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EC number: 225-218-5 | CAS number: 4724-48-5
- 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
No human data are available and no specific toxicokinetic (TK) study using octylphosphonic acid has been performed.
The available experimental data in animals show evidence of oral absorption and systemic distribution of the test substance since adverse effects were reported in the kidneys of rodents following repeated exposures. No systemic effects were observed when the test substance was dermally applied in the acute dermal toxicity study. No indication on the test substance excretion was obtained.
Key value for chemical safety assessment
Additional information
No human data are available and no specific toxicokinetic (TK) study using octylphosphonic acid has been performed. Therefore, the assessment of absorption, distribution, metabolism and excretion of octylphosphonic acid is based on the physico-chemical properties of the test substance and on the results of the available toxicity studies.
Physico-chemical properties:
- The test substance has a low volatility with a vapor pressure of 1.6*10-4 Pa at 25°C
- The estimated partition coefficient in n-octanol/water is 2.7 (at 25°C)
- The estimated water solubility is 0.188g/l at 25°C
- Density: 1.09 (at 20°C)
- Boiling point: > 450°C
Absorption:
Inhalation:
No data were available for this route of exposure. However, the submitted substance is a waxy solid with a low volatility, as evidenced by the very low vapour pressure. Therefore it can be considered that the absorption by the inhalation route is limited.
Oral:
Mortality was observed in rats exposed to one single administration of octylphosphonic acid at 1600 mg/kg and above (see Ac. tox. oral V2 1979HOEC). Clinical signs observed were passivity, prone or side position, creeping gait, partially closed eyes, noisy, irregular or increased rate of respiration, decreased pupillary reflex, rough coat and increased heart rate. It can be therefore considered that octylphosphonic acid is absorbed by the oral route.
Dermal route:
In the acute dermal toxicity study performed in rats, no mortality and no signs of systemic toxicity were observed at 2000 mg/kg bw. Signs of skin irritation noted were very slight to well-defined erythema, very slight to slight oedema, scabbing, blanching of the skin, superficial cracking of the epidermis, crust formation, desquamation and glossy skin. No abnormalities were noted at necropsy.
Octylphosphonic acid is corrosive to the skin, Therefore it is not relevant to evaluate its dermal penetration.
In conclusion, it can be assumed that octylphosphonic acid is absorbed only by oral route.
Distribution:
During the rat 28 days oral toxicity some effects were observed on the lung, kidney,adrenals, bone marrow, spleen and stomach in addition to local effects or consequences of local effects (seeRep. dose tox. oral V1 1989 HOFF). Based on these effects, octylphosphonic acid is classified into category 2 STOT RE, H373 (target organ: Kidneys). Therefore, these adverse effects demonstrated the systemic distribution of octylphosphonic acid.
Metabolism:
Several in-vitro and in vivo genotoxicity studies were performed in presence or absence of metabolic activation. In vitro, octylphosphonic acid (OPA) consistently gave negative results in the Ames test inS typhimuriumstrains TA 1535, TA 1538, TA98, TA 100 andE Colistrains WP2P, WP2Puvr Aand WP2 uvr A, both in the presence and absence of S9. In two out of five studies, Salmonella strain TA 1537; small increases in revertant colonies were seen on some occasions only in the presence of S9. In the mammalian cell mutation assay in L5178Y cells, small increases in mutant frequency were seen with one sample of OPA, but only in the absence of S9. A second sample showed no such increases. In an in vitro cytogenetic assay in human lymphocytes, OPA gave a negative response in both the presence and absence of S9. In vivo,OPA has been shown to be negative in the mouse bone marrow micronucleus assay for clastogenicity and in the rat liver UDS assay for general DNA damage/DNA repair. These two in vivo assays, using dose levels up to and including the maximum tolerated dose levels, confirm that OPA is not genotoxic in the entire animal.
Based on all these results, no conclusion on the metabolism can be drawn.
Excretion:
There is no information to indicate a route of excretion for Octylphosphonic acid but its high water and relatively fat solublity indicate that excretion of unchanged parent substance and/or metabolites could occur by renal or biliary routes and that bioaccumulation is unlikely. The parent substance could not be eliminated via the lungs in expired air due to its form (solid) and its low volatility.
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