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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.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.

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Key value for chemical safety assessment

Additional information

Non-human information

 

In vitro data

The key studies are considered to be a bacterial mutation assay (NOTOX, 2000), a mammalian cell cytogenetic assay (JETOC, 1998b), and a mammalian gene mutation assay (Harlan, 2014).  These are three recognised core assay types for investigating mutation in vitro.

Dicyclopentadiene (resin grade containing 75% dicyclopentadiene) was tested in a pre-incubation modification of a standard Ames test (NOTOX 2000). S typhimurium (TA1535, TA1537, TA98 and TA100) and E. coli (WP2uvrA) were treated with dicyclopentadiene both with and without auxiliary metabolic activation (S9). A range of doses was used up to 666 μg/plate where toxicity allowed, and with S9 levels of 5% and/or 10%. Dicyclopentadiene was negative in this assay.

Dicyclopentadiene was tested for cytogenetic activity in CHL cells both in the presence and absence of S9 (JETOC, 1998b).  A range of doses up to approximately 0.1 mg/ml (approximately 10 mM) was used, and both a continuous and short term exposure was employed in the absence of S9. Dicyclopentadiene was negative in this assay at concentrations causing up to 50% inhibition of cell growth, in both the absence and presence of S9. A small increase in aberrations was observed at a high concentration on continuous exposure in the absence of S9. This small increase is not considered to be significant, and dicyclopentadiene was reported as negative. 

Dicyclopentadiene was tested for gene mutation potential in L5178Y mouse lymphoma cells, both in the absence and presence of S9 (Harlan, 2014). An initial toxicity test indicated that concentrations would be limited by cyctoxicity to ca. 40-60μg/mL. Dicyclopentadiene did not induce a statistically significant, dose-related increase in mutant frequency, and was considered to be negative in this test.

There are additional reports of negative results for dicyclopentadiene in an in vitro mammalian cell micronucleus assay (JETOC, 1998b), in the Ames test (+/- S9) in Salmonella strains TA1535, TA1537, TA1538, TA98 and TA100 (Litton Bionetics 1980), in Salmonella strains TA1535, TA1537, TA98 and TA100 (Litton Bionetics 1980 ) and in S cerevisiae D4 (+/- S9) (Litton Bionetics, 1980) and S cerevisiae D3 (Litton Bionetics, 1980).The data from these assays all support the above conclusion that dicyclopentadiene is not mutagenic in vitro.

In vivo data

There are no available in vivo studies on dicyclopentadiene, however there is an important supporting bone marrow micronucleus study in the mouse available on dicyclopentadiene / codimer concentrate, containing 29.175% dicyclopentadiene (DuPont, 2004). This is a recognised core assay type for investigating mutation in vivo.

Male and female mice were given two doses of dicyclopentadiene / codimer concentrate by oral gavage, 24h apart, and bone marrow sampled 24h after the last dose. The dose levels used were 0, 437, 875, or 1750 mg/kg, and the highest dose induced clinical signs in both sexes and evidence of bone marrow toxicity (decreased PCE/NCE ratio) in females. A negative result was obtained in this assay.

 

Human information

There is no information indicating any adverse effects of dicyclopentadiene. 

 
Short description of key information:
Dicyclopentadiene has been evaluated for mutagenicity both in vitro and in vivo using recognised core assay studies and has shown negative results. It is concluded from the available data that dicyclopentadiene has no significant genotoxicity.

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

It is concluded that the available data indicate that dicyclopentadiene has no significant genotoxicity and therefore does not warrant classification for mutagenicity under CLP.