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EC number: 215-114-8 | CAS number: 1303-00-0
- 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
Specific investigations: other studies
Administrative data
Link to relevant study record(s)
Description of key information
One study on effects of hypoxia in in male B6C3F1 mice and one study on effects of hypoxia in male Wistar rats are reliable without restriction. The exposure to atmosphere with reduced oxygen content (measured 10.7%) of mice and rats caused changes of various hematology parameters and blood gas parameters, as responses and adaption reaction to the hypoxemia condition. In mice adaptive changes were also observed in histopathology of lungs, spleen and testis. In mice and rats, sperm parameters were not changed at any of the examined time points. The review article on human pulmonary alveolar proteinosis (Trapnell et al., 2003) is reliable with restrictions. Human pulmonary alveolar proteinosis is a disorder in which lipoproteinaceous material accumulates within alveoli. Recent studies led to the concept that human acquired pulmonary alveolar proteinosis is an autoimmune disease targeting granulocyte-macrophage colony-stimulating factor (GM-CSF). A neutralizing autoantibody against GM-GSF causes defects in the functioning of alveolar macrophages, including impairment of the catabolism of surfactant lipids and proteins and disruption of surfactant homeostasis. No correlation to an exposure of gallium arsenide was found. Eight studies are not reliable.
Additional information
The review article on human pulmonary alveolar proteinois (Trapnell et al., 2003) is reliable with restrictions. The other 8 studies on specific effects of GaAs such as: magnetometry, urine porphyrines, morphometry and cytochemistry are not reliable. Therefore they are disregarded.
The review article on human alveolar proteinosis revealed no association of the disease with an exposure to GaAs.
Human pulmonary alveolar proteinosis is a disorder in which lipoproteinaceous material accumulates within alveoli. An important feature of the disease is susceptibility to pulmonary infections, sometimes with opportunistic organisms. Recent studies led to the concept that human acquired pulmonary alveolar proteinosis is an autoimmune disease targeting granulocyte-macrophage colony-stimulating factor (GM-CSF). A neutralizing autoantibody against GM-GSF causes defects in the functioning of alveolar macrophages, including impairment of the catabolism of surfactant lipids and proteins and disruption of surfactant homeostasis.
One study on effects of hypoxia in in male B6C3F1 mice and one study on effects of hypoxia in male Wistar rats are reliable without restriction. The exposure to atmosphere with reduced oxygen content (measured 10.7%) of mice and rats caused changes of various hematology parameters and blood gas parameters, as responses and adaption reaction to the hypoxemia condition. In mice adaptive changes were also observed in histopathology of lungs, spleen and testis. In mice and rats, sperm parameters were not changed at any of the examined time points. The review article on human pulmonary alveolar proteinosis (Trapnell et al., 2003) is reliable with restrictions. Human pulmonary alveolar proteinosis is a disorder in which lipoproteinaceous material accumulates within alveoli. Recent studies led to the concept that human acquired pulmonary alveolar proteinosis is an autoimmune disease targeting granulocyte-macrophage colony-stimulating factor (GM-CSF). A neutralizing autoantibody against GM-GSF causes defects in the functioning of alveolar macrophages, including impairment of the catabolism of surfactant lipids and proteins and disruption of surfactant homeostasis. No correlation to an exposure of gallium arsenide was found.Eight studies are not reliable.
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