Internal exposure to heat-induced food contaminants in omnivores, vegans and strict raw food eaters: biomarkers of exposure to 2- and 3-monochloropropanediol (urinary excretion) and glycidol (hemoglobin adduct N-2,3-dihydroxypropyl-Val).

Fatty acid esters of 2/3-monochloropropanediol (2/3-MCPD) and glycidol are formed mainly during heat processing (deodorization) of vegetable oils, and are hydrolyzed by lipases in the gastrointestinal tract leading to the absorption of 2/3-MCPD and glycidol. The International Agency for Research on Cancer (IARC) has classified 3-MCPD as possibly and glycidol as probably carcinogenic to humans. The aims of the current work were to clarify the exposure to 2/3-MCPD and glycidol associated with different dietary habits (omnivore, vegan, raw-food eating), and the exposure development between 2017 and 2021 in German study participants. The questions were addressed using the daily urinary excretion of 2/3-MCPD and the hemoglobin adduct N-(2,3-dihydroxypropyl)-Val (DHP-Val) formed from glycidol as biomarkers of exposure, which were determined in two dietary studies including 36 omnivores, 36 vegans and 16 strict raw food eaters (abstaining from any heated food for at least four months). The median urinary excretion of 2- and 3-MCPD in non-smoking omnivores and vegans was 0.87 and 1.35 µg/day (2-MCPD), respectively, and 0.79 and 1.03 µg/day (3-MCPD), respectively. The 2/3-MCPD concentrations in urine samples of raw food eaters were usually below the limit of detection. The median DHP-Val levels in non-smoking vegans and omnivores were 3.9 pmol/g Hb each, and 1.9 pmol/g Hb in raw food eaters. Between 2017 and 2021, the exposure to 3-MCPD and glycidol did not change, however, the median 2-MCPD excretion decreased (p = 0.02, omnivores and vegans combined). The correlation between daily excretions of 2/3-MCPD determined 4 years apart was weak, whereas a moderate correlation was observed for DHP-Val (rS = 0.66) in this timeframe. In conclusion, the exposure to glycidol in omnivores and vegans was alike, whereas the 2/3-MCPD exposure was somewhat (albeit not significantly) higher in vegans. While 2/3-MCPD were hardly detectable in urine samples of raw food eaters, the median DHP-Val level (about 50% of those in omnivores) indicates a glycidol source independent of the dietary exposure.

Health risk assessment for dietary exposure to 3-monochloropropane-1,2-diol, 2-monochloropropane-1,2-diol, and glycidol for Italian consumers.

3-Monochloropropane-1,2-diol (3-MCPD), 2-monochloropropane-1,2-diol (2-MCPD) and 2,3-epoxy-1-propanol (glycidol), in their free form or esterified to fatty acids, are food contaminants formed during the refinement of oils and fats. We conducted a survey to quantify the levels of these compounds in 130 food items, in order to assess the exposure to them in food and the consequent health risk for consumers. Food samples, including infant formula, were analysed by gas-chromatography mass spectrometry with the indirect method, and we used the latest open access food consumption database for the Italian population for a probabilistic assessment of exposure. We adopted an in silico approach to fill the gap for the toxicity of 2-MCPD. The occurrence values for the three contaminants in food were in most cases lower than or comparable to those reported in previous surveys. Exposure assessment for the most exposed individuals (95thpercentiles of consumers only) of different age groups, gave values below the tolerable daily intake recommended by the European Food Safety Authority for 3-MCPD and below the simulated or predicted toxicity thresholds for 2-MCPD, indicating a negligible risk due to dietary exposure to these contaminants. For glycidol, however, estimated exposure indicated a non-negligible increase in cancer risk, and a margin of exposure <25,000 for younger population groups, indicating a potential health concern.

Determination of Free Glycidol and Total Free Monochloropropanediol in Fish and Krill Oil with Simple Aqueous Derivatization and High-Performance Liquid Chromatography-Tandem Mass Spectrometry.

This study introduces a novel method for detecting free glycidol and total free monochloropropanediol (MCPD) in fish and krill oil. Before analysis on high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS), p-(dimethylamino)phenol was used for derivatization of these compounds, enabling the sensitive determination of these contaminants. The sample preparation procedure includes a simple, efficient pretreatment using NaCl aqueous solution extraction and C18 sorbent cleanup (for demulsification), distinguishing glycidol from MCPD under varied reaction conditions for derivatization (weak acidic and strong alkaline aqueous environments). This approach shows broad linearity from 1 to at least 256 ng·mL-1, improved sensitivity compared to standard GC-MS methods, with the limit of detection (LOD) and limit of quantification (LOQ) for MCPD and glycidol in both oil samples verified at 0.5 ng·mL-1 and 1 ng·mL-1, respectively. Different from previous HPLC-MS methods for direct detection of glycidol esters or MCPD esters, this is the first HPLC-MS method used for the detection of free glycidol and total free MCPD in edible oil. Furthermore, this method can be potentially developed for glycidol or monochloropropane diol esters, which is similar to the current official methods adopted for indirect detection of these contaminants in different food matrices. Application of this detection method to real dietary supplements (fish oil and krill oil) revealed MCPD residues in fish oil (maximum detected: 32.78 ng·mL-1) and both MCPD (maximum detected: 2767.3 ng·mL-1) and glycidol (maximum detected: 22.2 ng·mL-1) in krill oil, emphasizing its effectiveness and accuracy for assessing contamination in these supplements.

Occurrence of 3-monochloropropane-1,2-diol and glycidyl esters in artisanal vegetable edible oils.

The safety of vegetable oils has come under intense scrutiny ever since the International Agency for Research on Cancer issued an alert on the carcinogenic properties of 3-monochloropropane-1,2-diol fatty acid esters (3-MCPDE) and glycidyl esters (GE). In this study, a total of 114 samples of artisanal palm oil (PO), palm kernel oil (PKO), and coconut oil (CO) were sourced from three regions in Ghana. The concentrations of 3-MCPDE and GE were quantified using the indirect method with gas chromatography-mass spectrometry. Subsequently, the statistical distribution functions of the concentrations of the esters were fitted using the Palisade @risk software. The relationships between the esters in the oils were determined using the Pearson correlation coefficient. The results showed no correlation (p > 0.05) between the concentrations of 3-MCPDE and GE. However, 18-60 % of the sampled PO contained 3-MCPDE above the European Commission's 2.5 mg/kg limit. In comparison, 24-35 % of the PO contained GE at levels exceeding the Commission's 1 mg/kg limit. Similarly, 25-35 % of PKO samples had GE concentrations above the limit. CO was the least contaminated oil, with little or no evidence of 3-MCPE and GE formation. Though the most frequently occurring (modal) concentrations of the esters were below the limits imposed by the Commission, it is the 95th percentile level of concentrations, especially for PO, that pose a health concern. Serious education and control must be exercised over the production of PO to enhance safety at the national and international markets.

Beyond the Charge: Interplay of Nanogels' Functional Group and Zeta-Potential for Antifungal Drug Delivery to Human Pathogenic Fungus Aspergillus Fumigatus.

The ubiquitous mold Aspergillus fumigatus (A. fumigatus) is one of the main fungal pathogens causing invasive infections in immunocompromised humans. Conventional antifungal agents exhibit limited efficacy and often cause severe side effects. Nanoparticle-based antifungal delivery provides a promising alternative, which can increase local drug concentration; while, mitigating toxicity, thereby enhancing treatment efficacy. Previous research underscores the potential of poly(glycidol)-based nanogels (NG) with negative surface charge as carriers for delivering antifungals to A. fumigatus hyphae. In this study, NG is tailored with 2-carboxyethyl acrylate (CEA) or with phosphoric acid 2-hydroxyethyl acrylate (PHA). It is discovered that quenching with PHA clearly improves the adhesion of NG to hyphal surface and the internalization of NG into the hyphae under protein-rich conditions, surpassing the outcomes of non-quenched and CEA-quenched NG. This enhancement cannot be solely attributed to an increase in negative surface charge but appears to be contingent on the functional group of the quencher. Further, it is demonstrated that itraconazole-loaded, PHA-functionalized nanogels (NGxPHA-ITZ) show lower MIC in vitro and superior therapeutic effect in vivo against A. fumigatus compared to pure itraconazole. This confirms NGxPHA as a promising antifungal delivery system.

A comparison of the exposure system of glycidol-related chemicals on the formation of glycidol-hemoglobin adducts.

Glycidol fatty acid esters that are present in foods are degraded in vivo to the animal carcinogen glycidol, which binds to the N-terminal valine of hemoglobin (Hb) to form N-(2,3-dihydroxypropyl)valine (diHOPrVal) adducts. The existence of other chemicals that are converted to glycidol is unknown. To determine the effect of different exposure conditions on the formation of diHOPrVal adducts, several glycidol-related chemicals (3-monochloropropane-1,2-diol; 3-MCPD, epichlorohydrin, glyceraldehyde, acrylic acid, and 1,2-propanediol) were evaluated using in vitro and in vivo (single/repeated dose) methods. In vitro, the reaction of 3-MCPD or epichlorohydrin with human Hb produced 17% and 0.7% of diHOPrVal, as compared to equimolar glycidol, respectively. Following a single administration of glycidol-related compounds to ICR mice, diHOPrVal formation was observed only in the epichlorohydrin-treated group after day 5 of exposure. After 14 days of repeated dosing, the amounts of diHOPrVal produced by epichlorohydrin and 3-MCPD in vivo were <1% of diHOPrVal produced by an equal molar concentration of glycidol. Furthermore, glyceraldehyde group produced 0.2% of diHOPrVal at the same molar concentration of glycidol equivalents, in which diHOPrVal formation could not be confirmed by the in vitro assay. The results indicate the usefulness of diHOPrVal as an exposure marker for glycidol; however, the contribution of its formation in vivo by exposure to various chemicals will be necessary to validate and interpret the results.

Novel approach for enhancing skin allograft survival by bioadhesive nanoparticles loaded with rapamycin.

Skin graft rejection is a significant challenge in skin allografts for skin defects, particularly in extensive burn injury patients when autografts are insufficient. Enhancing the survival duration of allogeneic skin grafts can improve the success rate of subsequent autologous skin grafting, thereby promoting the therapeutic efficacy for wound healing. Rapamycin (Rapa), a potent immunosuppressant with favorable efficacy in organ transplantation, is limited by its systemic administration-associated toxicity and side effects. Therefore, addressing the short survival time of allogeneic skin grafts and minimizing the toxicity related to systemic application of immunosuppressive agents is an urgent requirement. Here, we present a topical formulation based on bioadhesive poly (lactic acid)-hyperbranched polyglycerol nanoparticles (BNPs) with surface-modified encapsulation of Rapamycin (Rapa/BNPs), applied for local immunosuppression in a murine model of allogeneic skin grafts. Our Rapa/BNPs significantly prolong nanoparticle retention, reduce infiltration of T lymphocytes and macrophages, decrease the level of pro-inflammatory cytokines and ultimately extend skin allograft survival with little systemic toxicity compared to free Rapa or Rapamycin-loaded non-bioadhesive nanoparticles (Rapa/NNPs) administration. In conclusion, Rapa/BNPs effectively deliver local immunosuppression and demonstrate potential for enhancing skin allograft survival while minimizing localized inflammation, thus potentially increasing patient survival rates for various types of skin defects.

Determination of chemical constituent yields in e-cigarette aerosol using partial and whole pod collections, a comparative analysis.

Literature reports the chemical constituent yields of electronic nicotine delivery systems (ENDS) aerosol collected using a range of aerosol collection strategies. The number of puffs to deplete an ENDS product varies widely, but collections often consist of data from the first 50-100 puffs. However, it is not clear whether these discrete puff blocks are representative of constituent yields over the life of a pod. We aimed to assess the effect of differing aerosol collection strategies on reported yields for select chemical constituents in the aerosol of closed pod-based ENDS products. Constituents analyzed were chosen to reflect important classes of compounds from the Final Premarket Tobacco Product Application Guidance. Yields were normalized to total device mass loss (DML). Collection strategies that consisted of partial pod collection were valid for determining yields of constituents whose DML normalized yields were consistent for the duration of pod life. These included primary aerosol constituents, such as propylene glycol, glycerol, and nicotine, and whole pod yields could be determined from initial puff blocks. However, changes were observed in the yields of some metals, some carbonyl compounds, and glycidol over pod life in a chemical constituent and product dependent manner. These results suggest that collection strategies consisting of initial puff block collections require validation per chemical constituent/product and are not appropriate for chemical constituents with variable yields over pod life. Whole pod collection increased sensitivity and accuracy in determining metal, carbonyl, and glycidol yields compared to puff block-based collection methodologies for all products tested.

Food processing contaminants: Dietary exposure to 3-MCPD and glycidol and associated burden of disease for Italian consumers.

In this study we assessed Italian consumers' dietary exposure to 3-MCPD and glycidol followed by risk characterization, potential cancer risk and the associated burden of disease. Consumption data was retrieved from the most recent Italian Food Consumption Survey (2017-2020), while contamination data was obtained from the European Food Safety Authority. The level of risk due to exposure to 3-MCPD was negligible, below the tolerable daily intake (TDI), except for high consumption of infant formulas. For infants, the intake level was higher than the TDI (139-141% of TDI), indicating a potential health risk. Exposure to glycidol indicated a health concern for infants, toddlers, other children, and adolescents consuming infant formulas, plain cakes, chocolate spreads, processed cereals, biscuits, rusks, and cookies (margin of exposure (MOE) < 25,000). The risk of cancer due to exposure to glycidol was estimated and the overall health impact was quantified in Disability-Adjusted Life Years (DALYs). The risk of cancer due to chronic dietary exposure to glycidol was estimated at 0.08-0.52 cancer cases/year/100,000 individuals depending on the life stage and dietary habits in Italy. The burden of disease quantified in DALYs varied from 0.7 to 5.37 DALYs/year/100,000 individuals. It is crucial to continuously gather consumption and occurrence data for glycidol over time to track patterns, assess potential health risks, identify exposure sources, and develop effective countermeasures, as long-term exposure to chemical contaminants can lead to an increased risk for human health. This data is critical for protecting public health and reducing the likelihood of cancer and other health issues related to glycidol exposure.

Potential Role of Lipase Activity on the Internal Exposure Assessment of Glycidol Released from Its Fatty Acid Esters.

Glycidyl fatty acid esters (GEs) can be found in food, and they can be converted into genotoxic animal carcinogen glycidol in vivo by the action of lipase. This study examined whether human ingestion of charbroiled pork containing high levels of GEs (300 µg/day) increased glycidol-hemoglobin adduct (diHOPrVal), a marker of internal exposure to glycidol using LC-MS/MS. Contrary to expectation, the diHOPrVal value before ingesting charbroiled pork was 3.11 ± 1.10 pmol/g globin, which slightly decreased to 2.48 ± 0.47 pmol/g globin after 5 days of consumption. The decrease in lipase activity caused by the continuous consumption of lipid-rich foods such as meat in humans might decrease internal exposure to glycidol released from its esters. Thus, lipase activity was measured in C57/BL6J mice fed a high-fat diet (HFD) for 8 weeks, and diHOPrVal formation was measured after the administration of glycidyl oleate. Lipase activity was significantly lower in the HFD group than in the normal diet group. The amount of diHOPrVal was reduced in the HFD group. Therefore, the lipase activity was reduced by HFD, thereby decreasing the degradation of glycidol from glycidyl oleate. These results indicate that changes in lipase activity depending on the amount of lipids in the diet may affect the assessment of GEs exposure, and monitoring the lipase activity would provide a comprehensive understanding of exposure assessment.

Preparation and Boron Removal Performance of Glycidol Modified PANI Nanorods: An Optimization Study Based on Response Surface Methodology.

Boron removal from aqueous solutions has attracted increasing attention, offering benefits for animal and plant health as well as profound significance for exploiting Salt Lake boron resources. In this work, we synthesized novel glycidol-functionalized and hydrophilic polyaniline (PANI) nanorod adsorbents, which were prepared to separate boron compounds from boric acid aqueous solutions. The as-prepared adsorbents were significantly different from the traditional polymers' grafting reaction because they had a higher functional yield and more active position for adsorption. The maximum adsorption capacity (0.2210 mmoL∙g-1) and optimal adsorption conditions (boric acid concentration of 1307 mg/L, pH = 9.82, time of 10 h) were obtained with single-factor experimentation and the response surface method (RSM). In addition, adsorption kinetics studies showed that the adsorption reaction belonged to the pseudo-first-order kinetic model, and diffusion was the key limiting factor; therefore, the adsorption equilibrium time is more than 10 h. Finally, the related possible adsorption mechanism was investigated based on the species and the diffusion of boron in the aqueous phase.

Apigenin and its octoic acid diester attenuated glycidol-induced autophagic-dependent apoptosis via inhibiting the ERK/JNK/p38 signaling pathways in human umbilical vein endothelial cells (HUVECs).

Glycidol is a well-known food contaminant mainly formed in refined edible oils and various thermally processed foods. Here, we studied the toxicity effects and related mechanism of glycidol on Human umbilical vein endothelial cells (HUVECs). Glycidol was found to induce Gap period 2 (G2)/Mitosis (M) phase cell cycle arrest, apoptosis, and autophagy in HUVECs. Inhibition of autophagy by 3-methyladenine (3-MA) attenuated glycidol-induced cell death, suggesting that glycidol-induced apoptosis was autophagy-dependent. Moreover, glycidol treatment induced phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal protein kinase (JNK), and p38. Inhibition of ERK, JNK, and p38 phosphorylation by the inhibitors U0126, SP600125, and SB203580 attenuated glycidol-induced autophagy and prevented glycidol-mediated reduction in cell viability, demonstrating that glycidol inhibited HUVECs growth by inducing autophagic-dependent apoptosis through activation of the ERK, JNK and p38 signaling pathways. In addition, apigenin (API) and its octoic acid diester apigenin-7 (API-C8), 4'-O-dioctanoate were found to significantly attenuate glycidol-induced cell growth inhibition by inhibiting the above signaling pathways. Collectively, glycidol induces autophagic-dependent apoptosis via activating the ERK/JNK/p38 signaling pathways in HUVECs and API-C8 could attenuate the toxicity effects.

Occurrence of glycidyl esters in infant formula products on the Canadian market between 2015 and 2019.

Glycidyl fatty acid esters (GEs) are processing contaminants formed during refining steps of vegetable oils. 'In vivo' hydrolysis of GEs releases potentially carcinogenic and genotoxic glycidol (2,3-epoxy-1-propanol). Occurrence of GEs in vegetable oils used for infant formula manufacturing may pose a potential health concern for formula-fed infants. Refined oils are commonly used as the main fat ingredient in formula manufacturing. For this study, different infant formula products (powders, concentrates and ready-to-feed formula products) were purchased and analysed in 2015 (35 samples) and 2019 (33 samples). Seven individual GEs were analysed by LC-MS/MS via direct approach by stable isotope dilution analysis, and total bound glycidol concentrations were calculated. Concentrations of bound glycidol in reconstituted formula reached maxima of 40.3 ng/g in the 2015 samples and 31.5 ng/g in the samples collected in 2019, with respective means of 8.7 ng/g and 6.7 ng/g. The analysed bound glycidol concentrations are comparable with concentration ranges from other studies, but are higher than observed in studies from the European market. Temporal trend data show a reduction of bound glycidol concentrations in 2019. GE concentrations were compared across different manufacturers.

Development of physiologically based toxicokinetic models for 3-monochloropropane-1,2-diol and glycidol.

3-Monochloropropane-1,2-diol (3-MCPD), glycidol, together with their fatty acid esters are commonly presented in various food and have shown carcinogenicity in various laboratory animals. Public health risk assessment of 3-MPCD and glycidol exposure relies on quantitative tools that represent their in vivo toxicokinetics. In order to better understand the absorption, distribution, metabolism, and excretion profiles of 3-MCPD and glycidol in male rats, a physiologically based pharmacokinetic (PBTK) model was developed. The model's predictive power was evaluated by comparing in silico simulations to in vivo time course data obtained from experimental studies. Results indicate that our PBTK model successfully captured the toxicokinetics of both free chemicals in key organs, and their metabolites in accessible biological fluids. With the validated PBTK model, we then gave an animal-free example on how to extrapolate the toxicological knowledge acquired from a single gavage to a realistic dietary intake scenario. Three biomarkers, free compound in serum, urinary metabolite DHPMA, and glycidol-hemoglobin adduct (diHOPrVal) were selected for in silico simulation following constant dietary intakes, and their internal levels were correlated with proposed external daily exposure via reverse dosimetry approaches. Taken together, our model provides a computational approach for extrapolating animal toxicokinetic experiments to biomonitoring measurement and risk assessment.

An Approach to Flavor Chemical Thermal Degradation Analysis.

Toxicological evaluations of flavor chemicals for use in inhalation products that utilize heat for aerosol generation are complicated because of the potential effect heat may have on the flavor chemical. The objective was to develop a thermal degradation technique to screen flavor chemicals as part of a toxicological testing program for their potential use in ENDS formulations. Based upon published data for acetaldehyde, acrolein, and glycidol from ENDS products (common thermal degradants of propylene glycol and glycerin), the pyrolizer temperature was adjusted until a similar ratio of acetaldehyde, acrolein, and glycidol was obtained from a 60/40 ratio (v/v) of glycerin/propylene glycol via GC/MS analysis. For each of 90 flavor chemicals, quantitative measurements of acetaldehyde, acrolein, and glycidol, in addition to semiquantitative non-targeted analysis tentatively identifying chemicals from thermal degradation, were obtained. Twenty flavor chemicals transferred at greater than 99% intact, another 26 transferred at greater than 95% intact, and another 15 flavor chemicals transferred at greater than 90% intact. Most flavor chemicals resulted in fewer than 10-12 tentatively identified thermal degradants. The practical approach to the thermal degradation of flavor chemicals provided useful information as part of the toxicological evaluation of flavor chemicals for potential use in ENDS formulations.

Polyglycerols as Multi-Functional Platforms: Synthesis and Biomedical Applications.

The remarkable and unique characteristics of polyglycerols (PG) have made them an attractive candidate for many applications in the biomedical and pharmaceutical fields. The presence of multiple hydroxy groups on the flexible polyether backbone not only enables the further modification of the PG structure but also makes the polymer highly water-soluble and results in excellent biocompatibility. In this review, the polymerization routes leading to PG with different architectures are discussed. Moreover, we discuss the role of these polymers in different biomedical applications such as drug delivery systems, protein conjugation, and surface modification.

Chemical refining methods effectively mitigate 2-MCPD esters, 3-MCPD esters, and glycidyl esters formation in refined vegetable oils.

Esters of 3-monochloro-1,2-propanediol (3-MCPDE), 2-monochloro-1,3-propanediol (2-MCPDE), and glycidyl esters (GE) are processing contaminants that can be found in refined edible fats and oils. Recently, the European Commission has implemented maximum limits for the presence of free and bound 3-MCPDE in vegetable fats and oils and in marine and fish oils. This boosted the necessity of oil producers to develop refining methods to limit the concentration of both 3-MCPDE and GE in their final products. Physical refining may lack the potential to mitigate the formation of 2- and 3-MCPDE. Therefore, in this study, the chemical refining method were explored to provide a viable mitigation strategy aimed at industrial application. Several pilot plant treatments with organic palm oil were performed. The investigated refining methods included a neutralization, a water washing process, reduced deodorization temperature, and a combination of them. The best performing chemical refining treatment achieved a final concentration of 0.42 (-49%), 0.78 (-52%), and 0.99 (-73%) mg/kg for 2-MCPDE, 3-MCPDE, and GE in organic palm oil, respectively. Results thus showed chemical refining has great potential for the simultaneous mitigation of 2-, 3-MCPDE, and GE.

Urinary non-targeted toxicokinetics and metabolic fingerprinting of exposure to 3-monochloropropane-1,2-diol and glycidol from refined edible oils.

The widespread presence of 3-monochloropropane-1,2-diol (3-MCPD) and glycidol in refined edible oils have raised food industrial and public health concerns, but their specific biomarkers of exposure and urinary metabolic pathways indicating nephrotoxicity remain largely unknown. Here, we unraveled the in vivo biotransformation of these two contaminants and revealed how they affect metabolic pathways in rats. Urine metabolomes in rats administered with glycidol or 3-MCPD were investigated using ultra-high performance liquid chromatography combined with a quadrupole-orbitrap high-resolution mass spectrometry. Compared to the currently acknowledged metabolite which is only 2,3-dihydroxypropyl mercapturic acid, we identified 8 and 4 new specific exposure biomarkers of glycidol and 3-MCPD, respectively, via mapping the glyceryl polymerization and glutathione and sulfur conjugation. The changes of metabolites in the surrounding metabolic network were investigated to further gain insight into their metabolic fates. Exposure to glycidol up-regulated citrate, isocitrate, ketoglutarate, malate, and pyruvate in the tricarboxylic acid cycle and glycolysis pathways, while 3-MCPD intake down-regulated these signal molecules in both pathways. Nonetheless, L-cysteine, proline, and arginine were significantly decreased by the effect of either glycidol or 3-MCPD. Our findings first map the urinary metabolomics of both contaminants from edible oils and advance the omics-level recognition for their observational health hazards.

Associations of 3-monochloropropane-1,2-diol and glycidol with prevalence of metabolic syndrome: Findings from Lanxi Nutrition and Safety Study.

In this study, we investigated the association of 2,3-dihydroxypropyl mercapturic acid (DHPMA), a urinary biomarker of environmental and dietary exposure to 3-monochloropropane-1,2-diol and glycidol, with prevalent MetS in a Chinese middle-aged and elderly population. The urinary DHPMA concentrations were determined by ultra-high performance liquid chromatography tandem mass spectrometry (UHPLC-MS/MS) analysis and further calibrated by the urinary creatinine content. MetS cases were defined by the Adult Treatment Panel III criteria for Asian-Americans of National Cholesterol Education Program (NCEP/ATPIII). Multivariate-adjusted modified Poisson regression models were used to analyze the associations between the urinary DHPMA concentrations and MetS prevalence. Of the 1613 participants aged 45-75 years, we documented 552 (34.2%) MetS cases. After adjustment for potential risk factors, the relative risks (95% confidence intervals) of MetS prevalence across the increasing quartiles of DHPMA concentrations were 1.14 (0.93-1.39), 1.29 (1.06-1.56), and 1.50 (1.25-1.80), respectively, compared with the lowest quartile. We also observed strong positive association between urinary DHPMA concentrations and hypertriglyceridemia prevalence (P < 0.001 for trend). These positive associations remained unchanged in the subgroups stratified by general demographic, dietary and behavioral risk factors. These results suggested that urinary DHPMA was associated with higher prevalence of MetS among Chinese elderly people.

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.