Occurrence and risk assessment of glycidyl and 3-monochloropropanediol esters in infant formulas marketed in Taiwan.

Glycidyl esters (GEs) and 3-monochloropropanediol esters (3-MCPDEs) are process contaminants commonly found in refined edible oils which are often added to infant formulas. The Taiwan Food and Drug Administration (TFDA) launched regulations for GEs in infant formulas that went into effect on 1 July 2021. To investigate levels of GEs and 3-MCPDEs in infant formula powder, 45 products were sampled and analysed during 2020-2021. The contents of GEs and 3-MCPDEs in formulas of different brands significantly varied, but their concentrations in all of the formulas complied with European Union (EU) regulations. Infant formulas containing palm oil had significantly higher 3-MCPDE levels in both extracted oils and milk powder than those without palm oil. Concentrations of GEs and 3-MCPDEs in infant formula powder and extracted oils were significantly lower in products from Europe than those from Australia and New Zealand. Infants aged 0-1 years in Taiwan who consumed only infant formula showed a margin of exposure (MoE) exceeding 25,000. Mean consumer exposures to 3-MCPDEs stayed below the tolerable daily intake (TDI), while high exposures at the 95th percentile (P95) exceeded the TDI by 1.7-fold. Herein, we present the changing trends in the risk assessment results of infant formula across various countries in the decade. Implementation of regulations and mitigation strategy effectively reduced the risk of infants being exposed to GEs and 3-MCPDEs through infant formula.

Ginsenoside Rb1 alleviates 3-MCPD-induced renal cell pyroptosis by activating mitophagy.

Ginsenoside Rb1 (Gs-Rb1) is among the most significant effective pharmacological components in ginseng. 3-monochloropropane-1,2-diol (3-MCPD), a chloropropanol-like contaminant, is produced in the production of refined oils and thermal processing of food. Pyroptosis is a type of programmed cell death triggered by inflammasomes. Excessive pyroptosis causes kidney injury and inflammation. Previous studies have revealed that 3-MCPD induced pyroptosis in mice and NRK-52E cells. In the present study, we find that Gs-Rb1 attenuates 3-MCPD-induced renal cell pyroptosis by assaying GSDMD-N, caspase-1, IL-18, and IL-1ß in mice and NRK-52E cells. In further mechanistic studies, we show that Gs-Rb1 removes damaged mitochondria via mitophagy and reduces intracellular reactive oxygen species (ROS) generation, therefore alleviating 3-MCPD-induced NOD-like receptor family pyrin domain containing 3 (NLRP3) activation and pyroptosis. The above results are further validated by the addition of autophagy inhibitor Chloroquine (CQ) and mitophagy inhibitor Cyclosporin A (CsA). Afterward, we explore how Gs-Rb1 activated mitophagy in vitro. We determine that Gs-Rb1 enhances the protein expression and nuclear translocation of Transcription factor EB (TFEB). However, silencing of the TFEB gene by small interfering RNA technology reverses the role of Gs-Rb1 in activating mitophagy. Therefore, we conclude that 3-MCPD damages mitochondria and leads to ROS accumulation, which causes NLRP3 activation and pyroptosis in ICR mice and NRK-52E cells, while Gs-Rb1 mitigates this phenomenon via the TFEB-mitophagy pathway. Our findings may provide new insights for understanding the molecular mechanisms by which Gs-Rb1 mitigates renal injury.

3-Monochloropropane-1,2-diol esters induce HepG2 cells necroptosis via CTSB/TFAM/ROS pathway.

3-monochloropropane-1,2-diol esters (3-MCPDE) are toxic substances that form in food thermal processing and have a diverse range of toxicities. In this study, we found that 3-MCPDE triggered necroptosis by RIPK1/RIPK3/MLKL pathway in HepG2 cells. Previous studies have shown that ROS is an important activator of RIPK1 and RIPK3. The data showed that 3-MCPDE induced excessive ROS production through mitochondrial damage. After treatment with ROS inhibitor N-acetylcysteine (NAC), 3-MCPDE-induced necroptosis was relieved. Further, we explored how 3-MCPDE destroys mitochondria. The data suggested that 3-MCPDE induced mitochondrial dysfunction through the CTSB/TFAM pathway. Overall, the results indicated that 3-MCPDE induced necroptosis through CTSB/TFAM/ROS pathway in HepG2 cells. Our study provided a new mechanism for 3-MCPDE hepatotoxicity.

Alleviating 3-MCPD-induced male reproductive toxicity: Mechanistic insights and resveratrol intervention.

3-Monochloropropane-1, 2-diol (3-MCPD), a food-borne contaminant, is widely regarded as the primary cause of male infertility. At present, identifying a method to improve/reduce the male reproductive toxicity caused by 3-MCPD is important. In our study, we explored the potential application of resveratrol (RSV) in mitigating the adverse effects of 3-MCPD. Using 7-week-old Sprague-Dawley (SD) rats as animal models, we investigated the impacts and underlying mechanisms of 3-MCPD and RSV on reproductive function. The administration of 3-MCPD led to significant reductions in testicular and epididymal weights, as well as disruptions in spermatogenesis and histological abnormalities. However, co-treatment with RSV and 3-MCPD mitigated these adverse effects. In vitro study, RSV exhibited the ability to reverse the decline in Leydig and Sertoli cell populations inflicted by 3-MCPD treatment. Mechanistically, RSV reduced endoplasmic reticulum stress (PARP), inflammasome activation (NLRP3), and autophagy-mediated lysosome dysfunction (p62 and LC3BII) induced by 3-MCPD. In addition, 3-MCPD treatment increased the expression level of steroidogenesis-related proteins, steroidogenic acute regulatory (StAR) and CYP11A1, but RSV normalized StAR expression. Moreover, 3-MCPD-induced pro-inflammatory responses were counteracted by RSV treatment, with the cytokine reduction and modulation of CD206 expression, a marker of macrophage activation. These findings indicate that RSV attenuates 3-MCPD-induced reproductive toxicity, highlighting its application potential as an adjuvant agent for male reproductive health.

A simple fluorescence pyrocatechol-polyethyleneimine detection method for 3-MCPD.

A rapid fluorescence detection method was established for 3-monochloropropane-1,2-diol (3-MCPD). The detection system works based on the fluorescence quenching of pyrocatechol-polyethyleneimine (PCh-PEI) polymer by 3-MCPD. The fluorescence quenching ability of 3-MCPD for PCh-PEI polymer was measured at different pH and temperatures. Indeed, in the presence of 3-MCPD, the fluorescence intensity of PCh-PEI polymer solution was quenched best at 100 °C and pH 8.5. Also, the effect of different concentrations of 3-MCPD on the optical properties of the PCh-PEI polymer was examined. Under optimal experimental conditions, fluorescence detection was linear in a range of 0.08-2.0 mg per L 3-MCPD, with a calculated detection limit of 0.06 mg L-1 and a correlation coefficient of 0.9974. Concisely, the reported method has good sensitivity and can be used for the rapid detection of 3-MCPD contamination in food products.

Optimization of water washing for mitigation of 3-monochloropropane 1,2 diol ester in palm oil physical refining process.

The presence of 3-monochloropropane-1,2 diol ester (3-MCPDE) and glycidyl ester (GE) in processed palm oils is of concern, as these oils are widely used for edible purposes. The mitigation method studied here optimizes the removal of chloride through water washing of crude palm oil (CPO), to limit the formation of 3-MCPDE. The contaminant removal obtained via washing CPO supports the quantitative findings. By utilizing 5% water in the washing step, water-soluble chlorides in CPO are removed by up to 76%, resulting in a 71% reduction of 3-MCPDE to within statutory limits. In this study, a linear correlation was developed between the chloride and the corresponding 3-MCPDE with a correlation coefficient (R2) of 0.99. Using the correlations, 1.0 mg/kg of 3-MCPDE in refined, bleached and deodorized palm oil (RBDPO) will be obtained from CPO with 1.2 mg/kg chloride with 7% wash water usage. The study also showed minor GE reduction between 7 and 11% was attained after water washing.

Rapid Sample Enrichment, Novel Derivatization, and High Sensitivity for Determination of 3-Chloropropane-1,2-diol in Soy Sauce via High-Performance Liquid Chromatography-Tandem Mass Spectrometry.

A novel, simplified derivatization method and a rapid sample preparation process using carbon yarn as a sorbent for the determination of 3-chloropropane-1,2-diol (3-MCPD) in soy sauce via high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) was developed. 3-MCPD was first enriched and purified with carbon yarn and then eluted with a methanol-water solution. Subsequently, the analyte underwent derivatization with p-(dimethylamino)-phenol for sensitive detection via HPLC-MS/MS. The limit of detection and the limit of quantitation for 3-MCPD were validated to be 0.5 and 1.0 µg/kg, respectively. Spiking experiments showed recoveries between 83 and 94%, with a relative standard deviation of ≤10%. The method was further validated with a certified reference material. Furthermore, 11 real soy sauce samples from local markets were tested by using this method. These results reveal the widespread 3-MCPD contamination. Consequently, this study offers a preferable alternative for the sensitive, accurate, and precise determination of 3-MCPD in soy sauce.

3-MCPD Induced Mitochondrial Damage of Renal Cells Via the Rhythmic Protein BMAL1 Targeting SIRT3/SOD2.

Biorhythm regulates a variety of physiological functions and enables organisms to adapt to changing environments. 3-Monochloro-1,2-propanediol (3-MCPD) is a common food thermal processing contaminant, and the kidney is its toxic target organ. However, the nephrotoxicity mechanism of 3-MCPD has not been fully elucidated. In the study, we found that 3-MCPD caused mitochondrial damage in renal cells by inhibiting the SIRT3/SOD2 pathway. Further, we found that 3-MCPD could interfere with rhythm protein BMAL1 expression at protein and mRNA levels in mice kidney and NRK-52E cells. Simultaneously, the balance of the daily oscillation of SIRT3/SOD2 pathway proteins was impeded under 3-MCPD treatment. To determine the role of BAML1 in mitochondrial damage, we overexpressed the BMAL1 protein. The data showed that BMAL1 overexpression upregulated SIRT3 and SOD2 expression and attenuated mitochondrial damage caused by 3-MCPD. These results indicated that 3-MCPD inhibited the SIRT3/SOD2 pathway by affecting the expression of the rhythm protein BMAL1, thereby inducing mitochondrial damage in renal cells. Taken together, our work reveals that 3-MCPD may possess a toxic effect via circadian clock mechanisms.

Determination of process contaminants 2- and 3-MCPD esters and glycidyl esters in palm-based glycerol by indirect analysis using GC-MS.

Esters of 2- and 3-monochloropropanediol (2-MCPDE, 3-MCPDE) and glycidol (GE) are regarded as process contaminants that are found in refined vegetable oils and oil-based foods. Since glycerol is produced during fat splitting, saponification and biodiesel production, it is important to have methods for determining contaminants that might be formed during these processes. Due to the use of glycerol as a food additive, data on the presence of compounds of toxicological concern, including 3-MCPD, are of interest. This study focuses on modifying the indirect analysis of 2-MCPDE, 3-MCPDE and GE using GC-MS based on the AOCS Official Method Cd 29a-13, validating the modified method, and quantifying 2-MCPDE, 3-MCPDE and GE in glycerol. The AOCS Cd 29a-13 method was modified at the initial stage of sample preparation in which the targeted esters were extracted from glycerol by vortex-assisted extraction before sample analysis. This modification was performed based on the polarity of all compounds involved. The calibration functions for all analytes were fitted to linear regression with R2 above 0.99. Limits of detection (LOD) 0.02, 0.01 and 0.02 mg kg-1 were obtained for 2-MCPDE, 3-MCPDE and GE, respectively. Spiked glycerol with 3-MCPDE and 2-MCPDE (0.25, 0.51 and 1.01 mg kg-1) and GE (0.58, 1.16 and 2.32 mg kg-1) were used for recovery and precision measurements. Recoveries of 100-108%, 101-103%, and 93-99% were obtained for 2-MCPDE, 3-MCPDE and GE, respectively. Acceptable precision levels with relative standard deviations ranged from 3.3% to 8.3% were obtained for repeatability and intermediate precision. The validated method was successfully applied for the analysis of the target compounds in refined glycerol from commercial plants, which showed that 2-MCPDE, 3-MCPDE and GE levels in the analysed samples were below the detection limit.

3-Monochloropropane-1,2-diol reduced bioaccessibility of sn-2 palmitate via binding with pancreatic lipase in infant formula during gastrointestinal digestion.

Infant formula contains 3-monochloropropane-1,2-diol esters (3-MCPDE), which are formed during the deodorization step of vegetable oil refining. The European Food Safety Authority stated that 3-MCPDE can be hydrolyzed in the gastrointestinal tract to free-form 3-monochloropropane-1,2-diol (3-MCPD), which has potential toxicity and can be rapidly absorbed. Evaluating the effect of 3-MCPD on nutrition absorption is a prerequisite for establishing effective management strategies. A total of 66 crucial lipid molecules associated with 3-MCPD were identified based on debiased sparse partial correlation analysis. 3-MCPD affected triglyceride hydrolyzation and increased the concentration of undigested sn-2 palmitate (9.57 to 17.06 mg kg-1). 3-Monochloropropane-1,2-diol reduced the bioaccessibility of fatty acids, and more short- (31.42 to 58.02 mg kg-1) and medium-chain fatty acids (17.03 to 26.43 mg kg-1) remained unabsorbed. Lipidomic profiles of infant formula models spiked with different 3-MCPDE levels were investigated, and the results were consistent with the experiments with the commercial formula indicating lipid alteration was mainly affected by the digestive 3-MCPD. The formation of 3-MCPD ester-pancreatic lipase with the binding energy of -4.9 kcal mol-1 was more stable than triglyceride-pancreatic lipase (-4.0 kcal mol-1), affecting triglyceride hydrolyzation. 3-Monochloropropane-1,2-diol was bound to Glu13 and Asp331 residues of the pancreatic lipase via hydrogen bonds, which resulted in a conformational change of pancreatic lipase and spatial shielding effect. The existence of the spatial-shielding effect reduced the accessibility of pancreatic lipase and further affected triglyceride hydrolyzation. These findings indicated that 3-MCPD obstructed nutrient acquisition and laid the foundation for the subsequent nutrition enhancement design.

Simultaneous mitigation of 3-monochloropropane 1,2 diol ester and glycidyl ester in edible oils: a review.

The rising concern about the presence of 3-monochloropropane 1,2 diol ester (3-MCPDE) and glycidyl ester (GE) in food has prompted much research to be conducted. Some process modifications and the use of specific chemicals have been employed to mitigate both 3-MCPDE and GE. Alkalisation using NaOH, KOH, alkali metals or alkaline earth metals and post sparging with steam or ethanol and short path distillation have shown simultaneous mitigation of 51-91% in 3-MCPDE and of 13-99% in GE, both contaminants achieved below 1000 µg/kg. Some of the mitigation methods have resulted in undesirable deterioration in other parameters of the refined oil. When the processed oil is used in food processing, it results in changes to 3-MCPDE and GE. Repeated deep frying above 170 °C in the presence of NaCl and baking at 200 °C with flavouring (dried garlic and onion), resulted in increased 3-MCPDE. Repeated frying in the presence of antioxidants (TBHQ, rosemary and phenolics) decreased 3-MCPDE in processed food. The GE content in foods tends to decline with time, indicating instability of GE's epoxide ring.

The occurrence and probabilistic risk assessment of 3-MCPDEs and GEs in infant formulas from Chinese market employing Monte Carlo simulation technique.

3-monochloropropane-1,2-diol esters (3-MCPDEs) and glycidyl esters (GEs) are food contaminants and have arisen continuous attention due to their toxicity, especially towards infants. Current risk assessment of these contaminants was mostly employing deterministic approaches, lacking quantitative characterization of the likelihood, incidence, or severity of the risks involved. Herein, 3-MCPDE and GE levels in 46 representative infant formulas (IFs) from Chinese market were determined by GC-MS/MS. Then, combining the occurrence data and consumption data from China National Food Consumption Survey, the Monte Carlo simulation-based probabilistic model for risk assessment of 3-MCPDEs and GEs in IFs from Chinese market was established. The results showed that all P90 (90th percentiles) hazard quotient values were below 1, demonstrating 3-MCPDEs didn't pose health risks to most populations aged 0-36 months old. However, for 0-12 months old groups, P10 (10th percentiles) margin of exposure values were all below 25000, indicating GEs may pose potential risks to 10% of this group. Uncertainty analysis revealed that the probabilistic model had considered uncertainties of model input and distribution, and realized refined assessment. This study is the first report on probabilistic assessment of 3-MCPDEs and GEs in IFs, which also provided references for the formulation of related regulatory limits in China.

Mitigation of 3-monochloropropane 1,2 diol ester and glycidyl ester in refined oil - A review.

The 3-Monochloropropane-1, 2-diol ester (3-MCPDE) and glycidyl ester (GE) are formed at high processing temperatures with the presence of respective precursors. Both are potentially harmful to humans, causing adverse health impacts including kidney damage, reproductive problems, and increased risk of cancer. The presence of 3-MCPDE and GE in palm oil is of particular concern because of its widespread use by the food industry. There are a variety of methods for reducing 3-MCPDE and GE. For example, water washing eliminates mostly inorganic chlorides that, in turn, reduce the formation of 3-MCPDE. 3-MCPDE has also been reduced by up to 99% using combinations of methods and replacing stripping steam with alcohol-based media. Activated carbon, clay, antioxidants, potassium-based salts, and other post-refining steps have positively lowered GE, ranging from 10 to 99%. Several approaches have been successful in reducing these process contaminants without affecting other quality metrics.

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.

3-Chloropropane-1,2-diol exposure adversely influenced the bio-accessibility signatures of digested infant foods by suppressing the destabilization of α-lactalbumin and d-aspartate oxidase in a dose-dependent manner.

The potential mechanisms about the health risks of endogenous 3-MCPD remain elusive. Here, we researched the influences of 3-MCPD on the metabolic landscape of digested goat infant formulas via integrative UHPLC-Q-Orbitrap HRMS-MS/MS-based peptidomics and metabolomics (%RSDs ≤ 7.35 %, LOQ 2.99-58.77 µg kg-1). Digested goat infant formulas under 3-MCPD-interference caused metabolic perturbation by down-regulating levels of peptides VGINYWLAHK (5.98-0.72 mg kg-1) and HLMCLSWQ (3.25-0.72 mg kg-1) pertained to health-promoting bioactive components, and accelerated the down-regulation of non-essential amino acids (AAs, l-tyrosine 0.88-0.39 mg kg-1, glutamic acid 8.83-0.88 µg kg-1, and d-aspartic acid 2.93-0.43 µg kg-1), semi-essential AA (l-arginine 13.06-8.12 µg kg-1) and essential AAs (l-phenylalanine 0.49-0.05 mg kg-1) that provide nutritional value. Peptidomics and metabolomics interactions elucidated that 3-MCPD altered the stability of α-lactalbumin and d-aspartate oxidase in a dose-dependent manner, and affected the flavor perception of goat infant formulas, leading to a decline of nutritional value of goat infant formulas.

Identification of genes showing altered DNA methylation and gene expression in the renal proximal tubular cells of rats treated with ochratoxin A for 13 weeks.

Ochratoxin A (OTA) is a mycotoxin that causes renal carcinogenicity following the induction of karyomegaly in proximal tubular cells after repeated administration to rats. Here, we performed gene profiling regarding altered DNA methylation and gene expression in the renal tubules focusing on the mechanism of OTA-induced carcinogenesis. For this purpose, OTA or 3-chloro-1,2-propanediol (3-MCPD), a renal carcinogen not inducing karyomegaly, was administered to rats for 13 weeks, and DNA methylation array and RNA sequencing analyses were performed on proximal tubular cells. Genes for which OTA altered the methylation status and gene expression level, after excluding genes showing similar expression changes by 3-MCPD, were subjected to confirmation analysis of the transcript level by real-time reverse-transcription PCR. Gene Ontology (GO)-based functional annotation analysis of validated genes revealed a cluster of hypermethylated and downregulated genes enriched under the GO term "mitochondrion," such as those associated with metabolic reprogramming in carcinogenic process (Clpx, Mrpl54, Mrps34, and Slc25a23). GO terms enriched for hypomethylated and upregulated genes included "response to arsenic-containing substance," represented by Cdkn1a involved in cell cycle arrest, and "positive regulation of IL-17 production," represented by Osm potentiating cell proliferation promotion. Other genes that did not cluster under any GO term included Lrrc14 involved in NF-κB-mediated inflammation, Gen1 linked to DNA repair, Has1 related to chromosomal aberration, and Anxa3 involved in tumor development and progression. In conclusion, a variety of genes engaged in carcinogenic processes were obtained by epigenetic gene profiling in rat renal tubular cells specific to OTA treatment for 13 weeks.

The role of microRNAs in the toxic mechanisms of furan and 3-MCPD and links to cancer risk - a review.

Contaminants formed during food processing are of increasing concern to public and food safety experts, as well as international risk assessment organizations. The emergence of 'omic' technologies (e.g. genomics and transcriptomics) have greatly increased the mechanistic knowledge of the toxicity associated with these compounds, and consequently have provided a better understanding of their potential adverse effects. Of note, microRNAs (miRNAs) have emerged as being of key importance during the development of cancer as well as being associated with food-processing contaminants. MiRNAs have been demonstrated to trigger toxic processes in hepatic and renal tissues due to exposure to toxic compounds such as furan and 3-monochloropropane-1,2-diol (3-MCPD), respectively. In this review, we consider the roles of miRNAs in the toxicity process and the challenges that lay ahead in order to translate this knowledge to the benefit of industrial food processing.

Risk assessment of 3-MCPD esters and glycidyl esters from the formulas for infants and young children up to 36 months of age.

Esters of 2-monochloropropane-1,2-diol (2-MCPD), 3- monochloropropane-1,2-diol (3-MCPD), and glycidol are present in infant formulas, follow-on foods and similar compositions. They arise mainly from the vegetable oil content and may cause harmful effects in consumers. The contents of these substances in formulas were determined indirectly by converting the esters to the free form, followed by derivatization and analysis by gas chromatography-tandem mass spectrometry (GC-MS/MS). The validation results demonstrate that the method had sufficient specificity and adequate accuracy. The limits of detection (LOD) and limits of quantification (LOQ) for each of 2-MCPDE, 3-MCPDE, and GE were 1.5 and 5 µg/kg, respectively. Formula intake by children up to 36 months of age was surveyed, and the data was used to assess the risks due to 3-MCPD esters (3-MCPDE) and glycidyl esters (GE). The mean exposure dose of 3-MCPDE for different age groups ranged from 0.51 to 1.13 µg/kg bw per day. The corresponding mean GE exposure ranged from 0.031 to 0.069 µg/kg bw per day. Neither mean values nor the percentile 95% values of 3-MCPDE exposure doses exceed the recommended provisional maximum tolerable daily intake (PMTDI).

Determination of 3-chloro-1,2-propanediol in biological samples by quick-easy-cheap-effective-rugged-and-safe extraction coupled with gas chromatography-mass spectrometry and its biodistribution in rats.

3-Chloro-1,2-propanediol is a common food contaminant, but reports on its determination in biological tissues are lacking. In the present study, a method was developed to detect 3-chloro-1,2-propanediol contents in rat tissues by quick-easy-cheap-effective-rugged-and-safe extraction and gas chromatography-mass spectrometry analysis. Biological samples were extracted with ethyl acetate and purified with adsorbents. The optimized adsorbent for each sample was selected from 4-5 combinations of N-propylethylenediamine, octadecylsilane, graphitized carbon black, strong anion exchange, and florisil. Extracted 3-chloro-1,2-propanediol was derivatized with heptafluorobutyric anhydride and subjected to gas chromatography-mass spectrometry. This method had good linearity (correlation coefficients >0.99) in the range of 2-2000 ng/g for blood, kidney, liver, testis, and brain samples. The limits of detection were under 0.8 ng/g; the limits of quantification were 2 ng/g; the recovery rates were 85%-102%; and the matrix effects were 1.98%-7.67%. This method also had good precision. The dynamic changes in 3-chloro-1,2-propanediol in rats gavaged with 20 mg/kg b.w. for 24 h were detected using this method. The 3-chloro-1,2-propanediol content in each tissue sharply increased to a peak, rapidly decreased within 2 h, and stabilized at 12 h. 3-Chloro-1,2-propanediol persisted in the kidney, testis, and liver 24 h after gavage.

Optimization of Physical Refining Process of Camellia Oil for Reduction of 3-Monochloropropane-1,2-Diol (3-MCPD) Ester Formation Using Response Surface Methodology on a Laboratory Scale.

Refined and deodorized camellia oil has been reported to contain a high amount of 3-monochloropropane-1,2-diol esters (3-MCPDE) due to the high-temperature deodorization step. To reduce 3-MCPDE in camellia oil, the physical refining process of camellia oil was simulated on a laboratory scale. Response surface methodology (RSM) was designed to modify and optimize the refining process with five processing parameters (water degumming dosage, degumming temperature, activated clay dosage, deodorization temperature and deodorization time). The optimized new refining approach achieved a 76.9% reduction in 3-MCPDE contents, in which the degumming moisture was 2.97%, the degumming temperature was 50.5 °C, the activated clay dosage was 2.69%, the deodorizing temperature was 230 °C, and the deodorizing time was 90 min. A significance test and analysis of variance results demonstrated that the deodorization temperature and deodorization time contributed significantly to the reduction of 3-MCPD ester. The joint interaction effects of activated clay dosage and deodorization temperature were significant for 3-MCPD ester formation.