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EC number: 940-510-9 | CAS number: 103043-58-9
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Carcinogenicity
Administrative data
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:
- LOAEL
- 1 715 mg/kg bw/day
- Study duration:
- chronic
- Species:
- mouse
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.
Reference
WHO (2004)Di(2 -ethylhexyl)adipate in Drinking water WHO/SDE/WSH/03.04/68
Carcinogenicity: via oral route (target organ): digestive: liver
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