Objective of this work was determination of processing contaminant known as 3-MCPD (3-chloropropa-ne-1,2-diol) in its free and bound form in breads with defined parameters of processing. Selected and analysed were 24 samples, which represented two sets of breads produced in bakeries equipped with a continual line. In all cases determinations were carried out for breadcrumb and crust separately. The first set of samples were wheat-rye breads produced chronologically in ten days in the bakery Michelská pekárna, slightly different in temperatures and times of baking. The second set contained 14 samples of wheat-rye breads with a content of rye flour less than 40% differing in the yeast type and acidity. These breads were produced in the bakery Kontinua. The fat content was determined in all samples by Soxhlet extraction. Free and bound 3-MCPD was determined by gas chromatography-mass spectrometry method. Concentration of free 3-MCPD in samples was at interval < 9-54.5 µg/kg. Concentration of bound 3-MCPD was at interval 1.56-23.60 mg/kg of fat (i.e. 5.7-84.9 µg/kg of sample).

In order to quantify the relative bioavailability of glycidol from glycidyl fatty acid esters in vivo, glycidyl palmitoyl ester and glycidol were orally applied to rats in equimolar doses. The time courses of the amounts of glycidol binding to hemoglobin as well as the excretion of 2,3-dihydroxypropyl mercapturic acids were determined. The results indicate that glycidol is released from the glycidyl ester by hydrolysis and rapidly distributed in the organism. In relation to glycidol, there was only a small timely delay in the binding to hemoglobin for the glycidol moiety released from the ester which may be certainly attributed to enzymatic hydrolysis. In both cases, however, an analogous plateau was observed representing similar amounts of hemoglobin binding. With regard to the urinary excretion of mercapturic acids, also similar amounts of dihydroxypropyl mercapturic acids could be detected. In an ADME test using a virtual double tag (³H, ¹⁴C) of glycidyl palmitoyl ester, a diverging isotope distribution was detected. The kinetics of the ¹⁴C-activity reflected the kinetics of free glycidol released after hydrolysis of the palmitoyl ester. In view of this experimental data obtained in rats, it is at present justified for the purpose of risk assessment to assume complete hydrolysis of the glycidyl ester in the gastrointestinal tract. Therefore, assessment of human exposure to glycidyl fatty acid ester should be regarded as an exposure to the same molar quantity of glycidol.

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