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Diss Factsheets
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EC number: 232-260-8 | CAS number: 7803-51-2
- 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
Link to relevant study record(s)
Description of key information
Short description of key information on bioaccumulation potential result:
Following acute phosphine or phosphide exposure, phosphine is rapidly absorbed and distributed throughout the body leading to possible effects on the respiratory, circulatory and nervous system, liver, kidney and gastrointestinal tract.
The majority of absorbed phosphine is excreted in exhaled air. Minor amounts are slowly and incompletely oxidised and excredted in the urine as hypophosphite and phosphate.
Key value for chemical safety assessment
- Bioaccumulation potential:
- no bioaccumulation potential
Additional information
Metabolism and Disposition
A report of the International Programme on Chemical Safety indicated that inhaled phosphine is readily absorbed through the lungs and is primarily distributed to the blood, nervous system, and liver. The report also indicated that phosphine has been detected in the kidneys of fatal poisoning cases. In rats, phosphine not excreted in expired air is oxidized and is excreted in urine as hypophosphite and phosphite. The fact that phosphine is incompletely oxidized and that the proportion of an administered dose that is eliminated as expired phosphine increases with dose suggest that the oxidative pathway is slow (IPCS 1988).
Dermal absorption of phosphine is not considered a significant route of exposure.
IPCS (International Programme on Chemical Safety). 1988. Phosphine and Selected Metal Phosphides. Environmental Health Criteria 73. Geneva: World Health Organization. Available: http://www.inchem.org/documents/ehc/ehc/ehc73.htm
Mechanism of toxicity
In vitro, phosphine reacts with cytochrome C and cytochrome C oxidase, thereby inhibiting mitochondrial oxygen uptake (Chefurka et al. 1976; IPCS 1988). In vitro studies have shown that phosphine can react with the heme moiety of hemoglobin in the presence of oxygen (Chefurka et al. 1976). In rabbits treated with zinc phosphide, increases in serum glutamic-pyruvic and glutamicoxaloacetic
transaminases, leucine aminopeptidase, aldolase, alkaline phosphatase, and albumin were observed. Hepatic fat metabolism was also disturbed. Cell death and loss of cell membrane integrity accounted for the increased liver enzymes, bronchiolytic effects, cloudy swelling of renal tubular epithelia, and hemorrhagic myocardial lesions (IPCS 1988). Phosphine and arsine are often described as chemically similar. However, no explanation exists as to why hemolysis does not occur as a result of phosphine poisoning.
Chefurka, W., K.P. Kashi, and E.J. Bond. 1976. The effect of phosphine on electron transport in mitochondria. Pestic. Biochem. Physiol. 6:65-84.
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