Registration Dossier
Registration Dossier
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EC number: 215-114-8 | CAS number: 1303-00-0
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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