Registration Dossier
Registration Dossier
Data platform availability banner - registered substances factsheets
Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.
The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.
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: - | 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
Toxicokinetic behaviour of some pure substances present in these streams has been extensively studied and reported. In many circumstances the body burden of the substance and/or metabolites is dependent upon several factors such as the rate and extent of uptake, distribution, metabolism and excretion. In complex mixtures, however, the toxicokinetics of even well-studied pure substances may vary depending upon interaction with other chemical species available within the mixture. For example, the substances present may compete for the uptake, metabolism, and/or elimination of the complex mixture. This situation, already complicated, is further exacerbated when the composition of the mixture is uncertain and variable.
For this ‘Resin Oils and Cyclic Dienes (DCDP rich)’ category the marker substances, in their pure form, have well-defined toxicokinetic parameters that have been taken into account during the derivation of their respective DNEL’s. The overall DNEL of this category is driven by the DNELs for benzene and dicyclopentadiene.
The toxicokinetics of dicyclopentadiene has been evaluated in rats, mice and dogs (Litton Bionetics, 1976). Elimination from plasma was biphasic in all three species; terminal half lives were 18 to 27 hours. Radioactivity was rapidly and widely distributed into tissues in all three species; the highest concentrations were found in the body fat, adrenal glands and urinary bladder in the rat; in the urinary bladder, gall bladder and body fat in the mouse; and in the bile, gall bladder and bladder in the dog. In all three species, the majority of the radioactivity was excreted in the urine. Urinary radioactivity was present as 6 -7 constituents; conjugates but no unchanged dicyclopentadiene were present. A further studywascarried out in a lactating Jersey cow (Ivie, 1980). On the basis of this study it was concluded that exposure of livestock to small quantities of dicyclopentadiene would not result in perceptible contamination of the milk or meat.
ATSDR have also reviewed the toxicokinetics of naphthalene (ATSDR, 2005) and report that naphthalene is readily absorbed into the systemic circulation following inhalation or ingestion. Systemic absorption of naphthalene can also occur following dermal contact however, the rate and extent of naphthalene absorption for all routes is unknown in many instances. Naphthalene is initially metabolised into a number of reactive epoxide and quinone metabolites by cytochrome P450 oxidation. Metabolites of naphthalene are excreted in the urine as mercapturic acids, methylthio derivatives and glucuronide conjugates. Glutathione and cysteine conjugates are excreted in the bile. Following ingestion the urinary excretion of naphthalene metabolites is prolonged due to delayed absorption from the gastrointestinal tract.
Styrene toxicokinetics were reviewed by ATSDR in 2007. It can be concluded that styrene is well absorbed by the inhalation and oral routes and poorly absorbed through the skin. Once absorbed, styrene is widely distributed throughout the body, with the highest levels detected in fat. There are several metabolic pathways for styrene; the primary pathway is oxidation of the side chain by cytochrome P450 to form styrene 7,8-oxide. The styrene oxide is further metabolized to ultimately form mandelic acid or phenylglyoxylic acid or can be conjugated with glutathione. Styrene is rapidly eliminated primarily in the urine as mandelic acid and phenylglyoxylic acid.
Toluene toxicokinetics were reviewed by the EU (EU, 2003a). In summary, the major uptake of toluene vapour is through the respiratory system. It is absorbed rapidly via inhalation and the amount absorbed (approximately 50%) depends on pulmonary ventilation. Toluene is almost completely absorbed from the gastrointestinal tract. Liquid toluene can be absorbed through the skin but dermal absorption from toluene vapours is not likely to be an important route of exposure. Dermal absorption of liquid toluene was predicted using a model which considers absorption as a two stage process, permeation of the stratum corneum followed by transfer from the stratum corneum to the epidermis. The model predicted a maximum flux of 0.0000581 mg/cm2/min giving a dermal absorption value of approximately 3.6% of the amount applied as liquid toluene. Toluene is distributed to various tissues, the amount depending on the tissue/blood partition coefficient, the duration and level of exposure, and the rate of elimination. Biotransformation of toluene occurs mainly by oxidation. The endoplasmic reticulum of liver parenchymal cells is the principal site of oxidation which involves the P450 system. Analysis of blood and urine samples from workers and volunteers exposed to toluene via inhalation in concentrations ranging from 100 to 600 ppm (377-2,261 mg/m3) indicate that of the biotransformed toluene, ~ 99% is oxidised via benzyl alcohol and benzaldehyde to benzoic acid. The remaining 1% is oxidised in the aromatic ring, forming ortho-, meta- and para-cresol. In the rat, elimination of toluene is rapid with most toluene eliminated from fat after 12 hours. Within a few hours after termination of exposure the blood and alveolar air contains very little toluene. A proportion (around 20%) of the absorbed toluene is eliminated in the expired air. The remaining 80% of the absorbed toluene is metabolised in the liver by the P450 system, mainly via benzyl alcohol and benzaldehyde to benzoic acid. Benzoic acid is conjugated with glycine and excreted in the urine as hippuric acid.
The metabolism and kinetics of xylene isomers has been reviewed extensively by ATSDR (2007c). All the xylene isomers are well absorbed via the oral route. They are rapidly distributed through the body and any unmetabolised compound quickly eliminated in exhaled air. In gavage dosing experiments in animals, 90% absorption has been estimated. In humans, inhalation absorption has been estimated at about 60-65% based on human data. The major pathway of xylene metabolism in humans involves mixed function oxidases in the liver, with minor metabolism occurring in the lung and kidneys. Xylenes are transformed primarily to methylbenzoic acid followed by conjugation with glycine to form the main metabolites, the corresponding methylhippuric acid isomers, which are eliminated in the urine.
References
ATSDR (2005). Toxicological profile for naphthalene, 1-methylnaphthalene, and 2-methylnaphthalene. U.S. Department of Health and Human Services Public Health Service Agency for Toxic Substances and Disease Registry.
ATSDR (2007b). Draft toxicological profile for styrene. U. S. Department of Health and Human Services Public Health Service Agency for Toxic Substances and Disease Registry.
ATSDR (2007c). Toxicological profile for xylene. U. S. Department of Health and Human Services Public Health Service Agency for Toxic Substances and Disease Registry.
EU (2003a). European Union Risk Assessment Report for Toluene. EC Joint Research Centre http: //ecb. jrc. ec. europa. eu/DOCUMENTS/Existing- Chemicals/RISK_ASSESSMENT/REPORT/toluenereport032. pdf
Ivie GW and Oehler DD (1980). Fate of dicyclopentadiene in a lactating cow. Bull. Environm. Contam. Toxicol. 24, 662-670.
Litton Bionetics (1976). Mammalian toxicological evaluation of DIMP and DCPD. Testing laboratory: Litton Bionetics Inc.5516 Nicholson Ave. Report no.: DAMD 17. 75-C-5068. Owner company: U. S. Army Med. Res. and Dev. Command,, D. C. 20314,. Report date: 1976-06-25.
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.