Glycidol Fatty Acid Ester and 3-Monochloropropane-1,2-Diol Fatty Acid Ester in Commercially Prepared Foods

Glycidyl fatty acid esters (GEs), which are the main pollutant in processed oils, are potential mutagens or carcinogens. 3-Monochloropropane-1,2-diol fatty acid esters (3-MCPDEs) are also well-known food processing contaminants. 3-MCPDEs are believed to be a precursor to GEs in foodstuffs. In vivo, lipase breaks down the phosphate ester of GEs and 3-MCPDEs to produce glycidol and 3-MCPD, respectively, which are genotoxic carcinogens. Thus, it is important to determine human exposure to GEs and 3-MCPDEs through foodstuffs. There are only reports on the amount of GE and 3-MCPDE in cooking oils and cooked foods. The content in multiple types of foods that are actually on the market was not clarified. In this study, 48 commercially prepared foods were analyzed to identify other sources of exposure to GE and 3-MCPDE. All of them contained relatively high amounts of GEs and 3-MCPDEs. The correlation between GEs and 3-MCPDEs in individual foods was examined. There was a correlation between the amounts of GEs and 3-MCPDEs in the food products (r = 0.422, p < 0.005). This is the first report on the content in multiple types of commercially prepared foods that are actually on the market was clarified.

Does External Exposure of Glycidol-Related Chemicals Influence the Forming of the Hemoglobin Adduct, N-(2,3-dihydroxypropyl)valine, as a Biomarker of Internal Exposure to Glycidol?

Glycidyl fatty acid esters (GE) are constituents of edible oils and fats, and are converted into glycidol, a genotoxic substance, in vivo. N-(2,3-dihydroxypropyl)valine (diHOPrVal), a hemoglobin adduct of glycidol, is used as a biomarker of glycidol and GE exposure. However, high background levels of diHOPrVal are not explained by daily dietary exposure to glycidol and GE. In the present study, several glycidol-related chemicals (glycidol, (±)-3-chloro-1,2-propanediol, glycidyl oleate, epichlorohydrin, propylene oxide, 1-bromopropane, allyl alcohol, fructose, and glyceraldehyde) that might be precursors of diHOPrVal, were administered to mice, and diHOPrVal formation from each substance was examined with LC-MS/MS. DiHOPrVal was detected in animals treated with glycidol and glycidyl oleate but not in mice treated with other chemicals (3-MCPD, epichlorohydrin, propylene oxide, 1-bromopropane, allyl alcohol, fructose, and glyceraldehyde). The amount of diHOPrVal per administered dose produced from other chemicals was negligible compared to the amounts associated with dietary glycidol and GE. The present study provides important knowledge for exploring other sources for internal exposure to glycidol.