Abstract
The general population is exposed to the genotoxic carcinogen glycidol via food containing refined edible oils where glycidol is present in the form of fatty acid esters. In this study, internal (in vivo) doses of glycidol were determined in a cohort of 50 children and in a reference group of 12 adults (non-smokers and smokers). The lifetime in vivo doses and intakes of glycidol were calculated from the levels of the hemoglobin (Hb) adduct N-(2,3-dihydroxypropyl)valine in blood samples from the subjects, demonstrating a fivefold variation between the children. The estimated mean intake (1.4 μg/kg/day) was about two times higher, compared to the estimated intake for children by the European Food Safety Authority. The data from adults indicate that the non-smoking and smoking subjects are exposed to about the same or higher levels compared to the children, respectively. The estimated lifetime cancer risk (200/105) was calculated by a multiplicative risk model from the lifetime in vivo doses of glycidol in the children, and exceeds what is considered to be an acceptable cancer risk. The results emphasize the importance to further clarify exposure to glycidol and other possible precursors that could give a contribution to the observed adduct levels.
Highlights
Exposure to genotoxic compounds in interaction with other factors contributes to an increased risk of cancer development [1]
Quantification of the cancer risk from exposure to genotoxic compounds is usually based on data from carcinogenicity studies at high doses in rodents, with extrapolation of the obtained cancer risk coefficient to estimated human exposure doses of the studied compound
This is important for ongoing human exposures, where measured in vivo doses give an improved estimate of the exposure
Summary
Exposure to genotoxic compounds in interaction with other factors contributes to an increased risk of cancer development [1]. Quantification of the cancer risk from exposure to genotoxic compounds is usually based on data from carcinogenicity studies at high doses in rodents, with extrapolation of the obtained cancer risk coefficient to estimated human exposure doses of the studied compound. An improved estimate of the risk would be obtained if the internal (in vivo) dose of the studied compound/metabolite could be used for species extrapolations. This is important for ongoing human exposures, where measured in vivo doses give an improved estimate of the exposure. For which there is an ongoing human exposure, is the genotoxic compound glycidol [3]. This compound has received much attention during the last years, largely due to the detection of glycidyl fatty acid esters in food intended for children, such as as infant formula [4]
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