Analytical chemistry,formation, mitigation,and risk assessment of polycyclic aromatic hydrocarbons: From food processing to in vivo metabolic transformation

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in the air, oils, water, and food products we encounter every day. Among these exposures, food consumption is a major route of PAH exposure for nonsmokers. The PAH dietary exposure levels vary among different countries; however, many studies have shown PAH exposure to be highly concerning to human health. The levels of PAH contamination in food are mainly influenced by processing procedures and cooking methods, and they could be attenuated by modifying cooking procedures and adding antioxidant-rich marinades. Several PAHs have toxic, mutagenic, and carcinogenic properties. The PAH benzo[a]pyrene (BaP) is particularly regarded as carcinogenic. There are three major metabolism pathways for PAHs, and the final products can bind to DNA, thus exerting mutagenic effects. Biological monitoring through the use of biomarkers is necessary for comprehensive and accurate risk assessments of human PAH exposure. It is important to reduce dietary PAH exposure and to implement reasonable and effective risk management strategies to reduce PAH levels in food to improve public health.     

Current issues in dietary acrylamide: formation,mitigation and risk assessment

Acrylamide (AA) is known as a neurotoxin in humans and it is classified as a probable human carcinogen by the International Agency of Research on Cancer. AA is produced as by‐product of the Maillard reaction in starchy foods processed at high temperatures (>120 °C). This review includes the investigation of AA precursors, mechanisms of AA formation and AA mitigation technologies in potato, cereal and coffee products. Additionally, most relevant issues of AA risk assessment are discussed. New technologies tested from laboratory to industrial scale face, as a major challenge, the reduction of AA content of browned food, while still maintaining its attractive organoleptic properties. Reducing sugars such as glucose and fructose are the major contributors to AA in potato‐based products. On the other hand, the limiting substrate of AA formation in cereals and coffee is the free amino acid asparagine. For some products the addition of glycine or asparaginase reduces AA formation during baking. Since, for potatoes, the limiting substrate is reducing sugars, increases in sugar content in potatoes during storage then introduce some difficulties and potentially quite large variations in the AA content of the final product. Sugars in potatoes may be reduced by blanching. Levels of AA in different foods show large variations and no general upper limit is easily applicable, since some formation will always occur. Current policy is that practical measures should be taken voluntarily to reduce AA formation in vulnerable foods since AA is considered a health risk at the concentrations found in foods. © 2013 Society of Chemical Industry     

食品中5-羟甲基糠醛的形成与控制

5-羟甲基糠醛(5-hydroxymethylfurfural,HMF)是食品热加工和贮藏过程中产生的内源性污染物,主要通过美拉德反应和己糖在酸性条件下脱水产生,其形成过程受反应底物种类、加热温度、反应体系p H、水分活度及金属离子等影响。HMF具有一定神经毒性、遗传毒性;摄入后在磺基转移酶作用下可转化为具有致癌毒性的羟甲基糠醛次硫酸,因而近年来HMF受到了国内外的广泛关注。本文综述了HMF形成的途径、影响因素和控制措施。     

云南省部分食品黄曲霉毒素B1膳食暴露风险评估

目的评估云南省部分食品中黄曲霉毒素B1(aflatoxinB1,AFB1)膳食暴露风险。方法结合2012～2017年云南省部分地区市售大米及其制品、玉米及其制品等6类主要食品的黄曲霉毒素B1含量数据,以及本省营养监测消费量数据,采用点评估方法对云南省居民AFB1暴露水平进行评估。结果云南省全人群来源于6类食品的AFB1暴露量为1.02×10-3μg/kgbw,其中来源于大米的AFB1暴露量最高,占总暴露量的50.98%,其次是玉米及其制品,占18.63%。总暴露量为大城市贫困农村中小城市一般农村;云南省居民AFB1膳食暴露量对肝癌发病率的贡献为0.040/10万人;各地区居民暴露边界比(margin of exposure, MOE)值介于144.07～180.85之间。结论云南省AFB1污染状况相对良好,仍需持续关注; 6类食物中大米、玉米是云南省AFB1的主要暴露来源。     

婴幼儿配方食品及婴幼儿辅助食品中呋喃污染特征及膳食暴露概率评估

目的 了解我国市售婴幼儿配方食品及婴幼儿辅助食品中呋喃污染特征,并对其健康风险进行评估.方法 基于方便抽样法,于2017—2018年在北京市、浙江省、山东省和四川省采集260份市售婴幼儿配方食品及婴幼儿辅助食品,采用同位素稀释-顶空气相色谱-质谱法测定呋喃的含量,结合2015年婴幼儿食品消费量调查数据,通过概率评估方法...     

Consumer exposures to anthocyanins from colour additives,colouring foodstuffs and from natural occurrence in foods

Anthocyanins are responsible for the red/blue colour of grapes, currants, and other fruits and vegetables. They may also be extracted for use as colour additives (E163) or concentrated for use as colouring foods. Consumer exposures have been assessed using data on natural occurrence, use levels and frequencies from food manufacturers and European food consumption data. Intakes from natural occurrence can be up to 4 mg kg bw^?1 day^?1 at the mean and up to 17 mg kg bw^?1 day^?1 for children who are high level consumers of red/black berries and small fruits. High-level intakes for children from food colour and colouring food applications lie in the range 0.3–6.3 mg kg bw^?1 day^?1 and for adults at 0.6–2.8 mg kg bw^?1 day^?1. Exposures from food colour use and colouring foods separately or combined are therefore lower than those from natural occurrence in foods.     

食品中丙烯醛形成、危害及控制研究进展

食品中的丙烯醛是食品在高温加工过程中产生的内源污染物,碳水化合物、植物油、动物脂肪和氨基酸是其形成前体。碳水化合物的高温裂解、甘油脱水、多不饱和脂肪酸的脂质氧化等过程都可以产生丙烯醛。丙烯醛可以与谷胱甘肽、DNA、蛋白质等形成加合物,积累氧自由基,对呼吸系统、心血管系统、生殖系统、神经系统等形成不同程度的危害。目前主要通过减少或消除前体物质、改变加工方式和条件、加入抗氧化剂、含硫和含氮化合物等清除剂对丙烯醛进行控制。本文综述了国内外在食品中丙烯醛形成的途径、对人体的危害以及控制途径方面的研究进展,希望能为食品中有效地抑制丙烯醛形成的研究提供参考。     

Overview on mitigation of acrylamide in starchy fried and baked foods

Acrylamide in fried and baked foods has the potential to cause toxic effects in animals and humans. A major challenge lies in developing an effective strategy for acrylamide mitigation in foods without altering its basic properties. Food scientists around the world have developed various methods to mitigate the presence of acrylamide in fried food products. Mitigation techniques using additives such as salts, amino acids, cations and organic acids along with blanching of foods have reduced the concentration of acrylamide. The use of secondary metabolites such as polyphenols also reduces acrylamide concentration in fried food products. Other mitigation techniques such as asparaginase pre‐treatment and low‐temperature air frying with chitosan have been effective in mitigating the concentration of acrylamide. The combined pre‐treatment process along with the use of additives is the latest trend in acrylamide mitigation. © 2018 Society of Chemical Industry     

Recent advances in heterocyclic aromatic amines: An update on food safety and hazardous control from food processing to dietary intake

Heterocyclic aromatic amines (HAAs) as probable carcinogenic substances are mainly generated in meat products during thermal processing. Numerous studies have contributed to the analysis, formation, and mitigation of HAAs during food processing. However, few articles have comprehensively reviewed food safety aspects from both food processing and dietary intake regarding the formation, mitigation, metabolism, biomarkers for exposure, hazard control, and risk assessment of HAAs, and related food safety researches. Several factors may influence the generation of HAAs, including processing temperature, processing time, and chemical composition of the meat. Nonetheless, these mutagenic compounds are attenuated to different levels by the addition of natural or synthetic flavorings and antioxidant‐rich marinades, as well as pretreatments using technique such as microwave heating. After dietary intake, different types of HAAs are metabolized in humans by several enzymes, including cytochrome P450s, peroxidases, N‐acetyltransferases, sulfotransferases, uridine diphosphate‐glucuronosyltransferases, and glutathione S‐transferases. Their primary metabolites are further conjugated with DNA or ultimately excreted in urine and feces. The 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine in hair as well as DNA, hemoglobin, and serum albumin adducts has been considered as biomarkers for exposure assessment. Dietary intake information obtained from questionnaires and the results of epidemiological investigations have shown a positive relationship between the intakes of red meat and processed meat and high risk of cancer incidence. As several cancers have been reported to be associated with HAAs, HAAs should be both effectively reduced during food processing and controlled from dietary intake to facilitate human health.     

Furan formation from ingredient interactions and furan mitigation by sugar alcohols and antioxidants of bamboo leaves in milk beverage model systems

The cover image is based on the Research Article Furan formation from ingredient interactions and furan mitigation by sugar alcohols and antioxidants of bamboo leaves in milk beverage model systems by Jun Guo et al., DOI: 10.1002/jsfa.9739 .

     

吉林省主要食品中砷污染状况及居民膳食暴露风险评估

目的掌握吉林省主要食品中砷污染水平,评估吉林省居民砷暴露风险及对人体潜在的健康危害。方法 2012—2017年吉林省居民主要食品中砷的含量数据来自国家食品风险监测,共11种类别4 532份样品。食物消费量的数据来自2012年吉林省居民营养与健康调查。采用确定性评估方法 ,结合无机砷的原暂定每周可耐受摄入量(PTWI)和暴露边距(MOE),评价吉林省居民膳食中砷暴露情况。结果 11类食品中砷平均含量为0.030 mg/kg,谷物类、蔬菜类和水产类是膳食中砷的主要来源,三者贡献率之和为76.59%,其中谷物类贡献率高达54.44%。10个不同性别-年龄组平均摄入量为0.73～1.31μg/kg BW,一般人群暴露量MOE均1。结论吉林省居民膳食中砷暴露风险总体上是安全的。     

Occurrence and risk assessment of mycotoxins,acrylamide, and furan in Latvian beer

This work reports data on the occurrence of nine mycotoxins and two food processing contaminants – acrylamide and furan – in a total of 100 beers produced in Latvia. Mycotoxins were detected by high-performance liquid chromatography (HPLC) coupled with time-of-flight mass spectrometry, acrylamide by HPLC coupled with quadrupole-Orbitrap mass spectrometry, and furan by headspace gas chromatography-mass spectrometry. The most frequently occurring mycotoxins were HT-2 and deoxynivalenol (DON), which were detected in 52% and 51% of the analysed samples. The highest content was observed for DON, reaching the maximum of 248 µg kg^?1. Furan was ubiquitous, and 74% of the samples contained acrylamide. In terms of the estimated exposure, the biggest potential risk was identified for HT-2 representing more than 11% of tolerable weekly intake. The margin of exposure approach indicated the exposure to furan through beer as significant, this parameter being close to the critical limit.     

2012~2019年云南省蔬菜中毒死蜱膳食摄入风险评估

摘 要: 目的 了解云南省蔬菜中毒死蜱残留水平, 评估蔬菜中毒死蜱膳食暴露风险。方法 2012~2019年采集云南省市售蔬菜进行毒死蜱测定, 结合我国食物消费量数据, 采用点评估方法对毒死蜱进行急、慢性膳食暴露评估, 评估结果与急性参考剂量(acute reference dose, ARfD)、每日允许摄入量(acceptable daily intake, ADI)进行比较, 从而评价蔬菜中毒死蜱的暴露风险。结果 1~4岁人群的急性暴露量大于ARfD(0.1 mg/kg bw), 其余年龄组的急性暴露量均小于ARfD(0.1 mg/kg bw); 各年龄组平均暴露量低于ADI(0.01 mg/kg bw)。结论 蔬菜中毒死蜱的慢性暴露风险低, 但需关注急性暴露风险。     

典型膳食来源亚硝酸钠暴露对我国人群健康风险的研究

目的 评估中国居民膳食因素亚硝酸钠摄入量及对健康影响的潜在风险,为食品安全风险管理提供科学依据.方法 应用典型食品(酱类、肉制品和腌菜)中亚硝酸钠含量的实际监测结果和我国居民对含亚硝酸钠食品实际的膳食消费量数据,采用简单分布模型方法,对我国居民全人群的膳食亚硝酸钠摄入量进行估计,并与国际组织JECFA制定的亚硝酸钠每日允许摄入量(ADI)进行比较.结果 全人群的亚硝酸钠平均摄入量为0.021 mg/kgBW/day,占ADI的30.0％,而高暴露人群(亚硝酸钠摄入量的P97.5)的亚硝酸钠摄入量为0.150 mg/kg BW/day,是ADI的2.1倍;各性别-年龄组人群的膳食亚硝酸钠平均摄入量均未超过ADI,但就各组高暴露人群而言,亚硝酸钠摄入量范围为0.124 8 ～0.275 0 mg/kg BW/day,是ADI的1.8～3.9倍;酱/咸菜是我国居民膳食亚硝酸钠摄入的主要来源,占总摄入量的61.9％.结论 我国全人群平均膳食亚硝酸钠摄入量处于安全水平,但高暴露人群摄入的亚硝酸钠具有较高的健康风险,需予以重点关注;调整饮食习惯和行为,改进食品加工工艺,最大限度地减少外源性亚硝酸盐的添加和内源性亚硝酸钠的产生是降低我国居民膳食亚硝酸钠摄入的有效手段.     

浙江温州地区海产品中石油烃的含量分析及膳食风险评估

目的 掌握浙江温州地区海产品中石油烃的污染状况及其对人群膳食暴露影响。方法 采集2022年浙江温州地区30个品种217批次海产品, 取各样品可食部分, 经组织匀质后, 经6 mol/L氢氧化钠溶液40℃恒温振荡皂化6 h、二氯甲烷萃取、旋转蒸发浓缩至干、脱芳石油醚复溶, 取上清液采用分子荧光仪测定其石油烃含量。采用单因子指数法和商值法分别评价其污染程度和膳食暴露健康风险。结果 所有海产品均存在不同程度的石油烃检出(范围1.06~26.6 mg/kg, 均值9.70 mg/kg), 其中13.4%的样品中石油烃含量超出NY 5073—2006《无公害食品水产品中有毒有害物质限量》中规定的限值, 分别为缢蛏、泥蚶、馒头蟹。总体上检出浓度依次排序, 养殖贝类>海捕头足类>海捕蟹>海捕虾>海捕鱼>养殖藻类。所测海产品石油烃危害商在0.01226~0.3076之间, 均小于1, 致癌风险指数范围为4.9×10-7~7.6×10-5, 小于1×10-4, 其中养殖贝类中缢蛏、泥蚶、贻贝的危害商和致癌风险指数相对较高。结论 浙江温州地区海产品中石油烃的健康风险较低, 但应密切关注长期或大量食用缢蛏、泥蚶、贻贝带来的不利影响。     

Dietary N-epsilon-carboxymethyllysine as for a major glycotoxin in foods: A review

N-epsilon-carboxymethyllysine (CML), as a potential glycotoxin and general marker for dietary advanced glycation end products (dAGEs), exists in raw food and is formed via various formation routes in food processing such as Maillard reaction between the reducing sugars and amino acids. Although comprehensive cause-effect proof is not available yet, current research suggests a potential risk of chronic diseases such as diabetes is associated with exogenous CML. Thus, CML is causing public health concerns regarding its dietary exposure, but there is a lack of explicit guidance for understanding if it is detrimental to human health. In this review, inconsistent results of dietary CML contributed to chronic disease are discussed, available concentrations of CML in consumed foods are evaluated, measurements for dietary CML and relevant analytic procedures are listed, and the possible mitigation strategies for protecting against CML formation are presented. Finally, the main challenges and future efforts are highlighted. Further studies are needed to extend the dietary CML database in a wide category of foods, apply new identifying methods, elucidate the pathogenic mechanisms, assess its detrimental role in human health, and propose standard guidelines for processed food.     

Dityrosine in food: A review of its occurrence,health effects,detection methods,and mitigation strategies

Protein and amino acid oxidation in food products produce many new compounds, of which the reactive and toxic compound dityrosine, derived from oxidized tyrosine, is the most widely studied. The high reactivity of dityrosine enables this compound to induce oxidative stress and disrupt thyroid hormone function, contributing to the pathological processes of several diseases, such as obesity, diabetes, cognitive dysfunction, aging, and age-related diseases. From the perspective of food safety and human health, protein-oxidation products in food are the main concern of consumers, health management departments, and the food industry. This review highlights the latest research on the formation pathways, toxicity, detection methods, occurrence in food, and mitigation strategies for dityrosine. Furthermore, the control of dityrosine in family cooking and food-processing industry has been discussed. Food-derived dityrosine primarily originates from high-protein foods, such as meat and dairy products. Considering its toxicity, combining rapid high sensitivity dityrosine detection techniques with feasible control methods could be an effective strategy to ensure food safety and maintain human health. However, the current dityrosine detection and mitigation strategies exhibit some inherent characteristics and limitations. Therefore, developing technologies for rapid and effective dityrosine detection and control at the industrial level is necessary.