Registration Dossier
Registration Dossier
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EC number: 232-260-8 | CAS number: 7803-51-2
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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