
Repeated dose toxicity: via oral route - systemic effects
Endpoint conclusion
- Dose descriptor:
- NOAEL
- 2.2 mg/kg bw/day
- Study duration:
- chronic
- Species:
- rat
Repeated dose toxicity: inhalation - systemic effects
Endpoint conclusion
- Dose descriptor:
- LOAEC
- 0.06 mg/m³
- Study duration:
- chronic
- Species:
- rat
Additional information
NB. Effect levels above are expressed as mg Nickel/kg bw or mg Nickel/m3.
The repeated-dose toxicity of nickel was mainly assessed using a soluble form of the metal, nickel sulphate hexahydrate (NiSO4.6H2O).
By oral route, nickel sulphate hexahydrate was administered to rats for 2 years at 0, 10, 30 or 50 mg Ni sulphate/kg/day (equivalent to 2.2, 6.7 or 11.2 mg Ni/kg). Based on decreased survival rate (females) and reduced body weight gain (both genders) at higher dose levels, a NOAEL of 2.2 mg Ni/kg was identified.
By inhalation, rats and mice were exposed for up to 2 years to nickel sulphate hexahydrate at concentrations of 0, 0.12, 0.25 or 0.5 mg Ni sulphate/m3 (equivalent to 2.2, 6.7 or 11.2 mg Ni/m3) and 0, 0.25, 0.5 or 1 mg Ni sulphate /m3 (equivalent to 2.2, 6.7 or 11.2 mg Ni/m3), for rats and mice, respectively. The lung was clearly a target organ of nickel sulfate hexahydrate toxicity, with inflammation and fibrosis findings. Based on organ weight and microscopic changes in lungs and respiratory tract, no NOAEC was identified in 2-year studies. Following chronic exposure in rats for 2 years (6 hours a day, 5 days a week), the concentration of 0.25 mg Ni sulphate /m3 (equivalent to 0.06 mg Ni/m3) can be considered as a LOAEC based on the increased incidence of chronic active inflammation, macrophage hyperplasia, alveolar proteinosis, and fibrosis in the lungs of male and female rats.
Biochemical, morphometric and electron microscopy studies were conducted on the lungs of rabbits exposed to various forms of nickel by inhalation. Morphometric and ultrasructural analyses showed significant increases in the volume density of type II cells of alveolar epithelium, with no visible ultrastructural alteration, likely related to an overproduction of pulmonary surfactant. Repeated inhalation exposure of rabbits to metallic or ionic nickel dusts produced a typical pattern of lung lesions, characterized by accumulation of surfactant in alveolar spaces, impaired function of alveolar macrophages, and decreased lysozyme levels. Following repeated inhalatory exposure of rabbits to nickel dichloride, a significant decrease in the lysozyme activity in the lung lavage fluid as well as in the alveolar macrophages was observed, whereas the fibronectin content was unchanged in the lavage fluid and significantly increased in the macrophages.
Repeated dose toxicity: inhalation - systemic effects (target organ) respiratory: lung
Justification for classification or non-classification
Physico-chemical data tend to indicate that PBN1 mixture is a non-reactive inert substance and that its size and structure can not allow its absorption by skin or airways. Nevertheless by a conservative approach, the criteria for classification following the Directive 67/548/EEC or 1272/2008/EC will be applied.
Chronic lung inflammation and lung fibrosis are serious and potentially irreversible effects. According to Annex I of Directive 67/548/EEC, nickel fluoride (CAS No.: 10028 -18 -9) and nickel chloride (CAS No.: 7718 -54 -9), present in PBN1 mixture at 9.5 and 4.5% respectively, are both classified as T; R48/23, with a specific concentration limit of 1% for T; R48/23 classification. PBN1 mixture should therefore be classified as T; R48/23 (Directive 67/548/EEC) or STOT RE cat. 1 (H372) (Directive 1272/2008/EC).
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