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Administrative data

Key value for chemical safety assessment

Additional information

In-vitro studies

Bacterial systems

One bacterial gene mutation assay according to OECD guideline 471 is available with 2-propylheptyl acrylate (BASF SE, 2008). The assay was negative at doses up to 5300 μg/plate with and without S-9 mix in Salmonella typhimurium strains TA 98, TA 100, TA 1535, TA 1537 and E. coli WP2 uvr A. Since the experiment was negative with and without metabolic activation, there is no indication for a mutagenic potential of the test substance in bacterial cells.

Mammalian cell gene mutation test

No reliable studies concerning genetic toxicity in-vitro in mammalian cells were identified for 2-propylheptyl acrylate. However, data from the structural analogue 2-Ethylhexyl acrylate (CAS No. 103-11-7) are considered appropriate for the assessment. Two mouse lymphoma assays and two HGPRT tests with CHO cells were performed with the structural analogue 2-Ethylhexyl acrylate. A mouse lymphoma assay, with 4-hour treatment without S-9 mix, was reported by Dearfield et al. (1989). Small increases of mutation frequencies were obtained in high doses with strong cytotoxicity. Doses of 30, 31, 32, 33 and 34 nL/mL were tested in three independent experiments; according to combined data, mutation frequencies increased by factors of 1.6 to 1.9 without dose-effect relationship; relative survival ranged from 11 to 20.3 %. 2-Ethylhexyl acrylate produced an equivocal result for an increased mutant frequency. While a doubling of the mutant background frequency was seen at several tested concentrations, e.g. 31 µg/mL (experiment 2), other, sometimes higher concentrations and repeat experiments did not induce a consistent increase. No clear dose-response pattern was discerned. Rohm & Haas (1984) reported on a mouse lymphoma assay where doses of 15.6 to 150 nL/mL (with S-9 mix from Aroclor-induced rat livers) or 1.95 to 60 nL/mL (without S-9 mix) were tested in a 4-hour treatment. Treatment with doses of 70 to 150 nL/mL led to an increase of mutation frequency to 2.2- to 4.6-fold and was accompanied by moderate to strong cytotoxicity (relative growth varied from 4.8 to 54.6 % without clear dose-dependency). Without S-9 mix, an increase in mutation frequency at 15.6 nL/mL was not reproducible. Two investigations were conducted on induction of HGPRT mutations in CHO cells. According to Union Carbide Co. (1980) 2-Ethylhexyl acrylate did not induce HGPRT mutations after 5-hour treatment with or without S-9 mix. Doses of 3.13 to 50E-5 % (v/v; with S-9 mix) or 6.25 to 100E-5 % (without S-9 mix) were used; the maximum doses corresponded to 5 and 10 nL/mL; only minor toxicity was seen. In a 2nd investigation, cells were treated with doses of 5 to 80 μg/mL (monolayer assay) or 14 to 26 μg/mL (suspension assay) in the absence of S-9 mix (Moore et al. 1991). Whereas the suspension assay was clearly negative for all tested doses up to extreme toxicity, sporadic increases in mutation frequency were seen in the monolayer assay. In a 1st experiment, weak effects were seen at doses of 35 and 40 μg/mL which led to less than 20 % relative survival. In the 2nd experiment doses of 60 and 70 μg/mL resulted in slightly increased mutation frequencies, toxicity was moderate (33 % relative survival). Higher doses of 75 and 80 μg/mL were negative (40 and 7 % relative survival). In conclusion, 2 -ethylhexyl acrylate seems to have a low potential for induction of gene mutations in mammalian cells. Since the genetic effects were limited to doses with strong cytotoxicity and did not follow a clear dose-response reaction, the potential will probably not be expressed in vivo.

Chromosomal aberration and micronucleus tests

In mouse lymphoma cells, parallel investigations of structural chromosomal aberrations and micronuclei were performed by Dearfield et al. (1989) with the structural analogue 2-Ethylhexyl acrylate. Cells were treated with doses of 20, 25, 31 and 34 μg/mL 2 -ethylhexyl acrylate for 4 hours without S-9 mix. All treatments resulted in strong cytotoxicity (27, 16, 12 and 12 % relative survival). For analysis of chromosomal aberrations, cultures were exposed to BrdUrd after treatment and were sampled 14 to 15 hours after the beginning of the treatment in order to select 1st-division mitoses cells for analysis; however, co-treatment with BrdUrd, which is a genotoxin, is not recommended by the guidelines and makes findings difficult to interpret. 100 mitoses were analysed per experimental point. Aberration frequencies in treated cultures varied from 5 to 9 % (negative control, 4 %). Given the various methodological insufficiencies, the findings are evaluated as inconclusive. For analysis of micronuclei, cultures were exposed to cytochalasin B (3μg/mL) after treatment; sampling was 16 to 17 hours after the beginning of the treatment; 1000 cells were analysed per experimental point. The micronucleus frequency was 1.2 % in the negative control and varied from 0.8 to 1.1 % in the treated cultures, i.e. the result was negative. In conclusion, there is no relevant evidence for clastogenicity of 2 -ethylhexyl acrylate; a fully reliable finding, however, is lacking.

Mammalian cell indicator tests

A test for induction of unscheduled DNA synthesis (UDS) with primary rat hepatocytes was performed with the “liquid scintillation counting” methodology (Union Carbide Co., 1980) with the structural analogue 2 -ethylhexyl acrylate. A single experiment was conducted. The overall result for this test was negative for doses up to 100E-5 % (10 nL/mL). In conclusion, the data from mammalian cell indicator tests do not add relevant or conclusive information.

In vivo studies

The possible formation of cytogenetic damage in vivo was investigated in erythrocytes from bone marrow of NMRI mice, in accordance to OECD TG No. 474. Oral doses of 500, 1000, and 2000 mg/kg bw 2 -propylheptyl acrylate were given once to groups of 5 male animals. Sampling was 24 and 48 h after application of 2-propylheptyl acrylate. After 24 h no increase of MN frequency was observed. After 48 h, a statistically significant increase of MN in PCE (1.3 to 3.0 per mill) was observed. This increase was not biologically relevant because no dose-dependent increase was observed after 24 h. Furthermore, the increase did not significantly differ from data from historical controls (2 +/- 0.6 (mean +/- SD) with a max. value of 3.3) (BASF SE, 2008). Under the experimental conditions chosen, the test substance 2-propylheptyl acrylate does not have a chromosome-damaging (clastogenic) effect nor does it lead to any impairment of chromosome distribution in the course of mitosis (aneugenic activity) in bone marrow cells in vivo.

Conclusion

2-propylheptyl acrylate was negative in a bacterial mutation assay. Furthermore, no clastogenic or aneugenic potential of 2-propylheptyl acrylate was observed in an in-vivo micronucleus test. In addition, no relevant evidence for clastogenicity or gene mutation in mammalian cells was implicated to the structural analogue 2-Ethylhexyl acrylate. In a study conducted in compliance with GLP and OECD TG No. 486, 2-Ethylhexyl acrylate was negative in the in vivo UDS assay using rat hepatocytes. Thus, the negative results of 2-propylheptyl acrylate in terms of clastogenicity and gene mutation together with the results of the structural analogue 2-Ethylhexyl acrylate,strongly indicate that 2 -propylheptyl acrylate is not genotoxicity in vivo.


Justification for selection of genetic toxicity endpoint
Several studies with the substance itself and the structural analogue 2- Ethylhexyl acrylate were performed.

Short description of key information:
2-propylheptyl acrylate was negative in a bacterial mutation assay. Furthermore, no clastogenic or aneugenic potential of 2-propylheptyl acrylate was observed in an in-vivo micronucleus test. In addition no relevant evidence for clastogenicity or gene mutation in mammalian cells was implicated to the structural analogue 2-Ethylhexyl acrylate.

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

Based on the results of the in vivo and in vitro genetic toxicity studies, the test susbtance was neither found genotoxic nor mutagenic and is not subjected to classification and labelling according to Directive 67/548/EEC (DSD) and Regulation (EC) No 1272/2008 (CLP).