Abstract
Fatty acid esters of glycidol (glycidyl esters) are heat-induced food contaminants predominantly formed during industrial deodorization of vegetable oils and fats. After consumption, the esters are digested in the gastrointestinal tract, leading to a systemic exposure to the reactive epoxide glycidol. The compound is carcinogenic, genotoxic and teratogenic in rodents, and rated as probably carcinogenic to humans (IARC group 2A). Assessment of exposure from occurrence and consumption data is difficult, as lots of different foods containing refined oils and fats may contribute to human exposure. Therefore, assessment of the internal exposure using the hemoglobin adduct of glycidol, N-(2,3-dihydroxypropyl)-valine (2,3-diHOPr-Val), may be promising, but a proof-of-principle study is needed to interpret adduct levels with respect to the underlying external exposure. A controlled exposure study was conducted with 11 healthy participants consuming a daily portion of about 36 g commercially available palm fat with a relatively high content of ester-bound glycidol (8.7 mg glycidol/kg) over 4 weeks (total amount 1 kg fat, individual doses between 2.7 and 5.2 µg/kg body weight per day). Frequent blood sampling was performed to monitor the 2,3-diHOPr-Val adduct levels during formation and the following removal over 15 weeks, using a modified Edman degradation and ultrahigh performance liquid chromatography–tandem mass spectrometry (UHPLC–MS/MS). Results demonstrated for the first time that the relatively high exposure during the intervention period was reflected in corresponding distinct increases of 2,3-diHOPr-Val levels in all participants, following the expected slope for hemoglobin adduct formation and removal over time. The mean adduct level increased from 4.0 to 12.2 pmol 2,3-diHOPr-Val/g hemoglobin. By using a nonlinear mixed model, values for the adduct level/dose ratio (k, mean 0.082 pmol 2,3-diHOPr-Val/g hemoglobin per µg glycidol/kg body weight) and the adduct lifetime (τ, mean 104 days, likely the lifetime of the erythrocytes) were determined. Interindividual variability was generally low. 2,3-DiHOPr-Val was therefore proven to be a biomarker of the external dietary exposure to fatty acid esters of glycidol. From the background adduct levels observed in our study, a mean external glycidol exposure of 0.94 µg/kg body weight was estimated. This value is considerably higher than current estimates for adults using occurrence and consumption data of food. Possible reasons for this discrepancy are discussed (other oral or inhalational glycidol sources, endogenous formation, exposure to other chemicals also forming the adduct 2,3-diHOPr-Val). Further research is necessary to clarify the issue.
Highlights
Despite that industrial deodorization of vegetable oils and fats has been used to remove unwanted compounds since more than 100 years, the simultaneous generation of unwanted glycidyl fatty acid esters—due to the use of high temperatures during the processes—was discovered just about 10 years ago (Svejkovska et al 2004)
Glycidyl esters are nearly completely digested in the gastrointestinal tract, leading to a systemic exposure to the reactive epoxide glycidol (Appel et al 2013; Wakabayashi et al 2012)
The aims of this study were firstly to confirm that a high dietary exposure for a limited time is reflected in an increase and a following decrease of the adduct levels, and secondly to estimate the general exposure level from the relation of adduct levels before the intervention (“background”) to the adduct levels resulting from the controlled additional exposure using a defined dose
Summary
Despite that industrial deodorization of vegetable oils and fats has been used to remove unwanted compounds since more than 100 years, the simultaneous generation of unwanted glycidyl fatty acid esters (and 2-/3-monochloropropanediol esters)—due to the use of high temperatures during the processes—was discovered just about 10 years ago (Svejkovska et al 2004). Research has been initiated on industrial mitigation strategies on the one hand, and on toxicological properties of these heat-induced food contaminants on the other hand. As for other genotoxic compounds, the margin of exposure (MoE) concept is used in risk assessment. A T 25 of 10.2 mg glycidol/ kg body weight per day was selected for the occurrence of peritoneal mesothelioma in male rats (European Food Safety Authority 2016; Federal Institute of Risk Assessment (BfR) 2009). From a public health point of view, the daily exposure might be considered to be of low concern when it does not exceed 0.408 μg/kg body weight (T25 based MoE higher that 25,000)
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