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Toxicological information


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Administrative data

Description of key information

There are no relevant data for TCDE.  Considering the read-across substance, DCPD, this has been shown to be non-genotoxic both in vitro and in vivo.  These observations indicate that DCPD and therefore TCDE are not expected to be a genotoxic carcinogen.
 DCPD has been examined in repeat dose inhalation and oral studies and shown low levels of toxicity. The liver and adrenals showed limited changes on histopathological examination, and the kidneys in male rats showed changes consistent with the accumulation of alpha-2-microglobulin, a male rat specific protein.
It is concluded that there are sufficient data to indicate that dicyclopentadiene does not pose a risk of genotoxic carcinogenicity. There are also data available to understand that the cellular changes arising from repeated administration of dicyclopentadiene to animals are limited and to conclude that dicyclopentadiene is unlikely to be carcinogenic. The changes in the male rat kidney are consistent with a male rat specific mechanism and even if tumours were formed on chronic administration to male rats, these would be considered not relevant to humans. 
The conduct of animal carcinogenicity studies is therefore considered to be unwarranted.

Key value for chemical safety assessment

Justification for classification or non-classification

No classification of TCDE is warranted under DSD or CLP.

Additional information

As detailed in section 5.1.3 of the CSR (IUCLID 7.1.1),3a,4,7,7a-tetrahydro-4,7-methanoindene (DCPD) is considered an appropriate read-across candidate where data are not available for3a,4,5,6,7,7a-hexahydro-4,7-methano-1H-indene (TCDE).

There are no lifetime animal studies available on TCDE or DCPD in order to directly investigate for possible carcinogenic activity. However, there is sufficient information available to make an assessment of the likely carcinogenic potential of DCPD, the conclusions of which are considered to apply to TCDE.

Non-testing information relevant for carcinogenicity

DCPD is a relatively straightforward chemical structure. It contains two olefinic centres, but sufficiently distant as to be essentially two isolated mono-ene groups. These are potential centres of chemical functional activity and the only alert for possible genotoxic activity when the structure of DCPD is considered against the criteria established by Ashby and Tennant (1988).  For TCDE, one functional group is lost and consequently less potential for functional activity.

Testing data relevant for carcinogenicity

In vitro data 

DCPD has been examined for mutagenicity in a range of recognised core assay types. In vitro studies include assays for gene mutation in bacteria (the Salmonella mutation assay) and also for cytogenetic activity. It has shown negative results for mutagenicity in all these assays. The above assays would be considered appropriate for evaluating any activity that might have arisen from the two centres containing double bonds, and this indicates that the initial theoretical alert from consideration of the chemical structure is not expressed in reality.  It is concluded that the available data indicate that DCPD has no significant genotoxicity.

Animal data

A material containing DCPD has been examined for mutagenicity using a bone marrow cytogenetic assay in the mouse and was found not to be mutagenic. DCPD has therefore been examined in the key relevant mutagenicity assays both in vitro and in vivo and found to be non-genotoxic. There is therefore good evidence for DCPD being non-carcinogenic in animals with respect to a genotoxic mechanism. 

The repeat dose toxicity of dicyclopentadiene was examined in F344 rats and B6C3F1 mice by the inhalation route for 13 weeks, 5 days/week, 6 hours/day, at doses of 0, 5.4, 27.5 and 275mg/m3 (Bushy Run, 1982). No toxicity was reported in the female rats. In the male rats, histopathological examination of the kidneys revealed dose-dependent changes consistent with the accumulation of alpha2u-globulin, a male rat specific protein. The only significant toxicity reported in the mice was deaths that were seen at the top dose group, accompanied by congestion of the lungs and kidney failure.

DCPD has also been examined in SD(Crj:CD) rats in an OECD screening test for combined repeat dose and reproductive/developmental toxicity.  Doses used were 0, 4, 20, 100 mg/kg/day. In males, histopathological examination showed hyaline droplets and basophilic change in the tubular epithelium of the kidneys together with single cell necrosis in the liver. In both male and female animals an increase of fatty droplets was observed in the fascicular zone in the adrenals. No treatment related haematological changes were observed (JETOC, 1998a).

Similar findings of limited or no toxicity were reported in a range of other repeat dose studies, albeit with limited protocol features (e.g. animal numbers) or duration of exposure (e.g. Kinkead et al, 1971).


Ashby J and Tennant RW (1988) Chemical structure, Salmonella mutagenicity and extent of carcinogenicity as indicators of genotoxic carcinogenesis among 222 chemicals tested in rodents by the U.S.NCI/NTP. Mutat Res 204: 17-115.

 SIDS (1998)