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EC number: 270-790-1 | CAS number: 68478-10-4 A complex combination of hydrocarbons obtained by the distillation of debenzenized light steam-cracked naphtha. It consists predominantly of cyclic olefinic and aromatic hydrocarbons having carbon numbers predominantly in the range of C8 through C16 and boiling in the range of approximately 130°C to 300°C (226°F to 572°F).
- 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
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Endpoint summary
Administrative data
Description of key information
Oral and inhalation exposure to dicyclopentadiene resulted in nephrotoxicity (alterations in renal function and kidney morphology) in male rats only and characteristic
of hyaline droplet nephropathy, which is not relevant for human risk assessment. Other changes which were seen in male rats in all groups (including controls) were characteristic of chronic glomerulonephropathy. Mortality was seen in rats dosed with 100 mg/kg/day orally and in mice exposed to 51 ppm by inhalation. Apart from the effects on the kidney (in male rats only), there were few histopathological changes. Single cell necrosis in the liver and fatty changes in the adrenal glands were seen in the oral rat study only.
Key value for chemical safety assessment
Repeated dose toxicity: via oral route - systemic effects
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- NOAEL
- 4 mg/kg bw/day
- Study duration:
- subacute
- Species:
- rat
Repeated dose toxicity: inhalation - systemic effects
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed
- Dose descriptor:
- NOAEC
- 27.6 mg/m³
- Study duration:
- subchronic
- Species:
- mouse
Repeated dose toxicity: inhalation - local effects
Endpoint conclusion
- Endpoint conclusion:
- adverse effect observed
- Dose descriptor:
- NOAEC
- 27.6 mg/m³
- Study duration:
- subchronic
- Species:
- mouse
Repeated dose toxicity: dermal - systemic effects
Endpoint conclusion
- Endpoint conclusion:
- no study available
Repeated dose toxicity: dermal - local effects
Endpoint conclusion
- Endpoint conclusion:
- no study available
Additional information
Non human Information
Oral
The key study is considered to be a combined repeat dose toxicity study with reproduction/developmental toxicity screening (JETOC, 1998a). Systemic toxicity at 100 mg/kg/day was indicated by the mortality of two female rats and, decreased food consumption and bodyweight gain in both males and females. Pathological changes in the liver (single cell necrosis, males only) and adrenals (increase in fatty droplets, males and females). Similar changes were seen in the adrenals of some male rats dosed at 20 mg/kg/day. Male rat specific kidney pathology (hyaline droplet formation and basophilic changes in the tubular epithelium of the kidney) was observed in males in all dose groups. These findings are not relevant for human risk assessment.
The no effect level for systemic toxicity was therefore considered to be 20 mg/kg/day for females and 4 mg/kg/day for male rats (based on the adrenal effects at higher dose levels).
In the supporting study (Litton Bionetics, 1980), dicyclopentadiene was administered by incorporation into the diet at concentrations of 100, 300 and 1000 ppm to male and female beagle dogs for 13 weeks. No significant toxicity was seen at any dose level. Minor indications of intestinal distress (vomiting and soft stools) seen at the highest dose (1000 ppm) were considered to be of no toxicological significance. The NOAEL of dicyclopentadiene was therefore considered to be 1000 ppm (25 mg/kg/day) to beagle dogs following 13 week dietary administration.
Inhalation
Key studies were conducted in Fischer 344 rats and B6C3F1 mice (Bushy Run, 1982). Vapour generation was carefully controlled and analysed to ensure that no cyclopentadiene was formed during vapour generation. Animals were exposed (whole body) to vapours of 0, 1, 5 or 50 ppm dicyclopentadiene, 6 hr/day, 5 days/week for 13 weeks, followed by a 13-week recovery period. Animals were killed following completion of exposure at 2, 6, or 13 weeks and at post exposure weeks 4 or 13.
There was no mortality in any of the rats but approximately 20% of the mice (both sexes) of the 51 ppm exposure group died during the exposure period.
In rats exposed to 51 ppm, relative liver weights were significantly increased in males.
The kidney effects seen only in male rats exposed to dicyclopentadiene were reported by Bevan et al (1992) to be characteristic of alpha2u-nephropathy, which is considered to be of no relevance to human risk assessment.
The rat study indicates an overall low degree of systemic toxicity following sub-chronic inhalation exposure of dicyclopentadiene at exposure levels up to 51 ppm. As concluded by Bevan et al. (1992), increased liver weights in the absence of histopathologic changes were not considered to be an adverse effect. Excluding the male, rat-specific hyaline droplet nephropathy seen at 5.1 and 51 ppm during the exposure period, the no observed adverse effect concentration (NOAEC) in this study is therefore considered to be 51 ppm (276 mg/m3) for both male and female rats. Since approximately 20% of the mice (both sexes) of the 51 ppm exposure group died during the exposure period, the NOAEC is concluded to be 5.1 ppm (27.6 mg/m3) for male and female mice.
Human studies
In studies in human volunteers to ascertain the odour threshold of dicyclopentadiene vapour for man and to determine the human sensory response (Kinkead et al, 1981), some inadvertent exposure to dicyclopentadiene vapour occurred during the 5 month investigation period. Three workers experienced transitory headaches during the first 2 months, but not during the last 3 months.
Justification for selection of
repeated dose toxicity inhalation - systemic effects endpoint:
Mortality in male and female mice at 276mg/m3 was associated with
pulmonary congestion resulting from chronic irritation of the lung.
Justification for selection of repeated dose toxicity inhalation -
local effects endpoint:
Mortality in male and female mice at 276mg/m3 was associated with
pulmonary congestion resulting from chronic irritation of the lung.
Repeated dose toxicity: via oral route - systemic effects (target
organ) glandular: adrenal gland
Justification for classification or non-classification
Dicyclopentadiene is not classified for repeat dose toxicity under CLP.
While some effects were seen in repeat dose studies, these are believed to be due to chronic irritation of the lungs and gastrointestinal tract with secondary stress-related effects rather specific target organ toxicity. DCPD is irritating; therefore it is biologically plausible that the mortality is mostly attributable to respiratory and gastric irritation effects rather than systemic effects. Liver effects seen in the rat oral study were not considered sufficient to warrant classification.
Repeated exposure inhalation studies in rodents show mortality at levels that would be predicted by their LC50s, and appears related to respiratory irritation/portal-of-entry effects. The original Bushy Run 90-day study showed mortality in the mice at 276 mg/m3. The LC50 in mice is about half that of rats, which might be expected for a respiratory irritant (higher ventilation rate in the mouse). This justification for non-classification for the repeat dose toxicity (mortality in mice) is supported by the existing acute inhalation classification (Acute Cat 2).
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.
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