reaction products of diglycidyl ether bisphenol F (DGEBF) and oligomeric phenol diglycidyl ethers with acrylic acid

Endpoint summary

Additional information

In Vitro Studies

Bacterial reverse mutation assay

In a reverse gene mutation assay in bacteria according to OECD guideline 471, strains TA 97, TA 98, TA 100, TA 102 and TA 1535 of S. typhimurium were exposed to Epoxy half acrylate in the following concentrations: 

First Experiment:

Five concentrations of the test item, dissolved in dimethyl sulfoxide (DMSO) (ranging from 4999 to 50 µg/plate) were used. Five genetically manipulated strains of Salmonella typhimurium (TA 97a, TA 98, TA 100, TA 102 and TA 1535) were exposed to the test item both in the presence and in the absence of a metabolic activation system (S9) for 48 hours, using the plate incorporation method.

None of the concentrations caused a significant increase in the number of revertant colonies in the tested strains. The test item didn’t show any mutagenic effects in the first experiment.

No signs of toxicity towards the bacteria could be observed.

The sterility control and the determination of the titre didn’t show any inconsistencies. The determined values for the spontaneous revertants of the negative controls were in the normal range. All positive controls showed mutagenic effects with and without metabolic activation.

Second Experiment:

To verify the results of the first experiment, a second experiment was performed, using three concentrations of the test item (ranging from 5011 to 314 µg/plate) and a modification in study performance (pre-incubation method).

The test item didn’t show mutagenic effects in the second experiment, either.

No signs of toxicity towards the bacteria could be observed.

The sterility control and the determination of the titre didn’t show any inconsistencies. The determined values for the spontaneous revertants of the negative controls were in the normal range. All positive controls showed mutagenic effects with and without metabolic activation.

Under the conditions of the test, the test item didn’t show mutagenic effects towardsSalmonella typhimurium,strains TA 97a, TA 98, TA 100, TA 102 and TA 1535.

The test item Epoxy half acrylate is considered as not mutagenic under the conditions of the test.

 

Mammalian gene mutation assay

In a mammalian cell gene mutation assay according to OECD guideline 476 (HPRT assay), adopted July 21, 1997, Chinese hamster lung fibroblasts (V79) cultured in vitro were exposed to Epoxy half acrylate at the following concentrations in the presence and absence of mammalian metabolic activation (S9- mix):

experiment I:

without metabolic activation (4 h): 0.23, 0.47, 0.94, 1.9, 3.8, 7.5, 15.0, 30.0 µg/mL

with metabolic activation (4 h): 15.0, 30.0, 60.0, 120.0, 240.0, 480.0 µg/mL

experiment II:

without metabolic activation (24 h): 0.23, 0.47, 0.94, 1.9, 3.8, 7.5, 15.0, 30.0 µg/mL

with metabolic activation (4 h): 15.0, 30.0, 60.0, 90.0, 120.0, 180.0 µg/mL

The assay was performed in two independent experiments, using two parallel cultures each.

Phase separation of the test item was observed in both experiments at 60.0 μg/mL and above with and at 30.0 μg/mL without metabolic activation.

Relevant cytotoxic effects occurred in experiment I at 1.9 μg/mL without metabolic activation following 4 hours treatment. In all of the experimental parts with metabolic activation a very steep cytotoxic gradient was noted above 120.0μg/mL leaving insufficient cell numbers for mutation analysis. In the second experiment without metabolic activation such a steep cytotoxic gradient occurred above 7.5 μg/mL.

No relevant and reproducible increase in mutant colony numbers/1E06 cells was observed in the main experiments with and without metabolic activation. The mutation frequency did not exceed the historical range of solvent controls.

A linear regression analysis (least squares) was performed to assess a possible dose dependent increase of mutant frequency. A single significant dose dependent trend of the mutation frequency indicated by a probability value of <0.05 was determined in the second experiment at culture II without metabolic activation. However, the trend was judged as biologically irrelevant as the mutation frequency did not exceed the threshold described above.

There was no evidence of induced mutant colonies over background. Under the conditions of the study, the test substance was negative for mutagenic potential.

 

Chromosome aberration assay

In a mammalian cell cytogenetics assay (chromosome aberrations) according to OECD guideline 473, adopted 21 July 1997 and EU Method B.10, May 2008, peripheral human lymphocyte cultures were exposed to Epoxy half acrylate in acetone at the following concentrations:

Experiment IA (4 hour exposure time with S9 mix, recovery 18 h, preparation interval 22 h):
8.1, 14.3, 24.9, 43.7, 76.4, 133.7, 234.0, 409.4, 716.5, 1253.9, 2194.3, 3840.0 µg/mL

Experiment IB (4 hour exposure time without S9 mix, recovery 18 h, preparation interval 22 h)
1.6, 3.1, 6.3, 12.5, 25.0, 50.0, 100.0, 200.0, 400.0 µg/mL

The highest treatment concentration in this study, 3840.0 µg/mL (approx. 10 mM) was chosen with regard to the molecular weight of the test item and with respect to the OECD Guideline 473.

The number of cells with chromosome aberrations found in the solvent control cultures was within the laboratory historical control data range. The number of polyploid cells and cells with endoreduplicated chromosomes in the solvent control cultures was within the laboratory historical control data range. The positive control chemicals (EMS or CPA) both produced statistically significant increases in the frequency of cells with structural chromosome aberrations. It was therefore concluded that the test conditions were adequate and that the metabolic activation system (S9-mix) functioned properly.

No relevant influence on osmolarity or pH value was observed.

Phase separation was observed in Experiment IA at 14.3 µg/mL and above and in Experiment IB at 12.5 µg/mL and above at the end of treatment. In the absence and presence of S9 mix, cytotoxicity indicated by clearly reduced mitotic indices could be observed at the highest evaluated concentration.

Statistically significant increases of chromosome aberrations were observed after treatment with 12.5 and 25.0 µg/mL in the absence of S9 mix (8.0 and 24.5 % aberrant cells, excluding gaps) and with 234.0, 409.4 and 1253.9 µg/mL in the presence of S9 mix (8.5, 14.5 and 19.0 % aberrant cells, excluding gaps). These values clearly exceeded the range of the laboratory historical solvent control data (0.0 – 3.0 % aberrant cells, excluding gaps in the absence of S9 mix and 0.0 – 3.5 % aberrant cells, excluding gaps in the presence of S9 mix).

No evidence of an increase in polyploid metaphases was noticed after treatment with the test item as compared to the control cultures.There was evidence of structural chromosome aberrations induced over background.

 

In vitro chromosome aberration assays are also available for structurally related substances. These are included to justify the read-across for the in vivo micronucleus assays:

In a mammalian cell cytogenetics assay (chromosome aberration assay), CHO cell cultures were exposed to Resorcinol diglycidyl ether at concentrations of 0, 2.5, 8 and 25 µg/mL without metabolic activation for 6 and 24 h. Resorcinol diglycidyl ether was tested up to cytotoxic concentrations.

There was a concentration-dependent increase in chromosome aberrations induced over background.

 

In a mammalian cell cytogenetics assay (chromosome aberration assay), CHO cell cultures were exposed to Phenyl glycidyl ether at concentrations of 0, 8 and 25 µg/mL without metabolic activation for 6 and 24 h. Phenyl glycidyl ether was tested up to cytotoxic concentrations.

There was no concentration-dependent, statistically significant increase in chromosome aberrations induced over background.

 

Hydroxypropyl acrylate was tested in a cytogenetic assay according to OECD Guideline 473 at concentrations up to 100 μg/mL and was positive with and without metabolic activation in this assay.

 

Bisphenol-A-diglycidyl ether was positive for genotoxic effects in several in vitro test systems (MAK, 2012):

-      Ames test: positive in Salmonella typhimurium strains TA100 and TA1535 with and without metabolic activation / negative in TA 98, TA 1537, E.coli WP2 with and without metabolic activation

-      Mouse lymphoma assay: positive without metabolic activation

-      Gene mutation assay in CHO cells: negative without metabolic activation, positive with metabolic activation

-      Sister chromatid exchange in CHO cells: positive without metabolic activation

-      UDS assay: positive in rat primary hepatocytes / negative in human primary lymphocytes

 

 

In vivo genotoxicity assays

An in vivo chromosome aberration study with Epoxy half acrylate is not available. In vivo studies with the structurally related substances Bisphenol-A-diglycidyl ether, Resorcinol diglycidyl ether, Phenyl glycidyl ether and Hydroxypropyl acrylate are available.

 

Bisphenol-A-diglycidylether did not induce chromosome aberrations or micronuclei after oral administration in rat, mouse and chinese hamster in bone marrow or germ cells (details are summarized in the table below; MAK, 2012).

Additionally, the effect of Bisphenol-A-diglycidylether on the integrity of rat liver DNA was investigated using the alkaline comet assay. No effect on the integrity of liver DNA was demonstrated 6 h after a single oral exposure to 500 mg test substance/kg bw (MAK, 2012).

 

In vivo genotoxicity tests with Bisphenol-A-diglycidyl ether(MAK, 2012)

Test system	Endpoint / method	Application, dosage	Result	Comments / animals examined
mouse (B6D2F1), 10 females	micronucleus test, bone marrow	p.o., 1000 mg/kg bw/d, 5 d	negative	No data
chinese hamster, 6 males, 6 females	micronucleus test, bone marrow	p.o., 0, 825, 1650, 3300 mg/kg bw/d, 2 d	negative	24 h after 2nd application
chinese hamster, 4 males, 4 females	chromosome aberration assay, bone marrow	p. o., 0, 825, 1650, 3300 mg/kg bw/d, 2 d	negative	6 h after 2nd application
mouse (NMRI) , males: 12, 15, 18	chromosome aberration assay, germ cells	p. o., 0, 1000, 3000 mg/kg bw/d, 5 d (day 0, 2, 3, 5, 9)	negative	3 d after last application
mouse (Tif.MAGf) 24 males	chromosome aberration assay, germ cells	p. o., 0, 375, 750, 1500, 3000 mg/kg bw/d, 5 d	negative	1 d after last application
Rat (Wistar) 2 males, 2 females	DNA single strand breaks, liver, alkaline comet assay	p.o., 500 mg/kg bw	negative	6 h after application

 

In an ICR mouse bone marrow micronucleus assay, male and female mice were treated orally with Resorcinol diglycidyl ether at doses of 300 and 600 mg/kg bw.  Bone marrow cells were harvested at 24 h (300 and 600 mg/kg bw), 48 and 72 h (600 mg/kg bw only) post-treatment.  The vehicle was polyethylene glycol (PEG 400). Animals were treated up to acutely toxic levels (however, signs of toxicity are not described in the publication).

There was no significant increase in the frequency of micronucleated polychromatic erythrocytes in bone marrow after any treatment time and dose level.

 

In an ICR mouse bone marrow micronucleus assay, male and female mice were treated orally with Phenyl glycidyl ether at doses of 400, 500, 800, 1000 mg/kg bw.  Bone marrow cells were harvested at 24 h (all dose levels), 48 and 72 h (1000 mg/kg bw only) post-treatment.  The vehicle was polyethylene glycol (PEG 400). Animals were treated up to acutely toxic levels (however, signs of toxicity are not described in the publication).

There was no significant increase in the frequency of micronucleated polychromatic erythrocytes in bone marrow after any treatment time and dose level.

 

In an NMRI mouse bone marrow micronucleus assay according to with OECD Guideline 474, 5 male and female mice were treated orally with Hydroxypropyl acrylate at doses of 0(control), 100, 300 and 600 mg/kg bw. Bone marrow cells were harvested at 24 h and 48 h (only 600 mg/kg bw) post-treatment. The vehicle was carboxymethyl cellulose. Animals were treated up to acutely toxic levels.

There was no significant increase in the frequency of micronucleated polychromatic erythrocytes in bone marrow after any treatment time and dose level.

 

Discussion

Epoxy half acrylate was not mutagenic in bacterial or mammalian cell gene mutation assays. But the substance induced structural chromosome aberrations in vitro.

The conduct of an in vivo micronucleus assay is nevertheless not deemed necessary in accordance with REACh Regulation, Annex XI, 1.5 as data from structurally related substances are available to fulfill the information requirement REACh Regulation, Annex VIII, 8.4.A justification for read-across is given below.

After oral administration of the structurally related substances Bisphenol-A-diglycidyl ether, Resorcinol diglycidyl ether, Phenyl glycidyl ether and Hydroxypropyl acrylate no genotoxic activity was detected.

Thus, based on the available data from structurally related substances, Epoxy half acrylate is considered to be not clastogenic in vivo.

 

There are no data gaps for the endpoint genotoxicity. No human information is available for this endpoint. However, there is no reason to believe that these results would not be applicable to humans.

 

READ-ACROSS

Hypothesis for the analogue approach

This read-across is based on the hypothesis that source and target substances have similar genotoxicity properties because they share structural similarities with common functional groups:

-      benzene-ring,

-      glycidyl-ether (R-O-CH2-epoxide)

-      acrylate

This prediction is supported by genotoxicity data on the target and source substances.

 

The target substance Epoxy half acrylate is a UVCB substance containing the reaction products of diglycidyl ether bisphenol F (DGEBF) and oligomeric phenol diglycidyl ethers with acrylic acid. The main components are shown in Fig. 1.

 

 

Figure 1: Structures of target substance Epoxy half acrylate, main components; see attachment 

 

Figure 2: Structures of the source substances Bisphenol-A-diglycidyl ether, Resorcinol diglycidyl ether, Phenyl glycidyl ether and Hydroxypropyl acrylate; see attachment 

 

2. Analogue approach justification

The read-across hypothesis is based on structural similarity products of target and source substances. The strategy is supported by the available experimental data (in vitro chromosome aberration assays). The respective reliable data (RL 1 or 2) are summarized in the data matrix below; robust study summaries are included in the Technical Dossier.

 

2.1 Structural similarity

Structural similarity and functional groups

The target substance Epoxy half acrylate contains the following functional groups:

-      diphenylmethane derivative / bisphenol

-      glycidyl-ether

-      acrylate ester

The source substance Bisphenol-A-diglycidylether (BADGE or DGEBPA) has essentially the same structural elements as the man component of the target substance (Bisphenol-F-diglycidyl ether) but contains two additional Methyl groups at the center carbon atom, and it is not acrylated.

The source substances Resorcinol diglycidyl ether and Phenyl glycidyl ether contain a benzene-ring and one or two glycidyl-ether groups, respectively.

The source substance (Hydroxypropyl acrylate) is an acrylic acid ester.

 

Differences

The target substance contains two linked benzene-rings (diphenylmethane) whereas the source substances Resorcinol diglycidyl ether and Phenyl glycidyl ether each contain only a single benzene-ring. Those two source substances do not contain the acrylate functional group. However, the influence of the acrylate function on genotoxicity is assessed by data on a further source substance, Hydroxypropyl acrylate.

Acrylate esters can be expected to be hydrolysed by ubiquitously present esterases to result in acrylic acid and the respective alcohol (OECD SIDS report, 2005; toxicokinetics), the latter being 3-{4-[4-(oxiran-2-ylmethoxy)benzyl]phenoxy}propane-1,2-diol (Fig. 1) in the case of Epoxy half acrylate as starting material and Hydroxypropanol in the case of Hydroxypropyl acrylate.

 

4. Comparison of genotoxicity data

The source substance Epoxy half acrylate was negative in a Bacterial Reverse Mutation Test according to OECD guideline 471 using Salmonella typhimurium, strains TA 97a, TA 98, TA 100, TA 102 and TA 1535.

The test item was also non-mutagenic in an HPRT assay according to OECD guideline 476 when tested up to cytotoxic concentrations.

However, Epoxy half acrylate induced structural chromosomal aberrations (with and without metabolic activation; predominantly chromatid breaks) in human lymphocytes in vitro.

In contrast to the target substance, the source substances Bisphenol-A-diglycidylether, Resorcinol diglycidyl ether, Phenyl glycidyl ether and Hydroxypropyl acrylate were mutagenic in the bacterial reverse mutation assay. Hydroxypropyl acrylate was not mutagenic in the mammalian cell gene mutation assay. No reliable data were available for the other two source substances.

The source substances Bisphenol-A-diglycidyl ether, Resorcinol diglycidyl ether and Hydroxypropyl acrylate were positive in an in vitro chromosome aberration assay, whereas the source substance Phenyl glycidyl ether was negative. 

All four source substances were negative in an in vivo micronucleus assay. Bisphenol-A-diglycidyl ether was also negative in an in vivo chromosome aberration assay in germ cells as well as in an in vivo comet assay in rat liver.

 

Data matrix

	Target substance	Source substances
	Epoxy half acrylate	Resorcinol diglycidyl ether (RDGE)	Phenyl glycidyl ether (PGE)	Hydroxypropyl acrylate	Bisphenol-A-diglycidyl ether (BADGE / DGEBPA)
CAS number	n.a.	101-90-6	122-60-1	25584-83-2	1675–54–3
EC number	700-487-6	202-987-5	204-557-2	247-118-0	216-823-5
bacterial reverse mutation assay	OECD guideline 471;with and without metabolic activation       Cytotoxicity: no   GLP, RL1   negative	Ames test, no guideline, only one strain tested (TA 100), without metabolic activation     Cytotoxicity: yes   Non-GLP   positive       Ref:J.P. Seiler, 1984 (no study summary)	Ames test, no guideline, only one strain tested (TA 100), without metabolic activation   Cytotoxicity: no   Non-GLP   positive       Ref:J.P. Seiler, 1984 (no study summary)	OECD guideline 471;with and without metabolic activation       Cytotoxicity: no data   Non-GLP   positive       Ref:OECD SIDS report, 2005(no study summary)	Ames test, no guideline; with and without metabolic activation       Cytotoxicity: no data   Non-GLP   Positive in strains TA100 und TA1535 with and without metabolic activation   Ref: Bisphenol-A-diglycidylether [MAK Value Documentation in German language, 1997](no study summary)
Mammalian cell gene mutation assay	OECD guideline 476, HPRT assay, Chinese hamster lung fibroblasts (V79);with and without metabolic activation     Cytotoxicity: yes   GLP, RL1   negative	No reliable data	No reliable data	OECD guideline 476, Chinese hamster lung fibroblasts (V79);with and without metabolic activation     Cytotoxicity: yes   Non-GLP, RL2   Negative         Ref:OECD SIDS report, 2005(no study summary)	Mammalian cell gene mutation test inL5178Y cells (without metabolic activation) / in CHO cells (with and without metabolic activation); no guideline   Cytotoxicity: no data   Non-GLP   Positive in L5178Y cells without metabolic activation / positive in CHO cells with metabolic activation   Ref: Bisphenol-A-diglycidylether [MAK Value Documentation in German language, 1997](no study summary)
In vitrochromosome aberration	OECD Guideline 473;peripheral human lymphocyte cultures; with and without metabolic activation   Cytotoxicity: yes     GLP, RL1   Positive (with and without metabolic activation; structural chromosome aberrations)	No guideline followed; CHO cell cultures, only tested without metabolic activation     Cytotoxicity: yes     Non-GLP, RL2   positive	No guideline followed; CHO cell cultures, only tested without metabolic activation     Cytotoxicity: yes     Non-GLP, RL2   negative	OECD Guideline 473; Chinese hamster lung fibroblasts (V79); with and without metabolic activation   Cytotoxicity: no data     Non-GLP, RL2   Positive (with and without metabolic activation)	Chromosome aberration test in rat liver cells; no guideline followed; without metabolic activation     Cytotoxicity: no data     Non-GLP,   Positive (without metabolic activation)(no study summary)
In vivochromosome aberration	No data, read-across from source substances	No guideline followed; ICR mouse bone marrow micronucleus assay; treated up to acutely toxic levels; oral application       Non-GLP, RL2 negative	No guideline followed; ICR mouse bone marrow micronucleus assay; treated up to acutely toxic levels; oral application     Non-GLP, RL2   negative	OECD Guideline 474 (Mammalian Erythrocyte Micronucleus Test); treated up to acutely toxic levels; oral (gavage) GLP, RL1   negative	Several bone marrow micronucleus / chromosome aberration tests in chinese hamster and mouse; oral application     Non-GLP   Negative
In vivoComet Assay	No data	No data	No data	No data	Rat, alkaline single cell gel electrophoresis of liver cells; oral application, 500 mg/kg bw; Non-GLP   negative

 

 

Schematic description of read-across, see attachment

Bisphenol-A-diglycidyl ether (BADGE / DGEBPA)	Resorcinol diglycidyl ether (RDGE)	Phenyl glycidyl ether (PGE)			Epoxy half acrylate	Hydroxypropyl acrylate
Several bone marrow micronucleus / chromosome aberration tests in chinese hamster and mouse / in vivo comet assay in rat liver; oral application Non-GLP   Negative	No guideline followed; ICR mouse bone marrow micronucleus assay; treated up to acutely toxic levels   Non-GLP, RL2 negative	No guideline followed; ICR mouse bone marrow micronucleus assay; treated up to acutely toxic levels Non-GLP, RL2   negative			No data, read-across from source substances	OECD Guideline 474 (Mammalian Erythrocyte Micronucleus Test)     Non-GLP, RL2   Negative

 

Quality of the experimental data of the analogues:

All available studies / publications are reliable (RL = 1 or 2) and have been conducted according to OECD guidelines or are well-documented publications which meet basic scientific principles or from competent authorities reviewed data.

 

Conclusion

The structural similarities between and common functional groups of the source and the target substances presented above support the read-across hypothesis. Adequate and reliable scientific information indicates that the source and target substances have similar genotoxicity profiles.

Therefore, based on the considerations above, it can be concluded that the results of the in vivo chromosome aberration assays of the source substances are likely to predict the properties of the target substance and are considered as adequate to fulfil the information requirement ofAnnex VIII, 8.4.

Based on these data, the target substance Epoxy half acrylate is considered to be not clastogenic in vivo. No further testing is required.

 

 

References:

Bentley P et al., 1989, Hydrolysis of hisphenol A diglycidylether by epoxide hydrolases in cytosolic und microsomal fractions of mouse liver and skin: inhihition by bis epoxycyclopentylether and the effects upon the covalent binding to mouse skin DNA, Carcinogenesis, vol. 10, no. 2, pp. 321-327, 1989

 

Climie et al., 1981a, Metabolism of the epoxy resin component 2,Z-bis[4-(2,3-epoxypropoxy)phenyl]propane, the diglycidyl ether of bisphenol A (DGEBPA) in the mouse. Part I. A comparison of the fate of a single dermal application and of a single oral dose of 14C-DGEBPA; Xenobiotica, 1981, vol.11, no. 6, 391-399

 

Climie et al., 1981b, Metabolism of the epoxy resin component 2,2-bis[4-(2,3-epoxypropoxy)phenyl]propane, the diglycidyl ether of bisphenol A (DGEBPA) in the mouse. Part II. Identification of metabolites in urine and faeces following a single oral dose of 14C-DGEBPA, Xenobiotica, 1981, vol 11, no. 6, 401-424

 

MAK, 2012:Bisphenol-A-diglycidylether [MAK Value Documentation in German language, 1997].The MAK Collection for Occupational Health and Safety. 1–30

 

OECD SIDS report, 2005: HYDROXYPROPYL ACRYLATE CAS N°: 25584-83-2, SIDS Initial Assessment Report For SIAM 20

Seiler: The mutagenicity of mono- and di-functional aromatic glycidyl compounds, Mutation Research/Genetic Toxicology, Volume 135, Issue 3, March 1984, Pages 159–167 

Justification for selection of genetic toxicity endpoint
No single key study has been selected, since all available data are considered together.

Short description of key information:
In vitro studies:
- Ames test with S. typhimurium strains TA 97, TA 98, TA 100, TA 102 and TA 1535 (met. act.: with and without) (OECD TG 471, GLP); tested up to limit concentrations of 5000 µg/plate: negative with and without metabolic activation
- Mammalian cell gene mutation assay with V79 cells (HPRT test) (met. act.: with and without) (OECD Guideline 476, GLP); tested up to cytotoxic concentrations: negative with and without metabolic activation
- In vitro mammalian chromosome aberration test with cultured human lymphocytes (met. act.: with and without) (OECD Guideline 473, pre-GLP); tested up to cytotoxic concentrations: positive with and without metabolic activation, structural chromosomal aberrations (predominantly chromatid breaks)

In vivo micronucleus assays with read-across substances:
- mouse bone marrow micronucleus assay; oral; 300 and 600 mg/kg bw, treated up to acutely toxic levels; bone marrow cells were harvested at 24 h (300 and 600 mg/kg bw), 48 and 72 h (600 mg/kg bw only) post-treatment; no significant increase in the frequency of micronucleated polychromatic erythrocytes in bone marrow after any treatment time and dose level; read-across: Resorcinol diglycidyl ether
- mouse bone marrow micronucleus assay; oral; 400, 500, 800, 1000 mg/kg bw, treated up to acutely toxic levels; bone marrow cells were harvested at 24 h (all dose levels), 48 and 72 h (1000 mg/kg bw only) post-treatment; no significant increase in the frequency of micronucleated polychromatic erythrocytes in bone marrow after any treatment time and dose level; read-across: Phenyl glycidyl ether

Endpoint Conclusion: Adverse effect observed (positive)

Justification for classification or non-classification

Based on the available reliable, relevant and adequate data, Epoxy half acrylate does not need to be classified for genotoxicity according to Directive 67/548/EEC as well as GHS Regulation EC No 1272/2008. No labelling is required.