Registration Dossier
Registration Dossier
Diss Factsheets
Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 204-112-2 | CAS number: 115-86-6
- 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
Metabolism study of triphenyl phosphate (TPP) incubated with rat liver homogenate with and without NADPH and other enzyme systems showed that TPP is decomposed to diphenyl phosphate (DPHP, major metabolite) by mixed function oxidase system and arylesterase in microsomes. In a study on human liver microsomes TPP is metabolized into its diester metabolite DPHP and mono- and dihydroxylated metabolites by cytochromes P450 (CYP) in human liver microsomes, while CYP1A2 and CYP2E1 isoforms are mainly involved in such processes.
In human liver preparations other Phase-I metabolites of TPP were found, namely a mono hydroxylated metabolite (TPHP-M6), a di-hydroxylated metabolite (TPHP-M7, two isomers), and a metabolite resulting from hydroxylation and O-dealkylation of TPP (TPHP-M1). In primary human hepatocytes diphenyl phosphate corresponded to less than half of the depletion of TPP. Other metabolite structures were produced at 4- to 10-fold lower rates.
In FVB mice after intraveneous exposure to TPhP via vein-tail injection, this molecule could not be detected in blood (Limit Of Detection LOD TPhP = 0.7 ng/mL), or only after high doses and only in few of the treated animals. After quantification of DPhP in the same experiments, DPhP could not be detected in the blood of animals treated. Therefore, the large majority of injected or force-fed TPhP seemed not to have been metabolized into DPhP in the animals.
Key value for chemical safety assessment
Additional information
In a study on the metabolism of triphenyl phosphate (TPP) was incubated with rat liver homogenate with and without NADPH and other enzyme systems (Sasaki et al, 1984). Gas chromatography identified diphenyl phosphate as the major metabolite following decomposition of TPP. Arylesterase in the microsomes contributes to TPP metabolism. The metabolic reactions were inhibited almost completely by SKF-525A and carbon monoxide in the absence of NADPH whereas KCN, NAN3, dipyridyl and EDTA showed little effect. Therefore, mixed function oxidase system in the microsomes play a central role in the metabolism of TPP. Authors concluded TPP is degraded by hydrolysis in rat liver homogenate to diphenyl phosphate as the major metabolite.
In a study on human liver microsomes TPP is metabolized into its diester metabolite DPHP and mono- and dihydroxylated metabolites by cytochromes P450 (CYP) in human liver microsomes, while CYP1A2 and CYP2E1 isoforms are mainly involved in such processes (Zhang et al., 2018).
In human liver preparations other Phase-I metabolites of TPP were found, namely a mono hydroxylated metabolite (TPHP-M6), a di-hydroxylated metabolite (TPHP-M7, two isomers), and a metabolite resulting from hydroxylation and O-dealkylation of TPP (TPHP-M1). In primary human hepatocytes diphenyl phosphate corresponded to less than half of the depletion of TPP. Other metabolite structures were produced at 4- to 10-fold lower rates. (Van den Eede et al., 2015)
Para (p) and meta (m)- OH-TPHP glucuronides were detected in the urine of 4 human volunteers from Ottawa (Su et al., 2016).
Frederiksen M et al. (2018) investigated dermal uptake and percutaneous penetration of organophosphate esters (OPEs) in a human skin ex vivo model (Franz diffusion cell system). Large variation in penetration profiles was observed between the OPEs. Triphenyl phosphate (TPHP) tended to build up in the skin tissue and only smaller amounts permeated through the skin. The rates at which OPEs permeated through the skin decreased in the order TCEP > TCIPP _ TBOEP > TIBP _ TNBP > TDCIPP > TPHP > TMPP. Generally, the permeation coefficient, kp, decreased with increasing log Kow, whereas lag time and skin deposition increased with log Kow.
In FVB mice exposed to a single 0.1 or 1 µg concentrations of TPhP via vein-tail injection, this molecule could not be detected in blood (Limit Of Detection LOD TPhP = 0.7 ng/mL). After administration of 10 µg or 100 µg TPhP, TPhP was only quantified above the LOD in the blood of two animals at 2.33 ng/mL and 10.20 ng/mL, exposed to 100 µg following intravenous injection and oral gavage, respectively. In all other animals (18 out of 20 animals), TPhP remained undetected. To determine whether TPhP transformation into DPhP was the reason for the lack of detection of TPhP in the blood stream, DPhP was quantified in the same experiments. DPhP could not be detected in the blood of animals treated with 0.1 or 1 µg of TPhP (LOD DPhP = 0.3 ng/mL, LOQ DPhP = 0.5 ng/mL). At the highest doses of TPhP (10 and 100 µg), DPhP was detected in the blood of animals, but in a level comparable to that obtained after exposure to DPhP a hundred times lower. Therefore, the large majority of injected or force-fed TPhP seemed not to have been metabolized into DPhP in the animals.
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.
Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.

EU Privacy Disclaimer
This website uses cookies to ensure you get the best experience on our websites.