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Toxicological information


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Description of key information

No data on carcinogenicity are available for Dipropylheptyladipat. The potential to induce cancer was investigated for Diethylhexyladipat, a structural analogue to Dipropylheptyladipat, in a 103-week feeding study with F344 rats and B6C3F1 mice using dietary concentrations of 12000 or 25000 ppm, equivalent to a daily intake of 600 or 1250 mg/kg bw/day in rats and 1715 and 3570 mg/kg bw/day in mice. 
In rats relevant changes in tumor rates were found as compared with concurrend controls, whereas in mice hepatocellular tumor incidences were found in groups receiving remarkably high dose levels.

Key value for chemical safety assessment

Carcinogenicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no adverse effect observed
Dose descriptor:
1 715 mg/kg bw/day
Study duration:

Justification for classification or non-classification

Based on the results obtained from carcinogenicity testing with the read across substance Diethylhexyladipat, the target chemical Dipropylheptyladipat is not considered to be subject to classification and labelling for carcinogenicity according to Directive 67/548/EEC (DSD) and Regulation (EC) No 1272/2008 (CLP).


Additional information

No data on carcinogenicity are available for Dipropylheptyladipat. However, the potential to induce cancer was investigated for Diethylhexyladipat, a structural analogue to Dipropylheptyladipat (for more details please refer to the read across statement in chapter 13), in a 103-week feeding study (NTP, 1982). F344 rats and B6C3F1 mice were administered with Diethylhexyladipat in the diet at levels of 12000 or 25000 ppm, equivalent to a daily intake of 600 or 1250 mg/kg of bw in rats and 1715 or 3570 mg/kg of bw/day in mice (conversion based on data from the WHO report (2004)). Body weight, clinical signs and mortality were evaluated repeatedly during the study period. After animals were sacrificed gross and microscopic examinations were performed on major tissues, major organs, and all gross lesions form killed animals and from animals found dead. No test substance related changes in tumour rates were found in the rat (no increased tumour incidences). In the (female) mice an increased number of hepatocellular carcinomas was found at both doses. Hepatocellular adenomas and carcinomas occured combined in high-dose mice of both sexes and in low-dose female mice at incidences that were dose-related and significantly higher than those in control mice. The association of liver tumours in male mice with the administration of the test item was not considered to be conclusive because the increased number of liver tumours in males reflected only an increase in adenomas in the high-dose group and because the time to observation of tumours was not significantly different in dosed and control males. In addition, when comparing the incidence in historical laboratory control mice the liver tumours in male mice could not be clearly related to compound administration.

Under the conditions of the present study Diethylhexyladipat was carcinogenic for female B6C3F1 mice, causing increased incidences of hepatocellular carcinomas, and was probably carcinogenic for male B6C3F1 mice, causing hepatocellular adenomas.


As Diethylhexyladipat failed to elicit genotoxic responses in available test systems and did not form adducts with DNA, it may be an epigenetic carcinogen for which a dose threshold exists. Liver tumours are likely to occur only at very high doses causing proliferation of peroxisomes; as there is a dose threshold for such proliferation, there is probably also a dose threshold for tumour development. The available information suggests that primates are less sensitive to chemically induced peroxisomal proliferation than rodents (WHO, 2004; for further detailed discussion about the mechanism of peroxisome proliferation refer to the publications summarized in chapter 7.12).

Therefore, the animal data are not considered sufficient for a presumption that human exposure to Diethylhexyladipat might result in cancer.


WHO (2004)Di(2 -ethylhexyl)adipate in Drinking water WHO/SDE/WSH/03.04/68

Carcinogenicity: via oral route (target organ): digestive: liver