Glycerides, C16-18

Carcinogenicity

Key value for chemical safety assessment

Carcinogenicity: via oral route

Endpoint conclusion

Endpoint conclusion:

no adverse effect observed

Carcinogenicity: via inhalation route

Endpoint conclusion

Endpoint conclusion:

no study available

Carcinogenicity: via dermal route

Endpoint conclusion

Endpoint conclusion:

no study available

Justification for classification or non-classification

Based on studies from other substances of the same read-across category,‘glycerides, C16-18 (SDA Reporting Number: 19-001-00)’ are not expected to show carcinogenicity after oral exposure. This substance also does not contain any functional groups suggesting carcinogenic activity. Furthermore, no carcinogenicity is expected from dermal exposure as systemic uptake will be lower than from the oral route.Finally,based on its physical state (solid at ambient temperature) and low vapour pressure (< 1.33 x 10^-8Pa at 20°C), the possibility of inhalation exposure will be extremely limited. In many cases the substance is also used in industrial applications and transported and handled in liquid form (heated). If the substance is in powder form, sprayed or otherwise finely dispersed in the air, the use of respiratory protection (filter mask) is recommended at workplace.Thus,carcinogenicity as a result of respiratory exposure is considered unlikely.

‘Glycerides, C16-18 (SDA Reporting Number: 19-001-00)’ and the other substances from the same read-across grouphave a very long history of safe use in nutritional (food and feed), cosmetic and industrial applications.In the form of olive oil, corn oil, sunflower oil, etc., they are also frequently employed as vehicles in toxicity studies following international testing guidelines (e.g. OECD) for the evaluation of the repeated dose toxicity, carcinogenicity or reproductive/developmental toxicity of chemical substances, without any apparent adverse effects.

Based on the above information, the substance does not qualify for carcinogenicity classification according to EU CLP Regulation (EC) 1272/2008.

Additional information

A study was conducted to determine the long-term carcinogenic effects of 'glycerides, C8-18 and C18-unsatd.' (as coconut oil) in a life-span experiment in rats. 54 calorie (cal) % of the substance was fed through diet to 39-40 male and female Wistar rats per group during their entire life span (104 wks). No significant differences in the mean life span were found between groups. Considering the total population (males and females), the number of tumour bearers did not differ significantly. Parathyroid hyperplasia and necrocalcinosis in the heart were found mainly in males with slightly higher incidence in the coconut oil group in comparison with the control (soybean oil). Other pathological changes were randomly distributed among the different groups. However, the nature and incidence of these histopathological changes including tumours could not be related to the type of dietary fat or fatty acids used. Hence, under the test conditions, dietary administration of 54 cal% of the substance to wistar rats of either sex, for entire life span, has low carcinogenic potential (Vles and Gottenbus, 1972).

A study was conducted to determine the effects of diets high in ‘glycerides, C16-18 and C18 -unsatd.’ (as 20% palm oil or vegetable fat) on mammary tomourigenesis when fed to rats prior to or during the initial phase of carcinogenesis. 21 d old Sprague Dawley rats were fed ad libitum on diets containing 20% of the substance, 5% (normal fat) corn oil, 20% (high fat) corn oil, 20% beef tallow or 20% lard. Rats in the various dietary treatments (32/group) orally gavaged 7.5 mg 12 -dimethylbenz(a)anthracene (DMBA) at 52 d of age. One week later, they were shifted to a 5% corn oil control diet for the rest of the experiment. Animals were placed on a normal diet to determine the early effects of the various high fat diets on subsequent mammary tumourigenesis. Under the study conditions, that diets high in vegetable fat containing either the saturated substance or polyunsaturated (corn oil) fatty acids have no effects on subsequent mammary tumorigenesis (Sylvester, 1986).

A study was conducted to investigate whether ‘glycerides, C16 -18 and C18 -unsatd.’ (as palm oil), as a dietary fat, had an impact on mammary carcinogenesis in female rats induced by DMBA. Groups of 20 female rats were given one single dose DMBA and after three days were fed semisynthetic diets containing 20% of the substance, soybean oil, corn oil, deodorized palm oil or metabisulfite-treated palm oil, respectively, for a duration of 5 months. At autopsy, blood was collected from the tumor-bearing rats. The tumors were examined and lipid extractions were made for analysis of fatty acid profile, as well as tocopherols, tocotrienols and carotenes content. Under the conditions of the study, the substance was shown to have a non-promoting effect on chemically induced mammary carcinogenesis in female rats (Sundram, 1989).