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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
Key value for chemical safety assessment
Additional information
Animal data
Kligerman et al. (1994ab) did not observe any cytogenetic damage as measured by chromosome aberrations, sister chromatid exchange or micronuclei induction in hematopoietic tissues of mice and rat exposed to PH3 (16 ppm / 22.72 mg/m3 for 6 hours periods and 5 ppm / 7.1 mg/m3 for 9 days period). Furthermore, the peripheral blood lymphocyte was used to quantify cytogenetic damage, theses studies are more comparable to the human in vivo studies.
Barbosa et al. (1994b) reported a slight but statistically significant increase in micronuclei polychromatid erythrocytes in the bone marrow of female mice and in the bi-nucleated splenocytes of male and female mice exposed to 4.5 ppm (6.39 mg/m3) for 13 weeks. The interpretation of these results is ambiguous because the significantly difference between sexes in the control group and an adverse effect (on weight gain) was also observed at this concentration (it was the highest dose). At the same time no statistically significant increase in HPRT mutagenisis was seen in the splenocytes from the treated mice. Nevertheless, when the concentration of PH3 was 5.5 ppm (7.81 ppm) and the exposure was limited to 2 weeks, no statistically significant increases in micronuclei were seen in the peripheral blood polychromatide erythrocyte or in binucleated keratinocytes.
the table below summarizes the animal data:
Reference | Klig, 1994a | Klig, 1994a | Barb, 1994b | ||
Exposure | 6 hours | 9 days | 2 weeks | 13 weeks | |
highest concentration (ppm) | 16 +/-1.15 | 5 | 5.5 | 4.5 +/-0.8 | |
Type of study | Species | ||||
Micronuclei | mice | negative (bone marrow) |
negative (blood lymphocyte) |
negative (spleen lymphocyte) |
postive at the highest concentation (bone marrow) |
negative (splenocyte) |
negative (keratonocyte) |
postive at the highest concentation (spleen lymphocyte) |
|||
rat | negative (bone marrow) |
||||
Sister Chromatid Exchange | mice | negative (splenocyte) |
negative (bloodlymphocyte) |
||
rat | negative (blood lymphocyte) |
||||
Chromosome Aberration | mice | negative (splenocyte) |
negative (blood lymphocyte) |
||
rat | negative (blood lymphocyte) |
||||
HPRT | mice | negative (spleen lymphocyte) |
Human data (not epidemiological studies)
Barbosa et al. (1994a) did not associate occupational exposure to PH3 with increased levels of chromosome damage in peripheral blood lymphocytes (micronuclei) and urine mutagenicty of fumigant applicators
Garry et al. (1989) associated occupational exposure to PH3, with increased levels of chromosome damage in peripheral blood lymphocytes of fumigant applicators. However, when the subjects were studies 6 weeks to 3 months after fumigation with PH3 had ceased, there was no difference in the number of chromosome damage between men exposed and control subject. Due the lack of information in the age and conditions of exposure was not clear, the reliability was 3.
Conclusion
The slight but statistically significant increases in micronuclei observed by Barbosa et al. (1994b) may be due to the extended period of exposure that was used in that study compared to Kligerman et al. (1994ab).
The possibility also exists that the positive response seen in the Human studies were actually not due to PH3 but to other confounding factors in the fumigators’ environment.
The most likely explanation for the disparate cytogenetic responses seen after some of the in vivo rodent PH3 exposures, is that PH3 is at best, a weak genotoxicant, that sometimes will induce marginal increases in cytogenitic damage when exposures are near toxic levels.
Short description of key information:
The most likely explanation for the disparate cytogenetic responses seen after some of the in vivo rodent PH3 exposures is that PH3 is at best, a weak genotoxicant, that sometimes will induce marginal increases in cytogenitic damage when exposures are near toxic levels (Kligerman et al., 1994b)
Endpoint Conclusion: No adverse effect observed (negative)
Justification for classification or non-classification
Phosphine is listed on Annex VI to Regulation (EC) No 1272/2008 includes lists of harmonised classification and labelling. No change is proposed for these effects.
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.
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