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.

Boric Acid and Borax Protect Human Lymphocytes from Oxidative Stress and Genotoxicity Induced by 3-Monochloropropane-1,2-diol.

3-chloro-1,2-propanediol (3-MCPD) is a member of the group of pollutants known as chloropropanols and is considered a genotoxic carcinogen. Due to the occurrence of 3-MCPD, which cannot be avoided in multiplexed food processes, it is necessary to explore novel agents to reduce or prevent the toxicity of 3-MCPD. Many recent studies on boron compounds reveal their superior biological roles such as antioxidant, anticancer, and antigenotoxic properties. In the current investigation, we have evaluated in vitro cytotoxic, oxidative, and genotoxic damage potential of 3-MCPD on human whole blood cultures and the alleviating effect of boric acid (BA) and borax (BX) for 72 h. In our in vitro experiments, we have treated blood cells with BA and BX (2.5, 5, and 10 mg/L) and 3-MCPD (at IC50 of 11.12 mg/l) for 72 h to determine the cytotoxic damage potential by using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and lactate dehydrogenase (LDH) release assays. Oxidative damage was assessed using total antioxidant capacity (TAC) and malondialdehyde (MDA) levels. Genotoxicity evaluations were performed using chromosome aberrations (CAs) and 8-hydroxy deoxyguanosine (8-OHdG) assays. The result of our experiments showed that the 3-MCPD compound induced cytotoxicity, oxidative stress, and genotoxicity in a clear concentration-dependent manner. BA and BX reduced cytotoxicity, oxidative stress, and genotoxicity induced by 3-MCPD. In conclusion, BA and BX are safe and non-genotoxic under the in vitro conditions and can alleviate cytotoxic, oxidative, and genetic damage induced by 3-MCPD in the human blood cells. Our findings suggest that dietary boron supplements may offer a novel strategy for mitigating hematotoxicity induced by xenobiotics, including 3-MCPD.

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.

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.

Lipidomics Analysis Explores the Mechanism of Renal Injury in Rat Induced by 3-MCPD.

3-monochloropropane-1,2-diol (3-MCPD) is a food-process toxic substance, and its main target organ is the kidney. The present study examined and characterized the nephrotoxicity and the lipidomic mechanisms in a model of kidney injury in Sprague Dawley (SD) rats treated with high (45 mg/kg) and low (30 mg/kg) doses of 3-MCPD. The results showed that the ingestion of 3-MCPD led to a dose-dependent increase in serum creatinine and urea nitrogen levels and histological renal impairment. The oxidative stress indicators (MDA, GSH, T-AOC) in the rat kidney altered in a dose-dependent manner in 3-MCPD groups. The lipidomics analysis revealed that 3-MCPD caused kidney injury by interfering with glycerophospholipid metabolism and sphingolipid metabolism. In addition, 38 lipids were screened as potential biomarkers. This study not only revealed the mechanism of 3-MCPD renal toxicity from the perspective of lipidomics but also provided a new approach to the study of 3-MCPD nephrotoxicity.

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.

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.

Association between dietary 3-monochloropropane-1,2-diol esters (3-MCPDE) and renal cancer in Peninsular Malaysia: exposure assessment and matched case-control study.

3-Monochloropropane-1,2-diol esters (3-MCPDE) are food contaminants commonly found in refined vegetable oils and fats, which have possible carcinogenic implications in humans. To investigate this clinically, we conducted an occurrence level analysis on eight categories of retail and cooked food commonly consumed in Malaysia. This was used to estimate the daily exposure level, through a questionnaire-based case-control study involving 77 subjects with renal cancer, with 80 matching controls. Adjusted Odds Ratio (AOR) was calculated using the multiple logistic regression model adjusted for confounding factors. A pooled estimate of total 3-MCPDE intake per day was compared between both groups, to assess exposure and disease outcome. Among the food categories analysed, vegetable fats and oils recorded the highest occurrence levels (mean: 1.91 ± 1.90 mg/kg), significantly more than all other food categories (p < .05). Risk estimation found the Chinese ethnic group to be five times more likely to develop renal cancer compared to Malays (AOR = 5.15, p = .001). However, an inverse association was observed as the 3-MCPDE exposure among the Malays (median: 0.162 ± 0.229 mg/day/person) were found to be significantly higher than the Chinese (p = .001). There was no significant difference (p = .405) in 3-MCPDE intake between the cases (median: 0.115 ± 0.137 mg/day/person) and controls (median: 0.105 ± 0.151 mg/day/person), with no association between high intake of 3-MCPDE and the development of renal cancer (OR = 1.41, 95% CI: 0.5091-2.5553). Thus, there was insufficient clinical evidence to suggest that this contaminant contributes to the development of renal malignancies in humans through dietary consumption. Further research is necessary to support these findings, which could have significant public health ramifications for the improvement of dietary practices and food safety measures.

Newly discovered developmental and ovarian toxicity of 3-monochloro-1,2-propanediol in Drosophila melanogaster and cyanidin-3-O-glucoside's protective effect.

3-Monochloro-1,2-propanediol (3-MCPD) is a pervasive environmental pollutant that is unintentionally produced during industrial production and food processing. Although some studies reported the carcinogenicity and male reproduction toxicity of 3-MCPD thus far, it remains unexplored whether 3-MCPD hazards to female fertility and long-term development. In this study, the model Drosophila melanogaster was employed to evaluate risk assessment of emerging environmental contaminants 3-MCPD at various levels. We found that flies on dietary exposure to 3-MCPD incurred lethality in a concentration- and time-dependent way and interfered with metamorphosis and ovarian development, resulting in developmental retardance, ovarian deformity and female fecundity disorders. Mechanistically, 3-MCPD caused redox imbalance observed as a drastically increased oxidative status in ovaries, confirmed by increased reactive oxygen species (ROS) and decreased antioxidant activities, which is probably responsible for female reproductive impairments and developmental retardance. Intriguingly, these defects can be substantially prevented by a natural antioxidant, cyanidin-3-O-glucoside (C3G), further confirming a critical role of ovarian oxidative damage in the developmental and reproductive toxicity of 3-MCPD. The present study expanded the findings that 3-MCPD acts as a developmental and female reproductive toxicant, and our work provides a theoretical basis for the exploitation of a natural antioxidant resource as a dietary antidote for the reproductive and developmental hazards of environmental toxicants that act via increasing ROS in the target organ.

Toxicology of 3-monochloropropane-1,2-diol and its esters: a narrative review.

3-Monochloropropane-1,2-diol (3-MCPD) is a chiral molecule naturally existing as a racemic mixture of (R)- and (S)-enantiomers. It was thoroughly investigated during the 1970s as a male antifertility drug until research was abandoned because of the side effects observed in toxicity studies. More than 20 years later, 3-MCPD, both in the free form and esterified to the fatty acids, was detected in vegetable oil and discovered to be a widespread contaminant in different processed foods. This review summarises the main toxicological studies on 3-MCPD and its esters. Current knowledge shows that the kidney and reproductive system are the primary targets of 3-MCPD toxicity, followed by neurological and immune systems. Despite uncertainties, in vivo studies suggest that renal and reproductive toxicity is mediated by toxic metabolites, leading to inhibition of glycolysis and energy depletion. Few acute, short-term, and subchronic toxicity studies have investigated the 3-MCPD esters. The pattern of toxicity was similar to that of free 3-MCPD. Some evidence suggests that the toxicity of 3-MCPD diesters may be milder than 3-MCPD, likely because of an incomplete enzymatic hydrolysis in the equivalent free form in the gastrointestinal tract. Further research to clarify absorption, metabolism, and long-term toxicity of 3-MCPD esters would be pivotal to improve the risk assessment of these compounds via food.

Development of a QuEChERS method for simultaneous analysis of 3-Monochloropropane-1,2-diol monoesters and Glycidyl esters in edible oils and margarine by LC-APCI-MS/MS.

A simple, fast and effective direct method based on HPLC-APCI-QqQ-MS/MS has been developed to simultaneously determine four 3-monochloropropane-1,2-diol monoesters (3-MCPDE) esterified with palmitic, linoleic, stearic, and oleic acid, and two glycidyl esters (GE) with palmitic and oleic acid in margarine and olive oil using a QuEChERS approach. Factors affecting the efficiency of the extraction process were assessed, including type and amount of salt, extraction solvent, test portion amount, and clean-up sorbent. The analytical method was validated according to Food and Drug Administration (FDA) guidelines using matrix-matched calibration with internal standards and showed good results in terms of linearity (r2 > 0.9992), accuracy (80

Ultrasound-assisted enzymatic indirect determination of total 3-monochloropropane-1,2-diol esters in canned fish oil fraction.

A novel, fast, and cost-effective indirect enzymatic method was successfully developed to assess the total 3-monochloropropane-1,2-diol (3-MCPD) in canned food's oil fraction by the action of Burkholderia cepacia lipase. The total 3-MCPD were derivatized with n-Heptafluorobutyrylimidazole (HFBI) for GC-MS analysis during dispersive liquid-liquid microextraction (DLLME). An asymmetrical 2213//8 screening design was used to study the influence of critical factors on the method's effectiveness. The analytical features of the proposed method were assessed following Food and Drug Administration (FDA) guidelines using extra virgin olive oil (EVOO) as a blank sample. Outstanding results were achieved in terms of linearity (r2 = 0.9995), sensitivity, precision (2.1 % to 10.4 % RSD), and accuracy (98.7 % ≤ recovery ≤ 101.9 %). Method efficacy was tested by comparing the results of 10 edible oils for total 3-MCPD with those reported in previous works. A total of 41 samples were analyzed. The lowest 3-MCPD content was found in samples of albacore canned in EVOO oil, while the highest amounts were found in albacore, mackerel, and Atlantic saury samples, all preserved in refined sunflower oil.

3-MCPD exposure enhances ovarian fibrosis and reduces oocyte quality in mice.

3-monochloro-1,2-propanediol (3-MCPD) is a food contaminant believed to be harmful to human health. Previous studies showed that 3-MCPD exerts toxic effects in multiple tissues, but whether 3-MCPD affects female reproductive function remained unknown. Here, using mouse gastric lavage models, we report that 3-MCPD exposure for four weeks affected body growth, decreased the ovary/body weight ratio, and increased atretic follicle numbers. Expression levels of follicular development-related factors decreased. Further studies found that ovaries from 3-MCPD exposed mice had activated the Transforming Growth Factor-ß (TGF-ß) signaling pathway and promoted ovarian fibrosis. Increased TNF-α, IL-1 and NF-κB expression also indicated the occurrence of ovarian inflammation. Exposure to 3-MCPD stimulated the caspase pathway and enhanced granulosa cell apoptosis. Consistent with disrupted ovarian homeostasis, 3-MCPD exposure interfered with mitochondrial function, generated more reactive oxygen species, increased ferrous ion and lipid peroxidation levels, and resulted in decreased oocyte development potential. Collectively, these findings indicated that 3-MCPD exposure induced ovarian inflammation and fibrosis, and caused disorders of mitochondrial function and ferrous ion homeostasis in oocytes, which consequently disturbed follicle maturation and reduced oocyte quality.

Risk assessment of 3-monochloropropane-1,2-diol esters through dietary exposure from edible oils for the Zhejiang population in China by Monte Carlo simulation.

The purpose of this study was to assess the risk of 3-monochoropropane-1,2-diol (3-MCPD) esters from edible oils for the Zhejiang population in China. Exposure assessment of 3-MCPD esters was evaluated by Monte Carlo simulation based on the concentrations of 3-MCPD esters in edible oils combined with survey data on the eating habits of Chinese residents classified by age group and gender. The simulation results indicated that the mean daily intakes (CDI) of 3-MCPD esters for children 7-10 years old were 2.154 µg (kg BW d)-1 for boys and 2.049 µg (kg BW d)-1 for girls, which are lower than the provisional maximum tolerable daily intake (PMTDI) of 4 µg (kg BW d)-1 for 3-MCPD and 3-MCPD esters individually or in combination, set by the Joint FAO/WHO Expert Committee on Food Additives. The range of mean dietary intakes of 3-MCPD esters in different subpopulation groups ranged 1.242-1.672 µg (kg BW d)-1, which was lower than the PMTDI. However, the CDI values of 3-MCPD esters in high percentile exposure subgroups (95th, 99th) of males (7-49 years old) and females (7-10 and 50-75 years old) were all above 4µg (kg bw d)-1. Outside of the senior group (50-75 years old), males had more exposure to 3-MCPD than females. The average hazard indexes (HI) of 3-MCPD esters to male and female children were 1.257 and 1.024, respectively, indicating there was a risk, but no immediate measures are required to address this risk. The average HI of 3-MCPD esters to adolescent, adult, and seniors were all below 1, indicating risk for those age groups were at an acceptable level.

Occurrence and Dietary Exposure of 3-MCPD Esters and Glycidyl Esters in Domestically and Commercially Prepared Food in Singapore.

This study investigated the prevalence and occurrence of 3-monochloropropanediol esters (3-MCPDEs) and glycidyl esters (GEs) in domestically and commercially prepared food in Singapore and assessed the total dietary exposure for the Singaporean population. Minimal impact on the formation of 3-MCPDEs and GEs was observed from the domestic cooking methods commonly practiced in Singapore such as deep frying and stir frying. The estimated total dietary exposure to 3-MCPDEs for the Singaporean population (aged 15 to 92) was 0.982 µg/kg bw/day for general consumers and 2.212 µg/kg bw/day for high consumers (95th percentile), which accounted for 49.1% and 110.6% of the tolerable dietary intake (TDI) at 2 µg/kg bw/day by the European Food Safety Authority (EFSA). The calculated margins of exposure (MOE) for GEs based on the dietary exposure for general consumers at 0.882 µg/kg bw/day and 2.209 µg/kg bw/day for high consumers were below 10,000, indicating a potential health concern. Our study showed that the occurrence of 3-MCPDEs and GEs varied among vegetable oils, and domestic cooking methods did not significantly impact the levels of 3-MCPDEs and GEs in prepared food. The critical factor influencing the prevalence and occurrence of 3-MCPDEs and GEs was the choice of oil used for cooking, which absorbed into the cooked food. It is essential to encourage the food industry to continue its innovation on mitigation measures to control and reduce 3-MCPDEs and GEs in vegetable oil production. Consumers are advised to make informed choices on food consumption and cooking oil for food preparation to reduce their exposure to 3-MCPDEs and GEs.

The Formation of 3-Monochloropropanediol Esters and Glycidyl Esters during Heat-Induced Processing Using an Olive-Based Edible Oil.

With the prevalence of edible diacylglycerol (DAG) oil, which is beneficial to human, the generation of 3-monochloropropanediol esters (3-MCPDE) and glycidyl esters (GE) as well as the stability of physical properties during heat-induced processing still need to be explored. In this study, the experiment used olive-based edible oil with different contents of DAG (40, 60, and 80%) to make crackers and fry chicken. They were heated at 160 and 180 °C to determine the changes in 3-MCPDE and GE, the crackers' hardness and gumminess, and the physical properties of the oil. During baking and frying, 3-MCPDE decreased, while the content of GE slightly increased with the prolonged heating duration. Finally, 3-MCPDE and GE were lower than 1.25 mg/kg and 1.00 mg/kg, respectively. The AV increased proportionally as duration increased and POV was below 0.30 g/100 g. In general, the changes in 3-MCPDE and GE were related to the heating temperature and duration, and not significantly (p > 0.05) related to the content of DAG.

Occurrence of 2- and 3-monochloropropanediol esters (MCPDE) in infant formula products on the Canadian market between 2015 and 2019.

2- and 3-monochloropropanediol esters (MCPDEs) are most commonly formed as process-induced contaminants during the refinement of vegetable oils used for food production. 'In vivo' hydrolysis of 3-MCPDEs releases the potential carcinogen 3-monochloropropanediol (3-MCPD). Levels of MCPDEs in infant formula are of particular concern, as refined oils are commonly used as main fat ingredients. For this study, infant formula samples (powders, liquid concentrates and ready-to-feed infant formula samples) from the Canadian market were purchased and analysed in 2015 (35 samples) and 2019 (33 samples). MCPDE concentrations (expressed as free MCPD equivalents) were examined through an indirect analytical approach, applying acid-catalysed ester cleavage and using cyclohexanone as derivatising agent. Labelled diesters were used as internal standards. 2015 Survey data were analysed by gas chromatography-mass spectrometry (GC-MS) in selected ion monitoring mode (SIM). 2019 Survey data were analysed with an updated method using GC-MS/MS in multiple reaction monitoring modes (MRM). In 2015, levels in reconstituted formula ranging from 3.7 ng/g to 111 ng/g for 3-MCPD and 2.2 ng/g to 56.2 ng/g for 2-MCPD were found. In 2019, levels ranging from 3.9 ng/g to 74.8 ng/g for 3-MCPD and 1.0 ng/g to 33.9 ng/g for 2-MCPD were found. A significantly reduced mean of combined MCPDEs was observed between 2015 and 2019 data (64.5 ng/g, standard deviation (SD) 8.6 ng/g in 2015 to 31.8 ng/g, SD 5.6 ng/g in 2019, p-value = 0.024). For the majority of manufacturers, the data comparison among brand products over time shows decreased levels of MCPDEs. Occurrence data of MCPDEs, including data from previously published surveys (2012/2013), were also compared and a temporal trend was established.

Molecularly imprinted sensing platform based on electrochemically modified graphite paper for efficient detection of 3-monochloropropane-1,2-diol.

In this study, a molecularly imprinted polymer (MIP) electrochemical sensor based on electrochemically modified graphite paper (EM-GP) was developed for the detection of 3-MCPD for the first time. To this end, Prussian blue (PB) was electrodeposited on EM-GP to yield uniformly distributed PtNPs. The successful preparation of Pt@PB/EM-GP was verified by SEM, Raman spectroscopy, XRD,XPS, and EDS. MIP was then prepared by CV electropolymerization with template molecules (3-MCPD), and density functional theory (DFT) at M06-2X/6-31 + g (d,p) level was used to calculate the molecular-level interaction between 3-MCPD and MIP. Under the optimum conditions, the dynamic linear range of the sensing platform varied from 1 × 10-8mol/L to 5 × 10-5mol/L with a detection limit estimated to 5 × 10-9 mol/L (S/N = 3). Overall, these findings look promising for the construction of selective and quick detection platforms of 3-MCPD in food samples.

Facile Synthesis of 3D Printed Tailored Electrode for 3-Monochloropropane-1,2-Diol (3-MCPD) Sensing.

Additive manufacturing (AM) has allowed enormous advancement in technology and material development; thus, it requires attention in developing functionalized printed materials. AM can assist in efficiently manufacturing complex tailored electrodes for electrochemical sensing in the food industry. Herein, we used a commercial fused deposition modeling (FDM) filament of acrylonitrile butadiene styrene (ABS) for FDM 3D printing of a self-designed electrode with minimal time and cost compared to a commercial electrode. A graphene-based ABS conductive filament (ABS-G) was used to fabricate the conductive electrode in a dual-nozzle FDM 3D printer. The electrochemically conductive 3D printed electrode was characterized using cyclic voltammetry and tested against standard 3-monochloropropane-1,2-diol (3-MCPD) with known concentrations using an amperometric detection method. Results showed a basis for promising application to detect and quantify 3-MCPD, a food contaminant known for its carcinogenic potential. The fabrication of functionalized 3D printed polymer electrodes paves way for the development of complete 3D printable electrochemical sensors. Under optimal conditions, this newly synthesized electrochemical sensor exhibited sensitivity with a linear response range from 6.61 × 10-4 to 2.30 × 10-3 µg/mL with an estimated limit of detection of 3.30 × 10-4 µg/mL against 3-MCPD.