Abstract 4692: Comparison of dietary exposure to acrylamide and acrolein: monitoring mercapturic acids in human urine after consumption of potato crisps

Abstract

Abstract Acrolein (AC) is an α,ß-unsaturated aldehyde, classified by the IARC in group 3B (not classifiable as to its carcinogenicity to humans). It is supposed to be formed by heating of fat containing foods, via heat induced formation from glycerides/glycerol. Formation of AC from carbohydrates has also been discussed [Stevens and Maier, 2008]. Moreover, it also has been suggested that AC might be formed by endogenous metabolism as a side product of carbohydrate and/or amino acid turnover or by oxidative desamination of polyamines. Analytical determination of AC in foodstuffs is difficult, due to its high volatility and reactivity. Data on exposure and contents of AC in heat treated foods therefore are scarce. It is unclear, to which extent AC contributes to the overall exposure of heat induced biologically active compounds such as acrylamide (AA) and furan. AC forms 1,4-Michael type adducts of biomolecular targets with nucleophiles like sulfhydryl and amino groups. In the organism, AC is mainly conjugated to glutathione and excreted after degradation and reduction as the mercapturic acid (MA), N-acetyl-S-(3-hydroxypropyl)-cysteine (3-HPMA). In the present study, AC exposure and detoxification kinetics were investigated within the scope of a human study with 13 healthy volunteers ingesting a test meal of 150 g potato crisps. Urine was collected for up to 72 hours (12 time points) and MA contents were measured after purifying and enrichment by solid phase extraction (SPE) [Fuhr et al., 2006]. Levels of 3-HPMA and of MAs derived from AA (N-acetyl-S-(2-carbamoylethyl)-cysteine (AAMA)) and glycidamide (N-acetyl-S-(2-hydroxy-2-carbamoylethyl)-cysteine (GAMA)) were determined by liquid chromatography tandem mass spectrometry (LC-MS/MS), and urinary concentrations were standardized by reference to urinary creatinine. The maximal urine concentrations found for 3-HPMA, AAMA, and GAMA were (mean ± SD) 146 ± 86, 2.5 ± 0.8, 0.14 ± 0.07 µmol/g creatinine, respectively and elimination half lives were 5, 12, and 38 hours. The AA uptake with a 150 g meal of potato crisps was about 1 mg, equivalent to 12.4 µg/kg body weight. The predose values for the sum of AAMA and GAMA were 0.15, that for 3-HPMA 35.9 µmol/g creatinine. On the basis of the AUC values of MAs excreted in urine, the total excretion of 3-HPMA was about 15 times higher than that of AAMA plus GAMA. Thus, the exposure to AC from the test meal was at least one order of magnitude higher than exposure to AA. The question as to what extent AC exposure has to be taken into account when considering risk assessment by heat induced toxicants has not been addressed before.