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EC number: 700-661-1 | CAS number: -
- 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
Key value for chemical safety assessment
Additional information
Chemical structure and synthesis
Peroxy sulfonated oleic acid (PSOA) is a long chain fatty acid derivative with three specific structural increments: a hydroperoxide structure, sulfonic acid and a monohydroxy structure.
PSOA is a reaction product of variable composition which is formed in the presence of H2O2in a sulfuric acidic environment from 9-Octadenenoic acid (Z)-, sulfonated.
The sulfonated oleic acid is mostly in the saturated 9-sulfo, 10-hydroxy form and as such forms mostly the monohydroxy sulfonated peracid with a molecular weight of 396 dalton. However, also other minor fractions are formed e.g. with a dihydroxy structure. From a regulatory perspective, PSOA falls into the legal definition of a UVCB substance (“unknown, variable composition or of biological origin”). The two major species typically represent more than 60 % of the peroxysulfonated acids formed in situ.
The commercial product PSOA contains
67.6% +/- 4.3% peroxysulfonated acids
2.7% +/- 1.2% H2O2
12.95% +/- 0.3% sulfuric acid
20.5% +/- 0.09% Water
The substance is characterized as a white liquid with a product specific odor.
General toxicological profile
Among the three specific structural increments of PSOA, the hydroperoxide structure, sulfonic acid and a monohydroxy structure it is the hydroperoxide moiety that stands out. It is expected to mainly define the toxicological profile of the substance. Hydroperoxides in general are considered corrosive in nature. An example of this is the ECHA guidance on the application of CLP. The guidance considers hydroperoxides per se as corrosive. Based on structure, hydroperoxides do not need to undergo further toxicological testing.
However, with the development of reconstructed human epidermis models definitive non-animal test methods exist for the investigation of local skin effects. A study in the human skin model confirmed the corrosive properties of PSOA. With this test result, as well as structural considerations, there is sufficient evidence that PSOA is corrosive. Given this conclusion, the accompanying test program for PSOA was limited due to animal welfare considerations. This approach aligns with the regulatory requirements: In compliance with REACH, no data were generated on the dermal systemic toxicity and skin sensitizing properties. The acute oral toxicity was determined up to a value of 300 mg/kg body weight. To avoid stress and undue suffering to the animals, the test design refrained from application of higher doses. Based on this approach the acute toxicity equivalent will be above 300 mg/kg bw.
In order to fulfill the regulatory requirements in the United States of America further tests were conducted. Hence, data on the toxicity after repeated exposure and the developmental toxicity are available. The study design for repeated dose and developmental toxicity accounted for experiences that were gained with respect to the local toxicity from other hydroperoxides. It is well known that severe effects on the mucosa of the gastro intestinal tract are seen after application of hydroperoxides such as peracetic acid.
Up to 50 mg/kg body weight and up to 0.5% the substance does not have adverse systemic and local effects, respectively. Again, and similar to the acute toxicity testing approach, higher concentrations/doses were not applied to avoid stress and undue suffering to the animals.
PSOA does not cause gene mutations in bacterial and mammalian systems. When applied directly to human lymphocytes in cell culture, PSOA can induce aberrations both with and without S-9 mix. However, this is not seen in the in-vivo situation: in the in-vivo micronucleus test, which was conducted under the US-FIFRA jurisdiction PSOA is devoid of a clastogenic effect.
Toxicokinetic behavior of PSOA
In the following, the expected toxicokinetic behavior of PSOA is described qualitatively, using the information from available toxicological data and taking into account its physico-chemical properties.
With a water solubility of 43 g/L the parent compound PSOA is considered very soluble in water. Water solubility is expected to be higher for the metabolites (see below).
A partition coefficient log Pow was determined. For the peroxide, the obtained value was 1.96, whereas for 10-hydroxy-9-sulfo-octadecanoic acid the log Pow was 3.12. This value exceeds the threshold of 3 which is considered as an indicator for bioaccumulation. However, the value must be put into the correct perspective given the fact that the substance has substantial surface activity with a surface tension of 32.91 mN/m. For substances with a high surface activity, a robust log Pow cannot be determined, since the substance will accumulate at the interface between water and octanol.
Especially at higher pH values or in the presence of organic matter or trace metals like copper, PSOA is expected to hydrolyze into the sulfonated oleic acid and the physiological substrate hydrogen peroxide. In biological systems, some oxidation of organic matter can also be expected to occur. Hydrolysis of PSOA was assessed in aqueous buffers at pH 4, 7 and 9 at 50 ± 0.5 °C. Indeed, after 5 days PSOA was shown to have hydrolyzed considerably at each pH. This indicates that PSOA is hydrolytically unstable and significant hydrolysis can occur.
Based on this data, it cannot be ruled out that the parent compound or its metabolites are absorbed to some extent. However, despite being bioavailable, PSOA does not cause systemic toxicity. This is demonstrated by the lack of specific target organ toxicity associated with repeated exposure to PSOA up to the highest locally-tolerable dose of 50 mg/kg body.
The molecular structure increments provide sites of attack to biotransformation. Sulfonated oleic acid will follow the route for fatty acid and is either integrated into the body fat or converted via the ß- oxidation to AcetylCoA and as such used as an energy source in the mitochondria. The two additional molecular increments, the sulfonic and monohydroxy moieties make the molecule and its ß-oxidised metabolites more hydrophilic and will facilitate renal elimination.
The degradation product hydrogen peroxide represents a quite potent physiological oxidizing agent, that is either enzymatically (e.g., via catalase or glutathione-mediated) or non-enzymatically converted mainly into water and oxygen.
In the in vitro mutagenicity test according to Ames et al., the cytotoxicity was markedly reduced in the presence of a metabolic activation system (S-9), which indicates that the (non-identified) metabolites are less cytotoxic than the parent compound. For example, in S. typhimurium strain TA1535, PSOA was cytotoxic at 2500 µg/plate without S-9 but non-cytotoxic in the presence of S-9 up to the highest dose of 5000 µg/plate. A similar picture can be observed in the other strains of S. typhimurium, whereas E. coli does not show this different influence of S-9-mix.
In mammalian cells the metabolizing system contributes to the reduction of cytoxicity, as shown in the HPRT test V79 with Chinese hamster cells.
Synopsizing these results, it can be concluded that PSOA is more reactive than the likely metabolite hydrogen peroxide, which is in line with the experience that has been made with other hydroperoxides such as peracetic acid. Effects remote from the portal route of entry are not observed which might be due to its low stability.
PSOA and its metabolites are prone to rapid degradation to molecules that are expected either to be used for catabolism or be readily excreted mainly via urine.
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