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Toxicological information


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Description of key information

no data available for 2-EHAc
Data from the analogous substance 2-ethylhexan-1-ol
2 years rat: no oncogenic effects up to 500 mg/kg bw/day (GLP, comp. to guideline, Astill 1996)
1.5 years mouse: weak adverse trends in hepatocellular carcinoma incidence at doses with increased lethality (750 mg/kg bw) were considered as not biologically relevant (GLP, comp. to guideline, Astill 1996)

Key value for chemical safety assessment

Carcinogenicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed

Justification for classification or non-classification

The available data do not justify a classification for carcinogenicity. Based on the available data, the US EPA concluded that 2 -ethylhexan-1 -ol is not carcinogenic in the mouse or rat. The same applies for 2 -ethylhexyl acetate.

Additional information

There were only reliable data available from the structural analogon and potential metabolite 2-ethylhexan-1-ol (2 -EH) to assess the cancerogenic potential of 2-EHAc.


The carcinogenic potential of 2 -EH was examined in two rodent long term studies under GLP and in accordance with OECD TG 451, using male and female Fischer F344 rats (dose levels 0, 50, 150, and 500 mg/kg bw/day) and B6C3F1 mice (dose levels 0, 50, 200, and 750 mg/kg bw/day). The studies are reported in the publication of Astill et al. (1996, rat and mouse).For rats there are two volumes containing the original two study report of BASF (Küttler, 1992; Hellwig et al., 1992). For mice the results are summarized in another BASF report (Hellwig et al., 1991).

2 -EH was neither carcinogenic in male or female rats in the 2 -year study, nor in male mice exposed for 18 months. A weak, or equivocal, carcinogenic potential was seen in female mice since the incidence of hepatic carcinoma was significantly increased in high dose females compared to the vehicle control group (p<0.05). The hepatic carcinoma incidence was, however, not significantly different from that in the control group given only water and no hepatic adenomas were observed in the top dose group.

In the study with Fischer 344 rats, in both sexes the sum of primary tumours, the sum of benign tumours and the sum of malignant tumours was lower in the top dose group than in either the vehicle control or the water control groups. The NOAEL (carcinogenicity) was therefore 500 mg/kg bw/day in male and female rats. A dose related increase in mortality was observed in female rats, with 52% mortality in those given 500 mg/kg bw/day 2-EH. Dose related reductions in weight gain were observed (for males: -5% at 50 mg/kg bw/day, -11% at 150 mg/kg bw/day, -23% at 500 mg/kg bw/day; for females: -9% at 150 mg/kg bw/day, -21% at 500 mg/kg bw/day). Increased focal lesions and lung discoloration was observed in rats at 500 mg/kg bw/day. The 50 mg/kg bw/day dose produced a 6% increase in relative female stomach weight. Significant increases in stomach, kidney and brain relative weights were observed in male rats at 150 mg/kg bw/day 2-EH, with testis relative weight increased at 500 mg/kg bw/day. Female rats had significantly increased relative weights of stomach, liver, kidney and brain at the 150 and 500 mg/kg bw/day doses. The effects seen on relative organ weights at 150 mg/kg bw/day were not accounted for as adverse as these presumably were due to the reduced body weights observed at the same dose levels. The NOAEL for systemic toxicity therefore was 150 mg/kg bw/day in this study based on the increased mortality and other effects in the high dose group (Astill et al., 1996).

In the study with mice, at the top dose of 750 mg/kg bw/d 2-EH caused a reduction of body weight gain in both sexes at early stages of the study (approx. from study week 6 onwards), a reduced terminal body weight, and an increased mortality of up to 30% in week 78. Relative organ weight changes were mostly limited to the top dose groups as evidenced by statistically significantly increased relative weights of the stomach, liver, brain and testes in males, and of the stomach, liver, kidneys, and brain in females.

No neoplastic lesions were seen in males. In top dose females, the incidence of hepatocellular lesions (basophilic foci and carcinoma) was significantly increased compared to vehicle control, but this was attributed to the toxicity (fatty infiltration of the liver was also observed) that was associated with the high dose (750 mg/kg bw/d).This was supported by the observation that the incidence of liver carcinoma was high (50%) in decedents. The NOAEL (carcinogenicity) was therefore 750 mg/kg bw/day in male and female mice. The NOAEL for systemic toxicity was 200 mg/kg bw/day in this study.

Overall it is concluded, that 2-ethylhexanol was not oncogenic in B6C3F1 mice in a valid GLP carcinogenicity study (Astill et al., 1996).The authors of the carcinogenicity study provided data, which indicate that the increased incidences of hepatic carcinoma in female mice that were seen associated with DEHP, DEHA, or other compounds, which may liberate 2-EH during their metabolism, is unlikely to be caused by 2-EH (e. g. different tumour pattern; Astill et al., 1996).

Read across justification to 2-ethylhexan-1-ol for filling data gaps of 2-ethylhexyl acetate:

As indicated by toxicokinetic studies (see chapter on toxicokinetics, metabolism and distribution), 2-ethylhexyl acetate is rapidly hydrolyzed to 2-ethyhexan-1-ol and acetate (acetic acid). Available data on 2-ethyhexan-1-ol is therefore suitable for filling data gaps of 2-ethylhexyl acetate.