No full-text available
To read the full-text of this research,
you can request a copy directly from the author.
Scientific Opinion on acrylamide in food
Abstract
EFSA was asked to deliver a scientific opinion on acrylamide (AA) in food. AA has widespread uses as an industrial chemical. It is also formed when certain foods are prepared at temperatures above 120 °C and low moisture, especially in foods containing asparagine and reducing sugars. The CONTAM Panel evaluated 43 419 analytical results from food commodities. AA was found at the highest levels in solid coffee substitutes and coffee, and in potato fried products. Mean and 95th percentile dietary AA exposures across surveys and age groups were estimated at 0.4 to 1.9 µg/kg body weight (b.w.) per day and 0.6 to 3.4 µg/kg b.w. per day, respectively. The main contributor to total dietary exposure was generally the category ‘Potato fried products (except potato crisps and snacks)’. Preferences in home-cooking can have a substantial impact on human dietary AA exposure. Upon oral intake, AA is absorbed from the gastrointestinal tract and distributed to all organs. AA is extensively metabolised, mostly by conjugation with glutathione but also by epoxidation to glycidamide (GA). Formation of GA is considered to represent the route underlying the genotoxicity and carcinogenicity of AA. Neurotoxicity, adverse effects on male reproduction, developmental toxicity and carcinogenicity were identified as possible critical endpoints for AA toxicity from experimental animal studies. The data from human studies were inadequate for dose-response assessment. The CONTAM Panel selected BMDL10 values of 0.43 mg/kg b.w. per day for peripheral neuropathy in rats and of 0.17 mg/kg b.w. per day for neoplastic effects in mice. The Panel concluded that the current levels of dietary exposure to AA are not of concern with respect to non-neoplastic effects. However, although the epidemiological associations have not demonstrated AA to be a human carcinogen, the margins of exposure (MOEs) indicate a concern for neoplastic effects based on animal evidence.
... After absorption in the intestine, AA is widely distributed to various organs and tissues, for instance, the liver, where conjugation with glutathione and/or activation by cytochrome P450 (CYP) 2E1 to the highly reactive metabolite glycidamide (GA) takes place [15]. The genotoxicity of AA is mostly mediated through the metabolism to GA, which is a known mutagen, whose genotoxic effect is mediated via DNA adduct formation [4,16]. Hence, CYP2E1 enzymes are of major importance for AA toxicity. ...
... However, knowledge about the toxicity of single substances does not guarantee the correct prediction of their toxicity in a mixture [2]. Due to their generally high occurrence in foods, the mycotoxin deoxynivalenol (DON), produced by Fusarium spp., and acrylamide (AA), a product of the Maillard reaction, are of particular interest [3][4][5][6]. The co-occurrence of AA and DON was reported once in Latvian beer [7,8] and co-occurrence in a broad ...
... The tested concentrations and ratios in the present study were selected based on occurrence data and mimic a realistic exposure to AA and DON [4,12,24,26]. Previously, AA in vitro concentrations exceeding 6 mM were considered unrealistic [54]. Nonetheless, many in vitro studies were carried out at the highest non-cytotoxic AA concentration, e.g., 5 mM in undifferentiated Caco-2 cells, 2 mM in normal human liver cells HL7702, or 2.5 mM in HepG2 cells [17,21,55]. ...
Acrylamide (AA) can be formed during the thermal processing of carbohydrate-rich foods. Deoxynivalenol (DON), a mycotoxin produced by Fusarium spp., contaminates many cereal-based products. In addition to potential co-exposure through a mixed diet, co-occurrence of AA and DON in thermally processed cereal-based products is also likely, posing the question of combinatory toxicological effects. In the present study, the effects of AA (0.001–3 mM) and DON (0.1–30 µM) on the cytotoxicity, gene transcription, and expression of major cytochrome P450 (CYP) enzymes were investigated in differentiated human hepatic HepaRG cells. In the chosen ratios of AA–DON (10:1; 100:1), cytotoxicity was clearly driven by DON and no overadditive effects were observed. Using quantitative real-time PCR, about twofold enhanced transcript levels of CYP1A1 were observed at low DON concentrations (0.3 and 1 µM), reflected by an increase in CYP1A activity in the EROD assay. In contrast, CYP2E1 and CYP3A4 gene transcription decreased in a concentration-dependent manner after incubation with DON (0.01–0.3 µM). Nevertheless, confocal microscopy showed comparably constant protein levels. The present study provided no indication of an induction of CYP2E1 as a critical step in AA bioactivation by co-occurrence with DON. Taken together, the combination of AA and DON showed no clear physiologically relevant interaction in HepaRG cells.
... Others have found adverse effects in renal cells, pre-and postnatal development and an increased risk for endometrial and ovarian cancer, but the evidence are limited and inconsistent. In June 2015, the CONTAM Panel (Panel on Contaminants in the Food Chain) of the European Food Safety Authority (EFSA) published the first comprehensive risk assessment of AA in food, identifying four possible adverse effects, including toxicity (i.e., neurotoxicity, also confirmed in humans), male reproductive effects, developmental toxicity, and carcinogenicity, for which further studies are needed [10]. Given the conflicting results of studies in humans, the International Agency for Research on Cancer has classified AA in Group 2A, listing it as a "probable human carcinogen" [11]. ...
... The BMDL 10 value considered for neurotoxic risk was 0.43 mg/kg BW/day, while a value of 0.17 mg/kg BW/day, derived from evidence of Harder's gland cancer in mice, was used to assess for carcinogenic risk [10]. ...
... The increased contaminant concentration can be explained by the fact that plums are an asparagine-rich food matrix [28]. This result agrees with the EFSA assessment, even if it shows higher AA concentrations than those of our study [10]. Concerning vegetable-based homogenized foods (Figure 2d), OVE1 has the highest AA content of 16.80 ± 0.57 µg/kg. ...
Acrylamide (AA) is a contaminant resulting from the Maillard reaction and classified by the International Agency for Research on Cancer (IARC) as a probable carcinogen in Group 2A, with proven neurotoxic effects on humans. European Union (EU) Regulation No. 2017/2158 is currently in force, which establishes measures meant to reduce AA levels in food and sets reference values, but not legal limits, equal to 40 and 150 μg/kg AA in processed cereal-based foods intended for infants and young children and in biscuits and rusks, respectively. For this reason, sixty-two baby foods were analyzed using ultra-high performance liquid chromatography with diode array detector and quadrupole time-of-flight mass spectrometry (UHPLC-DAD-Q-TOF/MS) to check whether industries were complying with these values, even though AA control is not legally mandatory. In total, 14.5% of the samples exceeded the reference values; these were homogenized chicken products (211.84 ± 16.53, 154.32 ± 12.71, 194.88 ± 7.40 μg/kg), three biscuits (276.36 ± 0.03, 242.06 ± 0.78, 234.78 ± 4.53 μg/kg), a wheat semolina (46.07 ± 0.23 μg/kg), a homogenized product with plaice and potatoes (45.52 ± 0.28 μg/kg), and a children’s snack with milk and cocoa (40.95 ± 0.32 μg/kg). Subsequently, the daily intake of AA was estimated, considering the worst-case scenario, as provided by the consumption of homogenized chicken products and biscuits. The results are associated with margins of exposure (MOEs) that are not concerning for neurotoxic effects but are alarming for the probable carcinogenic effects of AA.
... The obesity-inducing Western diet is made up of foods that have high acrylamide contents [28,29], suggesting that individuals with obesity may be exposed to higher levels of acrylamide. Current estimates suggest that chronic dietary exposure of adolescents and adults is, on average, between 0.4 and 0.9 µg/kg body weight per day [30]. Recommendations to reduce acrylamide production in food are provided by the United States Federal Drug Administration [31]. ...
... Recommendations to reduce acrylamide production in food are provided by the United States Federal Drug Administration [31]. The European Food Safety Authority concluded that margins of exposure indicate a concern for neoplastic effects based on animal evidence [30], and European companies selling foods containing acrylamide are required to report acrylamide levels due to its adverse health effects [32]. Recently, acrylamide exposure was found to enhance weight gain in mice [33] and zebrafish [34], as well as increase fat droplet accumulation in differentiated 3T3-L1 cultured adipocytes [33]. ...
... Here, a high-fat (HFD) model of obesity and chronic exposure to acrylamide in mice was utilized. The dose of acrylamide administered was similar to acrylamide exposure levels observed in humans [30]. Given the role of acylamide as a potential obesogen, the potential for acrylamide to enhance weight gain was examined in mice fed either a low-fat diet (LFD) or HFD. ...
Obesity and environmental toxins are risk factors for breast cancer; however, there is limited knowledge on how these risk factors interact to promote breast cancer. Acrylamide, a probable carcinogen and obesogen, is a by-product in foods prevalent in the obesity-inducing Western diet. Acrylamide is metabolized by cytochrome P450 2E1 (CYP2E1) to the genotoxic epoxide, glycidamide, and is associated with an increased risk for breast cancer. To investigate how acrylamide and obesity interact to increase breast cancer risk, female mice were fed a low-fat (LFD) or high-fat diet (HFD) and control water or water supplemented with acrylamide at levels similar to the average daily exposure in humans. While HFD significantly enhanced weight gain in mice, the addition of acrylamide did not significantly alter body weights compared to respective controls. Mammary epithelial cells from obese, acrylamide-treated mice had increased DNA strand breaks and oxidative DNA damage compared to all other groups. In vitro, glycidamide-treated COMMA-D cells showed significantly increased DNA strand breaks, while acrylamide-treated cells demonstrated significantly higher levels of intracellular reactive oxygen species. The knockdown of CYP2E1 rescued the acrylamide-induced oxidative stress. These studies suggest that long-term acrylamide exposure through foods common in the Western diet may enhance DNA damage and the CYP2E1-induced generation of oxidative stress in mammary epithelial cells, potentially enhancing obesity-induced breast cancer risk.
... There is evidence that acrylamide has adverse health effects, including neurotoxicity [7,8] and impaired fertility [9]. Moreover, experimental studies in rodents point to a possible carcinogenicity of this substance, as indicated by the Scientific Opinion on acrylamide in food of the European Food Safety Authority (EFSA) in 2015 [10]. In 1994, the International Agency for Research on Cancer (IARC) declared acrylamide as a probable human carcinogen (Group 2A) [11]. ...
... For the determination of the concentration of acrylamide in these 20 acrylamide-containing foods, the quantity of acrylamide for each food was derived from data published using Spanish populations, given the absence of an acrylamide database in this country [36][37][38][39][40][41][42][43]. If no previous Spanish study had evaluated the acrylamide concentration of a particular food, the Scientific Opinion on acrylamide in food of the EFSA was consulted [10]. The concentration of acrylamide in each food (µg/kg) and the source of information can be consulted in Supplementary Table S1. ...
... Specifically, these studies reporting higher intakes of acrylamide include crisp rye bread, a food that contains large amounts of acrylamide but is not part of the usual diet of the Spanish population [21,23,25]; (2) the concentration of acrylamide in each food differs depending on the source consulted. In our study, those indicated in Spanish publications were used, and failing that, the one reported by the Scientific Opinion on acrylamide in food of the EFSA [10]. Nevertheless, the food groups with a higher contribution to the acrylamide intake in our study were similar to those previously published, although most of them place coffee as the main or secondary source of acrylamide [19,21,[23][24][25]. ...
Acrylamide is a probable carcinogen. Its main sources are the diet and tobacco. The association between acrylamide intake from the diet and tobacco and prostate cancer (PCa) has not been previously evaluated. We aimed to evaluate the relationship between dietary acrylamide intake and exposure to acrylamide through cigarettes and PCa risk. A population-based case–control (CAPLIFE) study was conducted, including 428 incident PCa cases and 393 controls. Smoking and dietary information, with a validated food frequency questionnaire, was collected. We calculated the amount of acrylamide from both sources, and tertiles (Ts) were created. Multivariable logistic regression and restricted cubic spline models were applied to assess the association between exposure to acrylamide and PCa risk. The median was similar for acrylamide in both dietary and smoking acrylamide among PCa cases and controls. No association was observed between dietary acrylamide intake and overall PCa risk (adjusted ORT3vsT1 = 0.90 (95% CI 0.59, 1.37)). A risk trend was observed for acrylamide exposure from cigarette smoking (p-trend = 0.032), with the highest odds in those subjects with the high exposure to acrylamide through cigarettes (adjusted ORT3vsT1 = 1.67 (95% CI 0.92, 3.04)). The restricted cubic splines suggested a linear relationship. In conclusion, acrylamide from smoking could be positively associated with PCa risk, but no association was observed for dietary acrylamide.
... The Joint FAO/WHO on Food Additives (JECFA) classified acrylamide as a genotoxic c Acrylamide, a potentially harmful chemical formed in high-temperature processes such as roasting [4], has been a significant concern in food safety due to its classification as a probable human carcinogen (Group 2A) by the International Agency for Research on Cancer (IARC) [5]. Among various food products, coffee has been identified as a notable source of dietary acrylamide exposure, contributing significantly to total intake, specifically in populations with high prevalence of coffee consumption [6][7][8]. Although extensive research has been conducted on acrylamide in European-style medium-to dark-roasted coffees, there is a scarcity of data regarding its levels in very light-roasted Arabic coffee. ...
... The EFSA suggested that the margin of exposure of acrylamide indicates a health concern for neoplastic effects based on animal evidence [7]. Coffee is an important topic in reduction in acrylamide exposure because its consumption may lead to 20-30% of total daily intake [39]. ...
This study examines the acrylamide levels in a range of roasted coffee samples from Bahrain, with a particular focus on traditionally very light roasted coffees. Acrylamide, classified as a Group 2A carcinogen by the International Agency for Research on Cancer (IARC), is formed during the roasting process as a byproduct of the reaction between amino acids and reducing sugars present in coffee beans. The acrylamide levels were quantified using the standard method EN 16618:2015, which employs liquid chromatography in combination with tandem mass spectrometry (LC-MS/MS). The results demonstrated that the acrylamide levels in very light-roasted coffee samples (646 µg/kg, n = 4), which exhibited characteristics similar to green coffee, were significantly above the European Union (EU) benchmark level for roasted coffee of 400 µg/kg. In contrast, medium-roasted coffee samples (154 µg/kg, n = 4) and dark-roasted coffee samples (62 µg/kg, n = 2) did not exceed the benchmark level. These findings indicate a potential health risk associated with the consumption of very light-roasted coffee, emphasizing the need for awareness and possible mitigation strategies to reduce acrylamide exposure in traditional Arabic coffee practices.
... The European Chemical Agency has included acrylamide in its List of Substances of Very High Concern [5]. The European Food Safety Authority (EFSA) has announced that acrylamide can react with DNA, RNA and proteins to form compounds with genotoxic and neurotoxic effects [6,7]. Different studies have reported that acrylamide intake may cause various birth defects [8][9][10], damage the peripheral, autonomic and central nervous systems [11,12], and increase the risk of developing various types of cancer in respiratory, reproductive and gastrointestinal systems [13][14][15][16][17]. ...
... In addition, other formation mechanisms called the acrolein pathway have been identified in foods [20]. The level of acrylamide in foods varies according to many factors such as the type of raw material, chemical composition of the raw material, climatic conditions, production and storage conditions, and temperature and time applied during the preparation of foods [6]. The European Commission has established benchmark levels for acrylamide in certain foods: French fries (ready-to-eat) 500 µg/kg; potato-based crisps, crackers, and other potato products 750 µg/kg; roast coffee 400 µg/kg; instant (soluble) coffee 850 µg/kg; coffee substitutes 500-4000 µg/kg; biscuits and wafers 350 µg/kg; crackers (except potato-based) 400 µg/kg; crispbread 350 µg/kg; gingerbread 800 µg/kg; soft bread 50-100 µg/kg; breakfast cereals 150-300 µg/kg; baby foods (processed cereal-based foods) 40 µg/kg; and biscuits and rusks (for infants and young children) 150 µg/kg. ...
Acrylamide is a contaminant formed during heat treatment that poses potential health risks and occurs naturally in foods. Therefore, it is crucial to evaluate exposure from the consumption of foods containing acrylamide since dietary exposure continues throughout life. In this study, the acrylamide exposure level of people living in Türkiye is estimated. Consumption of a total of 28 foods in 9 different food groups was calculated using a deterministic model under two different scenarios. The exposure levels were evaluated in terms of carcinogenic, non-carcinogenic and neurotoxic health risks. The daily total acrylamide exposure levels of individuals aged 15 and older were determined as 58 µg/day (0.85 µg/kg bw/day) and 196 µg/day (2.80 µg/kg bw/day) for the good and bad scenarios, respectively. The highest daily acrylamide exposure in the good scenario came from brewed black tea (29%), whereas French fries (50%) were the source of highest daily acrylamide exposure in the bad scenario. According to the hazard index (HI) and margin of exposure (MOE) data, the good scenario (all food) is considered safe, while the bad scenario (all food) has potential and serious health risks. According to the carcinogenic risk (CR) data, both scenarios carry significant health risks. It is therefore important that consumers, producers and official institutions collaborate and take measures to reduce acrylamide exposure.
... These substances have been shown to be genotoxic and carcinogenic to rats; thus, they are classified as 2A carcinogenic effects in humans, according to a statement released by the International Institute for Research on Cancer (IARC) [1]. Even though additional pathways have been proposed to contribute to AA production, the main formation route of AA in foods is accepted to be through Maillard reaction, and fried potato products are the greatest source of AA of the diet, according to the European Food Safety Authority (EFSA) [2]. ...
... While this study provides insights into the impact of garlic treatment on acrylamide formation, its effect on the bioavailability of acrylamide was neglected. Following oral intake, unbound AA is absorbed from the gastrointestinal tract and rapidly distributed systemically into the tissues circulation, where it is metabolized to form glycidamide (GA), the major accepted route for its genotoxic and carcinogenic profile [2]; thus, it is of great importance to decrease the bioavailability of acrylamide. Martinez et al. observed the bioaccessibility of acrylamide and found that, specifically during the gastric phase of the digestion, newly generated small peptide chains and some amino acid residues such as cysteine and lysine, all related to the action of pepsin, have the ability to interact with acrylamide and form adducts, resulting in a decreased level of acrylamide absorption [54]. ...
Fried potato products are the largest dietary source of acrylamide, a potential carcinogen formed at high temperatures. Previous studies suggested that garlic powder could decrease the development of acrylamide; however, there has not been much focus on the effect of garlic extract. The aim of this study was to investigate the effect of garlic extract exposure on the development of acrylamide in French fries in popular home cooking techniques such as pan-frying, air-frying, and oven-frying. Initially, the antioxidative profile, total phenolic content, and chlorogenic acid content of garlic were analyzed. Subsequently, potatoes were treated with garlic extract and fried using pan-frying, air-frying, and oven-frying techniques. Acrylamide levels were then quantified through HPLC and compared to control groups. The findings showed that garlic exposure increased the acrylamide formation in French fries obtained with air-frying (311.95 ± 0.5 μg/kg) and with oven-frying (270.32 ± 23.4 μg/kg) (p < 0.005 *). This study offers new insights into varying acrylamide formation levels in domestic practices. Unlike previous studies, this study is the first to question the effect of aqueous garlic extract exposure. Further research is required to comprehend the interaction between garlic exposure and acrylamide formation in household settings.
... The collected data has been scrutinized and presented in a series of published reports (CONTAM Panel, 2015; EFSA, 2009EFSA, , 2010EFSA, , 2011EFSA, , 2012EFSA, , 2015. In the study report (CONTAM Panel, 2015) shows that, selected foods (vegetable crisps, coffee substitute, coffee/dry, potato crisps & snakes, potatoes fries, biscuits, crackers & crisp bread, breakfast cereals, roasted nuts & seeds processed cerealbased baby food, cakes and pastas, soft, bread and non-cereal baby foods). The higher AA levels were found in vegetable crisps and coffee substituents. ...
... The estimate of average daily human intake was 1 μg/kg bw/day, and it can be 4 μg/kg bw/day for high consumers. Several toxic effects of AA are summarized and described by Dilini N. Perera with collaborators (2021) Previous results of epidemiological studies on dietary acrylamide intake and cancers of the urinary tract, cancers of the gastro-intestinal tract, cancers of reproductive organs, and cancers of the respiratory tract, are presented by (CONTAM Panel, 2015). Many investigations have demonstrated that AA significantly affects a variety of physiological processes, such as the transmission of signals in peripheral nerves, the regulation of enzymatic and hormonal processes, muscular function, reproduction, and so forth. ...
Due to environmental problems from food packaging, in recent times the tendency to use different techniques for environmental protection and reducing waste from packaging has increased significantly. The main purpose of this paper is to research and assess the impact of the design of ecological packaging as a method for reducing waste from food packaging, and the impact of the ecological packaging design on consumers’ perception of purchasing food products. The research was developed in the form of a review of other researchers as well as through a survey by Google Docs., in Montenegro. The study included 300 people who participated by filling out an online questionnaire. This paper further elaborates on the research findings by comparing age groups, gender, perception of ecological packaging, consumer awareness, and the main problem that pushes consumers not to try to change their lifestyle for a cleaner environment and derives the results of analyzes that best summarize the problem and lead to its solution, especially the possibility for its solution. The tool used to analyze the answers is the IBM SPSS program, through which the statistical and graphic data for the choices of the participants in the questionnaire were obtained. This study makes diverse contributions in terms of theory, methodology, and policy-making, and with the recommendation for packaging industries to design packaging with ecological designs that stimulate the curiosity of consumers for their purchase.
Keywords: Environmental protection, food package, ecological design.
... The collected data has been scrutinized and presented in a series of published reports (CONTAM Panel, 2015; EFSA, 2009EFSA, , 2010EFSA, , 2011EFSA, , 2012EFSA, , 2015. In the study report (CONTAM Panel, 2015) shows that, selected foods (vegetable crisps, coffee substitute, coffee/dry, potato crisps & snakes, potatoes fries, biscuits, crackers & crisp bread, breakfast cereals, roasted nuts & seeds processed cerealbased baby food, cakes and pastas, soft, bread and non-cereal baby foods). The higher AA levels were found in vegetable crisps and coffee substituents. ...
... The estimate of average daily human intake was 1 μg/kg bw/day, and it can be 4 μg/kg bw/day for high consumers. Several toxic effects of AA are summarized and described by Dilini N. Perera with collaborators (2021) Previous results of epidemiological studies on dietary acrylamide intake and cancers of the urinary tract, cancers of the gastro-intestinal tract, cancers of reproductive organs, and cancers of the respiratory tract, are presented by (CONTAM Panel, 2015). Many investigations have demonstrated that AA significantly affects a variety of physiological processes, such as the transmission of signals in peripheral nerves, the regulation of enzymatic and hormonal processes, muscular function, reproduction, and so forth. ...
Acrylamide's presence in food has recently drawn considerable interest on a global
scale. One of the antecedents of acrylamide is asparagine, an amino acid that is frequently present
in both plant and animal proteins. Acrylamide is listed as a potential cause of cancer, abnormal
birth outcomes, and nerve damage in people. It appears naturally in foods that have been heated
to high degrees as a synthetic chemical. Acrylamide is generally associated to the Millard reaction,
which is prevalent in foods that mostly contain asparagine and starch, and forms during high-temperature cooking such as frying, roasting, and baking. According to the FDA, although it’s
unclear exactly what risk acrylamide poses to humans, research investigations in animals' labs
demonstrate that excessive quantities of the chemical caused cancer. Since acrylamide exposure
is so high, it's important to recognize its hazardous effects, especially in nations where people are
still mostly unaware of the danger’s acrylamide poses to their health. This article gives a summary
of relevant scientific data on the production of acrylamide, its potential health risks, and methods
for reducing it in the food industry and at home. Depending on the producer, cooking time,
temperature, and production process, different foods contain different amounts of acrylamide. To
control the manufacture and use of acrylamide, some nations have put regulations and laws into
place. For the purpose of regulating the manufacture and use of acrylamide, maximum amounts
of acrylamide in foods have been established in the USA, Europe, Japan, and Canada, and which
are expected to be updated in the coming year.
... Acrylamide is naturally formed in starchy food products during high-temperature cooking (above 120 • C), such as frying, baking, and grilling, but also in industrial processing [4]. Acrylamide is, therefore, commonly found in bread, biscuits, crackers, and chips. ...
... Acrylamide is, therefore, commonly found in bread, biscuits, crackers, and chips. European authorities such as the European Food Safety Authority (EFSA) offer some advice to reduce the production of this harmful compound at a domestic level: e.g., avoid excessive burning when frying, do not keep potatoes in the fridge to avoid an increase in sugar levels, and limit the toasting of bread [4]. ...
The Maillard reaction (MR) is one of the main reactions that occurs during the thermal processing of food. It contributes positively to the flavor, aroma, and color of food but also produces harmful by-products, including acrylamide and advanced glycation end products (AGEs). Bakery products are major staples consumed daily by people from all walks of life and of all ages; the identification of strategies to hamper acrylamide formation in bread and bread-like products is thus crucial for public health. Several strategies have been proposed to inhibit the MR in food processing, including biochemical approaches such as the use of enzymes; innovative technologies such as ohmic heating, pulsed electric field, high pressure processing, or encapsulation of metal ions; and the chemical modification of reactants, intermediates, or products of MR. Recently, phenolic compounds have been reported to have an inhibitory effect on the formation of harmful by-products resulting from the MR. The aim of this paper is, therefore, to provide a state-of-the-art overview of the use of phenolic compounds in the formulation of bakery products to inhibit the MR. A systematic review of the most up-to-date scientific literature was thus performed. It emerged that the inhibitory action was mainly investigated in bread. Phenolic extracts and powders obtained from plant-based foods have been included in the formulation of bakery products. The effect of pure phenolic standards was also considered.
... Especially, the estimated dietary intake of MGO is approximately three orders of magnitude lower than the predicted BMDL 10 values. Drawing from the European Food Safety Authority (EFSA)'s risk assessment for acrylamide, which is neurotoxic and genotoxic, this study adopted a similar MOE approach for further risk characterization for MGO 56 . Accordingly, an MOE of 100 or above for neurotoxicity endpoints including mitochondrial function, cytotoxicity, and apoptosis, was considered of no health concern. ...
This study aimed to evaluate human neurotoxicity and genotoxicity risks from dietary and endogenous methylglyoxal (MGO), utilizing physiologically based kinetic (PBK) modeling-facilitated reverse dosimetry as a new approach methodology (NAM) to extrapolate in vitro toxicity data to in vivo dose-response predictions. A human PBK model was defined based on a newly developed and evaluated mouse model enabling the translation of in vitro toxicity data for MGO from human stem cell-derived neurons and WM-266-4 melanoma cells into quantitative human in vivo toxicity data and subsequent risk assessment by the margin of exposure (MOE) approach. The results show that the MOEs resulting from daily dietary intake did not raise a concern for endpoints for neurotoxicity including mitochondrial function, cytotoxicity, and apoptosis, while those for DNA adduct formation could not exclude a concern over genotoxicity. Endogenous MGO formation, especially under diabetic conditions, resulted in MOEs that raised concern not only for genotoxicity but also for some of the neurotoxicity endpoints evaluated. Thus, the results also point to the importance of taking the endogenous levels into account in the risk assessment of MGO.
... One of the substances developed during frying is acrylamide. This substance is classified as potentially carcinogenic and genotoxic [17]. One of the theories describing acrylamide development says that water from fried products contributes to the hydrolysis of triacylglycerols, which release free fatty acids and glycerol. ...
This paper analyzed the effects of adding rice bran wax (RW) and beeswax (BW) to rapeseed oil as a deep-frying medium and the quality parameters of potato fries, including acrylamide contamination. It was found that the addition of RW and BW caused an increase in the oil’s acidity. However, oil deterioration based on peroxide values and fatty acid profiles did not differ very much from the oil without waxes. The study showed that the addition of rice bran wax at the level of 2.5 g/L of rapeseed oil was able to significantly decrease oil uptake in potato fries. The addition of waxes did not influence the color parameters in the first frying cycle; however, changes were observed later. The browning index indicated that 10 g of BW per liter may darken fries in comparison to rapeseed oil without additives. It was found that with an increase in wax content in the frying medium, potato fries contained more acrylamide.
... UPFs are often high in saturated fat, sugar, and sodium, whereas low in fiber [9], with some of these nutritional characteristics being related to diabetic microvascular complications [10][11][12]. Moreover, food processing can result in potentially toxic compounds (e.g., acrylamide) [13]. Additionally, the contaminants (e.g., bisphenols), which can migrate from contact packaging to UPFs, may also exacerbate the progression of diabetic microvascular complications [14]. ...
... Los metabolitos alterados se relacionaron con distintas vías metabólicas, comenzado con las relacionadas directamente con regulación del estrés oxidativo, en donde se incrementaron la linoleil-carnitina, la cervonilcarnitina y la estearidonil-carnitina; la vía del metabolismo del colesterol también se vio afectada, se detectó un incremento en los niveles de ácidos biliares tales como el ácido tauro-b-muricólico y ácido taurodeoxicólico; la alteración en la vía del metabolismo de los esfingolípidos, se puse de manifiesto en los niveles de esfingosina 1-fosfato (comúnmente identificada como marcador de funcionamiento hepático); la vía del metabolismo de los glicerofosfolípidos, y de oxidación de ácidos grasos también presentando alteraciones. Autofagia Los estudios relacionados a las alteraciones provocadas por la exposición de AA sobre procesos de autofagia son pocos; este mecanismo ha sido estudiado en células de tejido óseo (células U2OS) y en tejido nervioso, sin embargo, en el presente trabajo solo se encontró un documento que aborda autofagia en hígado, este estudio fue realizado en ratas Wistar gestantes sometidas a exposición a AA durante 5,10 y 15 días (3 mg/kg por vía oral).Tras finalizar el experimento, fue posible observar en los productos cambios en biomarcadores relacionados con autofagia y muerte celular programada en hígado tales como LC3B y Beclina-1, así como aumento en la actividad de caspasa 3. (Tomaszewska et al., 2022) Discusión La AA es un compuesto comprobado como neurotóxico y probable carcinógeno, al cual se le ha asociado con efectos tóxicos generados en hígado, riñón y sistema reproductor (Benford et al., 2015). En la actualidad los trabajos dedicados a evaluar exclusivamente la hepatotoxicidad asociada a la exposición a AA son escasos, sin embargo, estos estudios presentados en el presente documento abordan varios mecanismos implicados en la generación de la toxicidad, así como manifestaciones observables que evidencian el daño. ...
RESUMEN Introducción: La acrilamida es un compuesto tóxico que puede formarse en alimentos preparados a altas temperaturas, en exposición crónica provoca neurotoxicidad, genotoxicidad, y puede ser carcinógena. El hígado es el principal encargado de su metabolismo, la acrilamida y sus metabolitos pueden producir daños e inflamación crónica hepática que pueden desencadenar patologías graves. Objetivo: Analizar la información más reciente con relación a la hepatotoxicidad asociada a la ingesta de acrilamida. Material y Método: Se realizó una revisión hemerográfica en PubMed, ScienceDirect y Google Académico, utilizando términos MeSH: liver, toxicity, acrylamide, oxidative stress, Wistar Rat y Booleanos: "and", "or", "not" considerando artículos a partir del 2018, seleccionando los que describieran en su contenido datos relacionados las palabras clave. Resultados: La hepatotoxicidad por exposición a acrilamida está relacionada a alteraciones de biomarcadores de estrés oxidativo, cambios en metabolómica y en procesos de autofagia, activación del inflamasoma, y modificaciones estereológicas e histológicas. Conclusión: La información actualizada demuestra que a la hepatotoxicidad asociada a acrilamida le subyacen diversos mecanismos celulares en los que generalmente está involucrado el estrés oxidativo, por ello el abordaje de estrategias para entender y disminuir el impacto de la exposición debe considerar dichos aspectos. ABSTRACT Introduction: Acrylamide is a toxic compound that can be formed in foods prepared at high temperatures; chronic exposure to it causes neurotoxicity, genotoxicity, and it is consider as a potential carcinogenic. Liver is the main organ that metabolizes acrylamide and there, acrylamide and its metabolites can cause damage and chronic inflammation that might trigger serious pathologies. Objective: To analyze the most recent information regarding hepatotoxicity associated with the ingestion of acrylamide. Material and method: A journal search was conducted in PubMed, ScienceDirect and Google Scholar, using MeSH terms: liver, toxicity, acrylamide, oxidative stress, Wistar Rat and Booleans: "and", "or", "not", and considering articles from 2018, selecting those that described in its content data related keywords. Results: Hepatotoxicity due to exposure to acrylamide is related to alterations in oxidative stress biomarkers, changes in metabolomics and autophagy processes, inflammasome activation, and stereological and histological modifications. Conclusion: The updated information in the available literature demonstrates that hepatotoxicity associated with acrylamide consumption is underlain by various cellular mechanisms in which oxidative stress is generally involved, therefore the approach to develop strategies to understand and reduce the impact of exposure must consider these aspects.
... Los metabolitos alterados se relacionaron con distintas vías metabólicas, comenzado con las relacionadas directamente con regulación del estrés oxidativo, en donde se incrementaron la linoleil-carnitina, la cervonilcarnitina y la estearidonil-carnitina; la vía del metabolismo del colesterol también se vio afectada, se detectó un incremento en los niveles de ácidos biliares tales como el ácido tauro-b-muricólico y ácido taurodeoxicólico; la alteración en la vía del metabolismo de los esfingolípidos, se puse de manifiesto en los niveles de esfingosina 1-fosfato (comúnmente identificada como marcador de funcionamiento hepático); la vía del metabolismo de los glicerofosfolípidos, y de oxidación de ácidos grasos también presentando alteraciones. Autofagia Los estudios relacionados a las alteraciones provocadas por la exposición de AA sobre procesos de autofagia son pocos; este mecanismo ha sido estudiado en células de tejido óseo (células U2OS) y en tejido nervioso, sin embargo, en el presente trabajo solo se encontró un documento que aborda autofagia en hígado, este estudio fue realizado en ratas Wistar gestantes sometidas a exposición a AA durante 5,10 y 15 días (3 mg/kg por vía oral).Tras finalizar el experimento, fue posible observar en los productos cambios en biomarcadores relacionados con autofagia y muerte celular programada en hígado tales como LC3B y Beclina-1, así como aumento en la actividad de caspasa 3. (Tomaszewska et al., 2022) Discusión La AA es un compuesto comprobado como neurotóxico y probable carcinógeno, al cual se le ha asociado con efectos tóxicos generados en hígado, riñón y sistema reproductor (Benford et al., 2015). En la actualidad los trabajos dedicados a evaluar exclusivamente la hepatotoxicidad asociada a la exposición a AA son escasos, sin embargo, estos estudios presentados en el presente documento abordan varios mecanismos implicados en la generación de la toxicidad, así como manifestaciones observables que evidencian el daño. ...
Introducción: La acrilamida es un compuesto tóxico que puede formarse en alimentos preparados a altas temperaturas, en exposición crónica provoca neurotoxicidad, genotoxicidad, y puede ser carcinógena. El hígado es el principal encargado de su metabolismo, la acrilamida y sus metabolitos pueden producir daños e inflamación crónica hepática que pueden desencadenar patologías graves. Objetivo: Analizar la información más reciente con relación a la hepatotoxicidad asociada a la ingesta de acrilamida. Material y Método: Se realizó una revisión hemerográfica en PubMed, ScienceDirect y Google Académico, utilizando términos MeSH: liver, toxicity, acrylamide, oxidative stress, Wistar Rat y Booleanos: “and”, “or”, “not” considerando artículos a partir del 2018, seleccionando los que describieran en su contenido datos relacionados las palabras clave. Resultados: La hepatotoxicidad por exposición a acrilamida está relacionada a alteraciones de biomarcadores de estrés oxidativo, cambios en metabolómica y en procesos de autofagia, activación del inflamasoma, y modificaciones estereológicas e histológicas. Conclusión: La información actualizada demuestra que a la hepatotoxicidad asociada a acrilamida le subyacen diversos mecanismos celulares en los que generalmente está involucrado el estrés oxidativo, por ello el abordaje de estrategias para entender y disminuir el impacto de la exposición debe considerar dichos aspectos.
... Many studies have linked deep fat frying to health issues like diabetes, cancer, coronary heart disease, and hypertension (Sun et al., 2019;Verma, Singh, & Yadav, 2019), the reason being that cooking causes chemical reactions that produce toxic substances called thermal process contaminants (Mogol & Gokmen, 2016). Foods high in carbohydrates, such as French fries, coffee, and cereal-based items, are the primary sources of acrylamide (AA) in the diet (EFSA, 2015). AA is generated in foodstuff when exposed to temperatures ranging from 120 − 170 • C. Asparagine, an amino acid present in the food, may react with any carbonyl group, such as reducing sugars, hydroxycarbonyls, dicarbonyls, alkadienals, 5-hydroxymethylfurfural (HMF) to produce AA, but α-hydroxy carbonyls form of reducing sugars, make much more AA. ...
... Acrylamide (2-propenamide) (ACR) is an organic pollutant that poses significant hazards to human and animal health, garnering widespread attention from both the public and scientific communities [17]. Its production and presence in various systems, including food and the environment, have raised concerns [18]. The discharge of ACR from industrial processes and laboratories can lead to substantial environmental pollution [19]. ...
In the modern era, there is a growing trend in drinking coffee, and this trend is attributed to the perceived beneficial effects of coffee on human health. Despite several health benefits of coffee, the presence of various contaminations can potentially make it harmful. Employing rapid and precise analytical methods is crucial to guarantee the safety of coffee and to detect any detrimental contaminations that might pose a risk to human health. Although substantial advancements in analytical methodologies led to the development of many sensing platforms in the analysis of coffee safety, some limitations can restrict their application. Interestingly, recent progress in biosensor technology presents a high potential detection approach for addressing limitations of conventional methods. Especially, the progress of nanotechnology introduces several nanomaterials with specific properties that can be used in the structure of biosensors. This review aims to explore the latest development of biosensors in the analysis of coffee safety based on detection of chemical pollutants including mycotoxins, heavy metals, and processing chemicals. In addition, the importance of different nanomaterials and biological elements is discussed for introducing high performance biosensing. The commercial feasibility of developed biosensors is investigated for quantification of contamination in coffee.
... This confirms the inverse relationship between the AA content and coffee roasting [76]. These results are consistent with those of an EFSA report, which found that light coffee roasts have a high acrylamide content because the AA content decreases as the roasting process continues [77]. ...
Approximately 8 million tons of dates (Phoenix dactylifera) are produced globally each year. The seeds of the fruit, which make up 10–15% of its weight, are typically discarded. Date seed coffee is a sustainable food system innovation rooted in the traditions of high date-producing regions. Dating back to the late 19th century, date seed coffee has evolved from a historical coffee substitute to a modern caffeine-free alternative. Date seed coffee has a long history of consumption in the European Union (EU). This indicates that it may not require novel food authorization. The composition of date seeds is evaluated in this review and a toxicological risk assessment for date seed coffee is conducted. Subchronic studies show that consuming date seed or date seed coffee has no adverse effects. Therefore, currently unavailable chronic toxicity, carcinogenicity, and reproductive toxicity studies may be unnecessary. However, for a comprehensive evaluation, it is recommended to conduct an in vitro mutagenicity test. This review provides information on the safety of date seed coffee and highlights the need for further research.
... Köppen et al. [16] analysed 140 samples (chocolates with various levels of cocoa and cocoa powders) sourced from German retail markets, and measured acrylamide levels of 9-1747 µg/kg. The EU database for acrylamide [17] records a mean acrylamide level of 178 µg/kg for 13 cocoa powder samples. Finally, Raters and Matissek [18] analysed commercial semi-finished cocoa products (cocoa beans, nibs, powder, masses and cocoa butter) and found acrylamide in 97% of the samples examined, with 61% presenting acrylamide levels ranging from 101 to 400 µg/kg. ...
The present study was conducted to determine and analyse the content of furosine, acrylamide and furan in fermented cocoa beans from the Chuao (“criollo variety”) and Barlovento (“trinitario variety”) regions of Venezuela, after roasting (in the shell at 110–180 °C for 15–60 min) and alkalisation (with sodium bicarbonate or potassium carbonate, at concentrations of 10–25 g/kg in order to evaluate the impact of these operations. The highest furosine contents (up to 249 mg/100 g of protein) were found in fermented, sun-dried samples, and were higher in the nibs than in the shells. The acrylamide content increased in line with the temperature, to 160 °C in the shells, and to 180 °C in the nibs. At temperatures of up to 140 °C, the acrylamide content was higher in the shells than in the nibs. The furan content increased in line with the temperature and in this case too, was greater in the shells. The content of both furosine and furan decreased with alkalisation, while the presence of acrylamide was irregular and determined by the roasting temperature and the alkalising agent employed. Although the furosine, acrylamide and furan contents varied between the beans from the two regions and the varieties considered (Chuao and Barlovento), these three compounds were correlated to a statistically significant degree.
Asthma is a common, multifactorial chronic disease with a major impact on children and adolescents. Exposure to food contaminants is one of the contributing factors to asthma. This study aims to evaluate the intake and exposure of different contaminants and explore their association with childhood asthma.
The Childhood Asthma and Environment Research study evaluated Italian children aged 5–14 years, divided into control and asthma case groups. Dietary habits were recorded, and exposure to 11 food contaminants was estimated with the CONT11 database. The study included 428 children, 264 with asthma and 164 without.
The findings of this study were consistent with those reported in other studies, indicating that exposure to nitrates and acrylamide was significantly higher in asthmatic children. The results suggest that exposure to certain contaminants could have a more pronounced effect on asthmatic children.
The study demonstrates the importance of tools such as CONT11 in assessing food safety. Furthermore, it reinforces the need to prevent and reduce exposure to food contaminants to minimize health risks.
The present study evaluated the physicochemical parameters, polyphenolics content, levels of heat-induced compounds (acrylamide, furfural, 5-hydroxymethylfurfural), antioxidant properties, as well as sensory quality of shortbread cookies enriched with dried sea buckthorn fruit (SBF). The SBF-enriched cookies were prepared by replacing 1, 2, 3, or 5% of the flour with dried sea buckthorn fruit. Our results showed the presence of 12 phenolic acids and 5 flavonoids in the SBF, while two phenolic acids and two flavonoids were detected in the cookies. Most of the compounds were identified in the cookies enriched with 5% SBF. Among the phenolic acids, benzoic acid was the most abundant, while among the flavonoids, quercetin was the most abundant. 5-hydroxymethylofurfural was not detected in any cookies, and the addition of SBF contributed to the presence of furfural in baked products and increased the amount of acrylamide, and their content increased with the amount of SBF addition. The addition of sea buckthorn fruit at 5% distinctly exceeded the benchmark level of acrylamide in the cookies and worsened their sensory quality. It should also be noted that SBF significantly (p < 0.05) improved the antioxidant potential determined by two tests, ABTS and DPPH. The SBF-enriched cookies were characterized by significantly higher values of crispness and browning index compared to the control cookies. The results of the study indicate that SBF can be successfully used as a component of bakery products. In conclusion, the cookies with SBF can show improved technological and functional properties and constitute an added value bakery product that could provide health benefits.
Introducción: Una de las bebidas más consumidas a nivel mundial es el café, por su sabor, aroma y sus propiedades estimulantes. Estas propiedades organolépticas se deben a los compuestos que se forman durante el tueste. En procesos térmicos también se forman productos como acrilamida, contaminante del proceso, y con riesgo para salud. Metodología: Granos verdes de cafe arábigo de variedad Catuaí de dos tipos, pergamino y almendra, fueron procesados. Se obtuvieron tres grados de tueste y tres granulometrias. Para cuantificación de la acrialmida se seleccionó el café de mayor aceptación organoleptica por los consumidores al realizar el análisis sensorial. Resultados: Parámetros morfológicos para el tipo almendra resultaron ser superiores en diámetro ecuatorial (7,0±0,06 mm) y en peso (173,6±21,55 mg) que para el tipo pergamino. Acrilamida cuantificada en infusiones de café tipo almendra por GC-ECD arrojo un valor promedio de 20 mg/kg. Discusión: Parámetros morfológicos son indicadores de calidad de granos, siendo esenciales en la operación de equipos; los fisicoquimicos se relacionan con calidad organoléptica. Análisis sensorial mostro preferencia por tueste oscuro. Conclusiones: Resultados corroboran que concentración de acrilamida en bebida de café arábigo de variedad Catuaí tipo almendra no supera niveles máximos permitidos y no se ve influenciada por tamaño de la partícula.
The consumption of harmful substances, including environmental pollutants, endocrine disruptors, and certain food additives, has the potential to compromise food safety and the consumption of safe food, which are fundamental dynamics for society. Furthermore, it can pose a risk to health. This book, entitled Food Safety, aims to assist consumers in developing an awareness of healthy and safe food consumption, beginning with an understanding of the fundamental concepts of food safety, providing e_ective information for the prevention of foodborne diseases, and elucidating the possible e_ects on health. Furthermore, the book addresses contemporary concerns such as food terrorism, packaging safety, and the use of preservatives. Emphasizing food safety from a health perspective, this book is a vital reference for industry professionals, academics, and health professionals. By integrating current research _ndings and real-world examples, the book furnishes readers with a robust foundation of knowledge while raising awareness of food safety. Covering a wide range of food safety issues, this book is a comprehensive resource for anyone working in food toxicology.
Deep-fried foods are popular for their aroma, color, texture, and flavor but can form potentially toxic compounds like 5-hydroxymethylfurfural, polycyclic aromatic hydrocarbons, acrylamide, heterocyclic amines, trans fatty acids, and advanced glycation end products. Frequent consumption of these compounds can increase the risk of chronic conditions such as obesity, diabetes, heart disease, stroke, and certain cancers by exacerbating oxidative stress, inflammation, and tissue damage. Ensuring the safety of deep-fried foods and minimizing contaminants is crucial. Edible coatings, especially those with antioxidants, show promise in enhancing the quality and safety of fried foods. This review examines the chemistry of toxic compounds in deep-fried meat, discusses mitigation strategies, and evaluates novel technologies like gel-based coatings. These coatings, particularly protein-based ones, can reduce Maillard reaction products by competing with amino acids in meat, thus preserving quality and minimizing harmful compound formation.
The main focus of the study was to evaluate the level of knowledge, practices, and policies of potato-based product, manufacturers in Bangladesh regarding food safety and quality issues, particularly acrylamide, a probable human carcinogenic compound formed in potato-based products during heat processing. Among twenty-one processed potato product manufacturers, only fifteen were found interested in participating in this study. A pre-developed questionnaire was used to collect data from the respondents and descriptive statistical measures were used for data analysis. The results revealed that most of the manufacturers are not aware of the Maillard reaction (60%) and acrylamide formation (53.3%) during potato processing. Although the manufacturers are familiar with reducing sugar (80%) and amino acids (73.3%), they were unaware that these are acrylamide precursors that must be quantified before potato processing. Most of the manufacturers (83.3%) prefer 150-200°C temperature for frying and the remaining (16.7%) use above 200°C. However, no manufacturers performed acrylamide analysis as they didn’t have any standard policy. Only 16.7% of manufacturers adopted the mitigation strategy for acrylamide reduction. Additionally, almost 58.3% of manufacturers are not aware of the international trade barrier on the export of potato products based on the acrylamide level. There has been a crucial demand for further research on revising and updating the food safety policies and practices during the processing of potatoes to safeguard the health of the consumers by relevant regulatory bodies in Bangladesh for acrylamide to get on with the latest industrial and technological innovations along with skill developing training to remove the trade barrier on export.
This study investigated the effects of various characteristic components of tea—theaflavins, catechins, thearubigins, theasinensins, theanine, catechin (C), catechin gallate (CG), epicatechin (EC), epicatechin gallate (ECG), epigallocatechin (EGC), epigallocatechin gallate (EGCG), gallocatechin (GC), and gallocatechin gallate (GCG)—on acrylamide formation. The results revealed that most of tea’s characteristic components could significantly eliminate acrylamide, ranked from highest to lowest as follows: GC (55.73%) > EC (46.31%) > theaflavins (44.91%) > CG (40.73%) > thearubigins (37.36%) > ECG (37.03%) > EGCG (27.37%) > theabrownine (22.54%) > GCG (16.21%) > catechins (10.14%) > C (7.48%). Synergistic elimination effects were observed with thearubigins + EC + GC + CG, thearubigins + EC + CG, thearubigins + EC + GC, theaflavins + GC + CG, and thearubigins + theaflavins, with the reduction rates being 73.99%, 72.67%, 67.62%, 71.03%, and 65.74%, respectively. Tea’s components reduced the numbers of persistent free radicals to prevent acrylamide formation in the model system. The results provide a theoretical basis for the development of low-acrylamide foods and the application of tea resources in the food industry.
To investigate the impact of extrusion parameters on the formation of Nε-(carboxymethyl)lysine (CML), Nε-(carboxyethyl)lysine (CEL) and acrylamide in plant-based meat analogues (PBMAs), the content changes and the correlations of compounds related to their formation were studied. The extrusion promoted CML, CEL and acrylamide formation, with more CEL being formed than CML. Variations in the moisture level and barrel temperature exerted a greater influence on the CML, CEL, acrylamide and α-dicarbonyl compounds than the screw speed and the feed rate. An increase in the moisture content led to a decrease in the CEL content, whereas it enhanced CML formation. The impact of moisture on acrylamide formation varied depending on whether low- or high-moisture extrusion was applied. Elevated temperatures promoted the accumulation of CEL, methylglyoxal and 2,3-butanedione while diminishing the accumulation of CML, acrylamide, glyoxal and 3-deoxyglucosone. CML and CEL were positively correlated with glyoxal and methylglyoxal, respectively. CEL and methylglyoxal were negatively correlated with protein and water content, whereas CML, glyoxal and 3-deoxyglucosone displayed positive correlations. In summary, higher moisture levels and feed rates and lower screw speeds and barrel temperatures are advantageous for producing PBMAs with lower CEL and total advanced glycation end-products contents, while lower or higher moisture contents, a lower feed rate and a higher barrel temperature are beneficial to reducing the acrylamide content.
Thermal treatment of food can lead to the formation of potentially harmful chemicals, known as process contaminants. These are adventitious contaminants that are formed in food during processing and preparation. Various food processing techniques, such as heating, drying, grilling, and fermentation, can generate hazardous chemicals such as acrylamide (AA), advanced glycation end products (AGEs), heterocyclic aromatic amines (HAAs), furan, polycyclic aromatic hydrocarbons (PAHs), N-nitroso compounds (NOCs), monochloropropane diols (MCPD) and their esters (MCPDE) which can be detrimental to human health. Despite efforts to prevent the formation of these compounds during processing, eliminating them is often challenging due to their unknown formation mechanisms. It is critical to identify the potential harm to human health in processed food and understand the mechanisms by which harmful compounds form during processing, as prolonged exposure to these toxic compounds can lead to health problems. Various mitigation strategies, such as the use of diverse pre- and post-processing treatments, product reformulation, additives, variable process conditions, and novel integrated processing techniques, have been proposed to control these food hazards. In this review, we summarize the formation and occurrence, the potential for harm to human health produced by process contaminants in food, and potential mitigation strategies to minimize their impact.
Southern Chile native potatoes are an interesting raw material to produce novel snacks like colored potato chips. These novel products should be comprehensively evaluated for the presence of undesirable compounds such as acrylamide, 5-hydroxymethylfurfural and furan, the main neoformed contaminants in starchy rich fried foods. This study evaluated the neoformed contaminant levels and oil content on chips made from eleven Chilean potato accessions and compared them with commercial samples. The neoformed contaminant contents were related to Maillard reaction precursor levels (reducing sugars and asparagine) and secondary metabolites (phenolic compounds and carotenoids). Neoformed contaminants correlated well among them and were weakly correlated with reducing sugars and asparagine. Acrylamide level in native potato chips ranged from 738.2 to 1998.6 μ g kg 1 while from 592.6 to 2390.5 μ g kg 1 in commercial samples. Thus, there is need to implement neoformed contaminant mitigation strategies at different steps of the production chain of colored potato chips
Changing eating habits and an increase in consumption of thermally processed products have increased the risk of the harmful impact of chemical substances in food on consumer health. A 2002 report by the Swedish National Food Administration and scientists at Stockholm University on the formation of acrylamide in food products during frying, baking and grilling contributed to an increase in scientific interest in the subject. Acrylamide is a product of Maillard’s reaction, which is a non-enzymatic chemical reaction between reducing sugars and amino acids that takes place during thermal processing. The research conducted over the past 20 years has shown that consumption of acrylamide-containing products leads to disorders in human and animal organisms. The gastrointestinal tract is a complex regulatory system that determines the transport, grinding, and mixing of food, secretion of digestive juices, blood flow, growth and differentiation of tissues, and their protection. As the main route of acrylamide absorption from food, it is directly exposed to the harmful effects of acrylamide and its metabolite—glycidamide. Despite numerous studies on the effect of acrylamide on the digestive tract, no comprehensive analysis of the impact of this compound on the morphology, innervation, and secretory functions of the digestive system has been made so far. Acrylamide present in food products modifies the intestine morphology and the activity of intestinal enzymes, disrupts enteric nervous system function, affects the gut microbiome, and increases apoptosis, leading to gastrointestinal tract dysfunction. It has also been demonstrated that it interacts with other substances in food in the intestines, which increases its toxicity. This paper summarises the current knowledge of the impact of acrylamide on the gastrointestinal tract, including the enteric nervous system, and refers to strategies aimed at reducing its toxic effect.
Blood samples (n = 600) from participants in the Swedish dietary survey Riksmaten Adolescents 2016–17 were analyzed with respect to hemoglobin (Hb) adducts from acrylamide (AA) and its metabolite glycidamide (GA) as biomarkers of internal dose/exposure. The results are presented from statistical analyses of food consumption data (2-day dietary recall and questionnaires) and measured Hb adduct levels. The estimated exposure as well as consumption data were examined in relation to non-dietary factors such as sex, age (group medians of 12, 15, and 18 years), place of residence (urban/rural), smoking status, and parental education level. The median AA adduct level was estimated to be 34 pmol/g Hb (range 14–225). No significant difference was found for place of residence, parental education, sex, or age. A significant difference was found between the median adduct levels of daily smokers (n = 8) and never smokers (n = 323) in the older age groups, but not between occasional smokers (n = 47) and never smokers. The median differences between daily smokers and never smokers were 76, 40, and 128 pmol/g Hb for AA, GA, and AA + GA, respectively. The median AA intake for the whole group of adolescents, as estimated from dietary recall data combined with reported concentrations in food, was 0.40 μg/kg bw/day. The corresponding median intake estimated from measured Hb adduct levels of AA was 0.20 μg/kg bw/day. A significant, although low, positive Spearman correlation was found between the two intake estimates (p-value = 8 × 10⁻³; ρ = 0.11). From the estimated intake of AA from food frequency questionnaires, significance was found for the 15-year-old children with higher AA adduct levels observed at higher consumption frequencies of fried potatoes/French fries. AA is considered a genotoxic carcinogen. For the estimated intake of AA for any age group and method (dietary recall or AA adduct), both a calculated margin of exposure as well as lifetime quantitative cancer risk estimates indicate health concern. A future study on food consumption designed with respect to AA exposure would provide a better understanding of the correlation between consumption and exposure and should give a more reliable estimate of the contribution of dietary AA to the overall cancer risk.
In der EU-Acrylamid-Verordnung VO (EU) 2158/2017 sind Minimierungsmaßnahmen und Richtwerte festgelegt, die den Gehalt des gesundheitlich bedenklichen Prozesskontaminanten Acrylamid in Lebensmitteln soweit wie möglich verringern sollen. Seit dem Inkrafttreten der Verordnung im Jahr 2018 hat das CVUA Stuttgart den Acrylamid-Gehalt in mehr als 2000 Lebensmitteln untersucht. Die in der EU-Acrylamid-Verordnung geregelten Lebensmittelgruppen halten die vorgegebenen Richtwerte in der Regel gut ein. Jedoch finden sich zum Teil sehr hohe Acrylamid-Gehalte in Lebensmitteln, für die bislang noch kein Richtwert festgelegt wurde, wie zum Beispiel in Süßkartoffelpommes, Gemüsechips oder Oliven. Im Beitrag "5 Jahre EU-Acrylamid-Verordnung - Alles gut?" werden die Ergebnisse des CVUA Stuttgart dargestellt und diskutiert.
URL: https://www.ua-bw.de/pub/beitrag.asp?subid=1&Thema_ID=2&ID=3941
The urinary mercapturic acids N-acetyl-S-(2-carbamoylethyl)-L-cysteine (AAMA) and N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine (GAMA) are short-term biomarkers of exposure from acrylamide and its metabolite glycidamide, respectively. The medium-term exposure to acrylamide and glycidamide is monitored by the adducts N-(2-carbamoylethyl)-Val (AA-Val) and N-(2-carbamoyl-2-hydroxyethyl)-Val (GA-Val) in hemoglobin (Hb), respectively. Three questions were addressed by application of these biomarkers in two diet studies including 36 omnivores, 36 vegans and 16 strict raw food eaters (abstaining from any warmed or heated food for at least four months): first, what is the internal acrylamide exposure following a vegan or a raw food diet in comparison to that in omnivores? Second, did the exposure change between 2017 and 2021? And third, what is the stability over time of AAMA/GAMA excretion compared to that of AA-Val/GA-Val levels in Hb between both time points? Median urinary AAMA excretion per day in non-smoking omnivores, vegans and raw food eaters were 62.4, 85.4 and 15.4 µg/day, respectively; the corresponding median AA-Val levels were 27.7, 39.7 and 13.3 pmol/g Hb, respectively. Median levels in strict raw food eaters were about 25% (AAMA excretion) and 48% (AA-Val) of those in omnivores. In comparison to 2017, AAMA and GAMA excretion levels were hardly altered in 2021, however, levels of AA-Val and GA-Val in 2021 slightly increased. There was a weak correlation between AAMA excretion levels determined four years apart (rS = 0.30), and a moderate correlation between levels of AA-Val (rS = 0.55) in this timeframe. Our data in strict raw food eaters confirm a significant endogenous formation to acrylamide in a size range, which is—based on the levels of AA-Val—distinctly higher than reported previously based on levels of urinary AAMA excretion. The relatively lower AAMA excretion in raw food eaters likely represents a lower extent of glutathione conjugation due to missing hepatic first-pass metabolism in case of endogenous formation of acrylamide, which leads to a higher systemic exposure.
Supplementary Information
The online version contains supplementary material available at 10.1007/s00204-024-03798-z.
Acrylamide (AA) is formed in foods due to thermal processes. AA was analysed in 230 foods in the first German Total Diet Study and the highest mean levels of AA were found in vegetable crisps (1430 μg/kg), followed by potato pancakes (558) μg/kg) and pan-fried potatoes (450 μg/kg). In various foods, e.g. French fries and sweet potatoes, AA was also tested for different browning degrees and cooking methods. French fries cooked to a browning degree of 3 in all cooking methods exceeded the benchmark level set by the European Union. French fries prepared in the oven and sweet potatoes in the air fryer had the lowest AA levels. In foods from the German market, AA was found also in foods such as popcorn (243 μg/kg), salty sticks (190 μg/kg), and dark chocolate (130 μg/kg). Levels of AA found in our study may support future dietary exposure and food safety assessments.
High levels of food processing can have detrimental health effects independent of nutrient content. Experts and advocates have proposed adding information about food processing status to front-of-package labeling schemes, which currently exclusively focus on nutrient content. How consumers would perceive “ultraprocessed” labels has not yet been examined. To address this gap, we conducted a within-subjects online experiment with a convenience sample of 600 US adults. Participants viewed a product under three labeling conditions (control, “ultraprocessed” label, and “ultraprocessed” plus “high in sugar” label) in random order for a single product. The “ultraprocessed” label led participants to report thinking more about the risks of eating the product and discouraging them from wanting to buy the product more than the control, despite not grabbing more attention than the control. The “ultraprocessed” plus “high in sugar” labels grabbed more attention, led participants to think more about the risks of eating the product, and discouraged them from wanting to buy the product more than the “ultraprocessed” label alone. “Ultraprocessed” labels may constitute promising messages that could work in tandem with nutrient labels, and further research should examine how they would influence consumers’ actual intentions and behaviors.
Acrylamide (AA) is a potential neurotoxic chemical used widely in numerous large-scale industries and molecular research labs. It is a common toxic contaminant in potato and grain-based food products prepared at high temperatures. AA has received serious attention due to the cumulative toxic level exposure to the human population regularly through dietary, environmental, and cosmetics routes other than just occupational exposure. AA is a well-characterized neurotoxin in many rodents and human studies; however mechanistic pathway lacks detailed characterization. Putatively, AA exerts its neurotoxic effects primarily mediated by terminal nerve damage due to inhibition of neurotransmission upon formation of irreversible AA-neuronal protein adducts. Other potential contributors to the AA-induced neuropathological alterations involve an imbalance in redox potential in neuronal cells, inhibition of kinesin-based axonal transport, increased neuronal apoptosis, degenerative changes in cholinergic and dopaminergic neurons, and hyperphosphorylation of Tau. These neurological alterations substantiate the prognosis of the pathological development of severe neurodegenerative diseases. This review summarizes the possible advances in understanding the neuropathological mechanisms of AA-induced neurotoxicity and its clinical implications. Furthermore, we also discuss the potential therapeutic and mitigation strategies to counter the severe toxic health implications of AA.
We review the undertaking of a field trial of low asparagine wheat lines in which the asparagine synthetase gene, TaASN2, has been knocked out using CRISPR/Cas9. The field trial was undertaken in 2021–2022 and represented the first field release of genome edited wheat in Europe. The year of the field trial and the period since have seen rapid changes in the regulations covering both the field release and commercialisation of genome edited crops in the UK. These historic developments are reviewed in detail. Free asparagine is the precursor for acrylamide formation during high-temperature cooking and processing of grains, tubers, storage roots, beans and other crop products. Consequently, work on reducing the free asparagine concentration of wheat and other cereal grains, as well as the tubers, beans and storage roots of other crops, is driven by the need for food businesses to comply with current and potential future regulations on acrylamide content of foods. The topic illustrates how strategic and applied crop research is driven by regulations and also needs a supportive regulatory environment in which to thrive.
Data on nutrients, food additives, natural toxins, environmental and process-induced
contaminants in a selection of plant-based and gluten-free food products and their
meat and dairy and gluten-containing counterpart products have been mapped. The
level of the different substances has been compared.
Scientific Report of the Panel on Food Additives, Flavourings, Processing Aids, Materials
in Contact with Food, and Cosmetics of the Norwegian Scientific Committee for Food
and Environment
This study was conducted to provide data on the amount of acrylamide (AA) in 270 heat-treated carbohydrate-rich foods in Turkey, determined by gas chromatography-mass spectrometry (GC-MS). A total of 270 samples were analysed and it was found that 85% of potato chips, 80% of biscuits, 85% of cakes, 80% of bread, 80% of roasted peanuts, 80% of roasted nuts and 85% of pretzels contained AA above the limit of quantification (LOQ). Analytical results indicated that 10 corn chips samples, 4 biscuits samples, all bread samples, all wheat bread samples, 2 dried bread samples and 1 pretzel sample contained AA levels above the benchmark levels of 150, 350, 50, 50, 300 and 300 µg/kg, respectively, as set by the European Commission.
This study analysed the probabilistic risk to consumers associated with the presence of iAs, Cd, Cr, Hg, Pb, acrylamide (AA) and ochratoxin A (OTA) in instant coffee from Brazil, Colombia, Mexico and Peru. The results found iAs to be the metal with the highest concentrations (3.50 × 10−2 to 6.00 × 10−2 mg/kg), closely followed by Pb (1.70 × 10−2 to 2.70 × 10−2 mg/kg) and Cr (5.00 × 10−3 to 1.00 × 10−2 mg/kg), although these differences were not significant between countries. Cd and Hg were not detected. Focusing on AA, the concentrations ranged from 1.77 × 10−1 mg/kg (Peru) to 4.77 × 10−1 mg/kg (Brazil), while OTA ranged from 1.32 × 10−3 (Peru) to 1.77 × 10−3 mg/kg (Brazil) with significant differences between countries in both cases. As regards risk, the hazard quotient and hazard index were less than 1, meaning that the consumption of instant coffee represents a low level of concern for non-genotoxic effects. The results of the combination of margin of exposure and probability of exceedance indicated that the non-genotoxic effects of Pb, AA and OTA pose no threat. However, the probability values of suffering cancer from iAs and AA (between 1 × 10−6 and 1 × 10−4) indicated a moderate risk and that management measures should be taken.
Turkish desserts are consumed in Turkey, Middle East and some parts of Europe. This study investigates acrylamide contents of some Turkish desserts and their raw materials which are possible sources. For this aim, LC-MSMS based method was used which is simplifying sample treatment, reducing analyzing time and more reliable. Desserts are thought to have high levels of acrylamide contents due to the compositions and high cooking temperatures. In acidic condition, asparagine, which is primary substance to occurrence of acrylamide, is converted to aspartic acid so that acrylamide formation is prevented. Other factors affecting acrylamide content were oven temperature, frying oil temperature, acrylamide content of raw materials and production steps.
Aim: To evaluate the effects of acrylamide treatment on the activities of rat liver, kidney arginase activities and nitric oxide levels considering the possible induction of oxidative stress. Materials and methods: Serum aminotransferase activities, blood-urea nitrogen (BUN) and creatinine concentrations and tissue malondialdehyde (MDA), reduced glutathione (GSH), total nitrite concentrations and arginase activities were evaluated in groups. Histopathological analysis was performed. Results: Acrylamide treatment did not modulate liver and kidney serum markers. Hepatic MDA, GSH concentrations did not change whereas they were elevated in kidney tissues of high dose treated group (p<0.05). Arginase activity in gram liver tissue decreased (p<0.0001), but specific activity did not alter. Total nitrite concentrations increased in high dose treated group (p<0.05). In kidney, high dose of acrylamide treatment elevated activity and specific activity of arginase (p<0.05). No alteration was detected in total nitrite levels. Ultrastructural alterations were detected in epithelial cells of proximal tubules in kidney sections of the rats treated with high dose of acrylamide. Conclusion: Liver seems to protect itself against acrylamide toxicity whereas, kidney can be considered as a probable target tissue for acrylamide-induced oxidative stress.
Acrylamide (ACR) has broad applications in different industries. It also forms in food during heating process. Oxidative stress has a critical role in ACR-induced neurotoxicity in both in vitro and in vivo models; therefore, the aim of the current study was the evaluation of effects of thymoquinone, the main constituent of volatile oil from Nigella sativa seeds in ACR-induced neurotoxicity.
Male Wistar rats were treated with ACR (50 mg/kg IP) alone or with thymoquinone (TQ) (2.5, 5, 10 mg/kg IP) for 11 days. Two protocols were used in this study, A: in this one TQ and ACR were used simultaneously, B: Administration of TQ was started 1 week before ACR treatment and continued during exposure to ACR. At the end of the treatment, behavioral index (gait score) was examined for rats. After that, rats were sacrificed and molondialdehyde (MDA) as a marker of lipid peroxidation and glutathione (GSH) content were determined in cerebral cortex.
Exposure to ACR led to severe gait abnormalities and treatment with TQ significantly decreased abnormalities. Level of MDA was elevated in cerebral cortex after exposure to ACR while TQ treatment significantly and in a dose-dependent manner reduced lipid peroxidation. Results clearly showed that there is no significant difference between two protocols of administration of TQ.
It suggests the neuroprotective effect of TQ in this model in part, may be because of due the antioxidant activity of this natural compound.
Assessment of genotoxic properties of chemicals is mainly conducted only for single chemicals, without taking mixture genotoxic effects into consideration. The current study assessed mixture effects of the three known genotoxic chemicals, 2,4-dichlorophenoxyacetic acid (2,4-D), acrylamide (AA), and maleic hydrazide (MH), in an experiment with a fixed ratio design setup. The genotoxic effects were assessed with the single-cell gel electrophoresis assay (comet assay) for both single chemicals and the ternary mixture. The concentration ranges used were 0-1.4, 0-20, and 0-37.7 mM for 2,4-D, AA, and MH, respectively. Mixture toxicity was tested with a fixed ratio design at a 10:23:77% ratio for 2.4-D:AA:MH. Results indicated that the three chemicals yielded a synergistic mixture effect. It is not clear which mechanisms are responsible for this interaction. A few possible interactions are discussed, but further investigations including in vivo studies are needed to clarify how important these more-than-additive effects are for risk assessment.
Acrylamide is a toxic, cancer-causing, industrial chemical used primarily in the preparation of polyacrylamide, which is used principally in water and wastewater treatment and in pulp and paper processing. A significant source of dietary acrylamide is foods cooked at high temperature. Till recently, only known human health effect is neurotoxicity at relatively high doses occurring through occupational exposures. Numerous gaps in knowledge concerning the formation, dietary exposure, and potential for adverse health risks of acrylamide were identified, and the resulting recommendations called for additional research on these topics. Hence the objective of this study was to assess the effects of dietary acrylamide at different doses on tissues and blood of Wistar rats. The results showed no evidence of carcinogenic effect of acrylamide on any of the vital organs, but the main features were growth depression and pathological changes on the liver, kidneys and intestines sufficient to impose significant haematological changes. DOI: http://dx.doi.org/10.3126/ijls.v7i1.8018 International Journal of Life Sciences 7(1): 2013; 21-25
The aim of this study was to investigate serum total antioxidant status (TAS), total oxidant status (TOS) and ischemia-modified albumin (IMA) levels in long term acrylamide (ACR) given rats, compared to control rats. In total, 25 male and 25 female Wistar rats were involved in this experiment. Animals in each sex were segregated into three groups. Two of them were treatment groups and one of them was control group. Each treatment group consisted of ten animals and each control group consisted of five animals. ACR was administered to the treatment groups at 2 and 5 mg/kg/day via drinking water for 90 days. In the end of the experiment, serum samples were analyzed for IMA, TAS, TOS and albumin levels with the spectrophotometric method. Serum IMA and adjusted IMA levels were significantly higher at concentrations of 2 mg/kg and 5 mg/kg in the male rats when compared with those of the control male rats. Serum TAS levels significantly decreased at concentrations of 5 mg/kg in the male rats when compared with those of the control rats. We also observed a significant increase in the levels of serum TOS at concentrations of 5 mg/kg in the male rats. There were no significant differences between serum IMA, TAS, TOS and albumin levels at concentrations of 2 mg/kg and 5 mg/kg in the female rats. Our findings show that long term treatment with 2 mg/kg and 5 mg/kg doses of ACR led to a significant depletion of serum TAS levels and overproduction of serum TOS and IMA levels, consequently, to an increase in oxidative stress.
A new liquid chromatography-tandem mass spectrometry (LC-MS-MS) method for the analysis of acrylamide in tobacco, alternative tobacco products (wet snuff, snus, orbs, strips, and sticks), and cigarette smoke was developed and evaluated. Besides the LC-MS-MS method, two additional procedures for acrylamide analysis were also developed with the purpose of comparison. A thorough evaluation of the LC-MS-MS technique was performed for typical characteristics of an analytical method such as selectivity, precision, accuracy, range of measurable levels, robustness. The method was found perfectly fit for the analyses of acrylamide in the tobacco, tobacco products, and smoke matrix. Although not essential, the sensitivity of the method was further increased by using a concentration step on a graphitized carbon solid phase cartridge, allowing the measurement of as low as 300 pg/mL and detection of 90 pg/mL acrylamide in solution. Several tobacco samples, alternative tobacco products, and smoke from several cigarettes including commercial cigarettes from the US market, 2R4F, and 3R4F Kentucky reference cigarettes were analyzed. The levels of acrylamide in tobaccos were about 100 ng/g, or lower. The levels found in snus and one brand of wet snuff was also below 100 ng/g. A wintergreen wet snuff had about 180 ng/g, strips had about 126 ng/g and the sticks about 367 ng/g acrylamide. The cigarette smoke had levels of acrylamide around 1 μg/cig or higher.
Purpose:
Acrylamide has been associated with carcinogenicity in experimental animals, but potential health risks of dietary acrylamide intake and endometrial cancer in human are inconclusive. Thus, a meta-analysis of prospective cohort studies was conducted to provide a quantitative assessment of the association between dietary acrylamide intake and endometrial cancer risk.
Methods:
PubMed database was used to identify prospective cohort studies on dietary acrylamide intake and endometrial cancer risk published up to June 2014. Since smoking is an important source of acrylamide and is inversely associated with endometrial cancer risk, the association was examined in women who never smoked as well. Multivariable relative risks (RR) adjusting for potential confounders were combined using random effects models.
Results:
Four large prospective cohort studies were identified, which included 453,355 female participants and 2,019 endometrial cancer cases. There was no association between dietary acrylamide intake and endometrial cancer risk overall [pooled RR for high vs. low intake = 1.10; 95% confidence interval (CI) 0.91-1.34]. High acrylamide intake, however, was significantly associated with increased risk of endometrial cancer among women who never smoked (pooled RR for high vs. low intake = 1.39; 95% CI 1.09-1.77). In dose-response analyses, pooled RRs for an increase of 10 µg/day were 1.04 (95% CI 0.97-1.11) among all women and 1.11 (95% CI 1.04-1.19) among never-smoking women.
Conclusions:
Endometrial cancer risk was not associated with dietary acrylamide intake overall. Among women who never smoked, however, there was a significantly increased endometrial cancer risk in women who consumed high dietary acrylamide.
Acrylamide is an important chemical with widespread industrial and other uses in addition to generalized population exposure from certain cooked foods. Previous rat studies to assess the carcinogenic potential of acrylamide have been carried out exclusively in the Fischer 344 rat with identification of a number of tumors amongst which mesotheliomas of the tunica vaginalis is an important tumor endpoint in the classification of acrylamide as a probably human carcinogen. In a rat carcinogenicity study to determine the human relevance of mesotheliomas Wistar Han rats were exposed to 0, 0.5, 1.5, or 3.0 mg acrylamide/kg body weight/day in drinking water starting at gestation day 6. At the end of two years, mammary gland fibroadenomas in females and thyroid follicular cell tumors in both sexes were the only tumors increased in acrylamide treated rats. These tumor endpoints have rat-specific modes of action suggesting less likelihood of human cancer risk than previously estimated. This study demonstrates that tunica vaginalis mesotheliomas are strain specific and not likely of genotoxic origin
Acrylamide, classified in 1994 by IARC as 'probably carcinogenic' to humans, was discovered in 2002 in some heat-treated, carbohydrate-rich foods. The association between dietary acrylamide intake and epithelial ovarian cancer risk (EOC) has been previously studied in one case-control and three prospective cohort studies which obtained inconsistent results, and could not further examine histological subtypes other than serous EOC. The present study was carried out in the European Prospective Investigation into Cancer and Nutrition (EPIC) sub-cohort of women (n=325,006). Multivariate Cox proportional hazards models were used to assess the association between questionnaire-based acrylamide intake and EOC risk. Acrylamide was energy-adjusted using the residual method, and was evaluated both as a continuous variable (per 10µg/day) and in quintiles; when subgroups by histological EOC subtypes were analyzed, acrylamide intake was evaluated in quartiles. During a mean follow-up of 11 years, 1,191 incident EOC cases were diagnosed. At baseline, the median acrylamide intake in EPIC was 21.3 μg/day. No associations, and no evidence for a dose-response were observed between energy-adjusted acrylamide intake and EOC risk (HR10µg/day:1.02, 95%CI:0.96-1.09; HRQ5vsQ1:0.97, 95%CI:0.76-1.23). No differences were seen when invasive EOC subtypes (582 serous, 118 endometrioid, and 79 mucinous tumors) were analyzed separately. This study did not provide evidence that acrylamide intake, based on food intake questionnaires, was associated with risk for EOC in EPIC. Additional studies with more reliable estimates of exposure based on biomarkers may be needed.
The goal of this project was to assess both behavioral effect and gene expression changes induced by acrylamide neurotoxicity in rats when administered during early postnatal life. Three week old male Wistar rats were administered acrylamide daily (30 mg/kg, p.o.) for twenty one days. Neurobehavioral effects were assessed using locomotor activity, weight, hind‐limb heel splay, fore‐limb and hind‐limb grip strength. Acrylamide treatment induced significant characteristic neurotoxic symptoms: increased heel splay, decrease in grip strength, and decrease in locomotor activity. Acrylamide caused significant loss of weight gain starting at day fourteen (p<0.001) and a significant reduction in hind‐limb grip strength (p<0.001). Similarly, on day fourteen hind limb heel splay was significantly increased (p<0.01). Reduction in locomotor activity began in the treated rats on day sixteen (p<0.01). On the other hand, fore‐limb grip strength was not affected. Gene expression changes were evaluated in the cerebellum, spinal cord, and sciatic nerve of acrylamide‐treated rats. At a 2 fold cutoff, one gene was up‐regulated and fifteen genes were down‐regulated among the three tissues. RT‐PCR was conducted to validate the microarray data. The identified differentially expressed genes play a role in neuronal development, muscle contraction, and control of motor function.
Acrylamide is a monomer with established human neurotoxic actions. Public concern was lately heightened by the finding that acrylamide is formed in starch‐based foods cooked at high temperatures. However, the extent of neurotoxicity particularly in children is not understood. The primary objective of this project was to assess gene expression and translational changes induced by acrylamide in juvenile rats. Animals were administered acrylamide daily (p.o., 30 mg/kg doses, n=6) for 21 days. Neurobehavioral effects were assessed and gene expression changes were evaluated in different brain regions, spinal cord, and sciatic nerve. Quantitative RT‐PCR followed by western blot analyses were conducted. Acrylamide treatment induced significant behavioral symptoms. Gene expression changes identified differentially expressed genes that play a role in neuronal development, pain pathways, and control of motor function. Western blot analyses revealed a significant decrease ( p<0.05 ) in expression of kappa opioid receptors (KOR) in motor cortex and cerebellar tissues, while the expression was significantly increased in the sciatic nerve ( p<0.01 ). The current study revealed that acrylamide‐caused down regulation of KOR expression in motor cortex and cerebellum. Such an effect might be responsible for the enhanced pain sensation observed in animal studies as well as in workers who have high acrylamide exposure.
p>Recommendations on the monitoring of acrylamide levels in food by the European Commission (EC) were extended in 2010 (EC, 2010). The new Recommendation includes a revised categorisation of food products for monitoring purposes. This report describes the results of European acrylamide monitoring during the period from 2007 to 2010 using the revised product categorisation with 10 main food categories and an additional 26 sub-categories. Twenty-five European countries submitted a total of 13 162 acrylamide results for the four-year period including 2 200 results for the year 2010. During the monitoring period, time trends in acrylamide levels for the food categories were estimated. In 2010, middle bound mean acrylamide values ranged from 31 μg/kg for ‘other processed cereal based foods for infants and young children’ to 1 350 μg/kg for ‘coffee substitutes’. The highest 95th percentile value of 8 044 μg/kg was reported for ‘instant coffee’. The trend analysis showed only few changes in acrylamide levels from 2007 to 2010. At main food category level, a ‘common European trend’ was a decrease in acrylamide levels for ‘processed cereal based foods for infants and young children’ and an increase for ‘coffee and coffee substitutes’. As a ‘common European trend’ at sub-category level, acrylamide levels of ‘biscuits and rusks for infants and young children’ and ‘non-potato savoury snacks’ showed a decrease and an increase was seen for ‘crisp bread’. A marginal decrease was observed for the sub-category ‘other processed cereal based foods for infants and young children’ and a marginal increase was observed for ‘French fries from fresh potatoes’ as well as for ‘instant coffee’. Although only applicable from 2011, acrylamide levels were compared with indicative values recommended by the EC. Indicative values were exceeded in the case of 3-20 % of samples in different food categories based on 2010 monitoring data. An extended time period and detailed descriptions of sample sources would be needed for a more accurate trend evaluation.</p
Acrylamide (AA), used in many fields, from industrial manufacturing to laboratory work, is also formed during the heating process through the interactions of amino acids. Therefore, AA poses a significant risk for both human and animal health. This study aimed to elucidate whether N-acetyl-L-cysteine (NAC) treatment could modulate AA-induced oxidative changes in the brain, lung, liver, kidney, and testes tissues of the rat. Rats were divided into 4 groups, as the control (C), NAC [150 mg/kg intraperitoneally (i.p.)], AA (40 mg/kg i.p.), and NAC + AA groups. After 10 days, the rats were decapitated and the tissues were excised.alondialdehyde (MDA) and glutathione (GSH)levels, and myeloperoxidase activity (MPO) were determined in the tissues, while oxidant-induced tissue fibrosis was determined using the collagen contents. Serum enzyme activities, cytokine levels, and leukocyte apoptosis were assayed in the plasma. In the AA group, GSH levels decreased significantly, while the MDA levels, MPO activity, and collagen content increased in the tissues suggesting oxidative organ damage. In the NAC + AA group, oxidant responses reversed significantly. Serum enzyme activities, cytokine levels, and leukocyte apoptosis, which increased following AA administration, decreased with NAC treatment. Therefore, supplementing with NAC can be useful when there is a risk of AA toxicity, as NAC inhibits neutrophil infiltration, balances the oxidant-antioxidant status, and regulates the generation of inflammatory mediators to protect tissues.
Background: Humans are exposed to dietary acrylamide (AA) during their lifetime. Accumulating evidence indicates that AA administration is associated with significant increase of oxidative stress; thus, dietary antioxidants may have a protective role against AA toxicity. It was reported that garlic, a natural antioxidant, is able to enhance the cellular antioxidant defence capacity, thereby protecting cells from oxidative stress. Aim: In this study, we evaluated the protective role of garlic on the oxidative damage induced by AA in rat tissues. Methods: Twenty eight Sprague Dawely male adult rats were divided into four groups (7 rats/ group). Group I, negative control group, was fed on basal diet for 22 days. Group II, positive control, fed on basal diet for 22 days and on the 11th day AA was added to the diet (0.34 g/Kg diet). The other two groups received the basal diet supplemented with either 2.5% or 5% garlic for 22 days and on the 11th day AA was added to the diet. Results: The administration of AA resulted in significant elevation in kidney, spleen, testes and brain malondialdehyde level (MDA) and significant reduction in the level of reduced glutathione (GSH) and the activity of copper-zinc superoxide dismutase (Cu/Zn SOD) in the same organs. Also serum urea and creatinine levels and lactate dehydrogenase (LDH) and alkaline phosphatase activities were significantly elevated whereas serum total proteins and albumin were significantly reduced in AA-treated rats as compared with negative control. Treatment with garilic prior to AA produced protective effects and attenuated these biochemical changes. The protective effects of garlic were more pronounced for the high dose. Conclusion: Garlic has been shown to possess antioxidant properties offering promising efficacy against oxidative stress induced by AA administration.
Acrylamide (AA) is neurotoxic to experimental animals and humans. Also, it has mutagenic and carcinogenic effects. This study was carried out to investigate the effects of green tea extract on liver function test in male rats received different doses of acrylamide. Animals were assigned at random to six groups: group 1 served as control, while groups 2, 3 were received 7, 14 mg/100g B.W /day of acrylamide, respectively in drinking water for 15 and 30 days. Group 4 received green tea 1.5% concentration and groups 5, 6 received 7, 14 mg/100 g B.W /day of acrylamide in a combination with green tea for 15 and 30 days. Aspartate amintransferase (AST), and Alanine aminotransferase (ALT) and Alkaline phosphates (ALP), significantly increased whereas cholinesterase activity declined significantly in rats received AA in both concentrations and time in comparison with the control. However, the values of cholinesterase activity decreased when rats received green tea alone or in combination with AA.
This work aimed to evaluate the ameliorating effect of grape seed oil (GSO) on the lesions of experimental Acrylamide (ACR) intoxication in male rat genital organs. Two experimental groups of concomitant administration of 2 dietary levels of GSO with the toxic dose of ACR were evaluated in comparison with a negative control group and other 3 positive control groups for each of the 2 dietary levels of GSO and the toxic dose of the ACR. The results, at the end of the experiment (3 weeks), revealed occurrence of the highest scale of the histopathologic changes in case of the group of ACR-intoxication. These changes were in the form of testicular degeneration, abnormal epididymal contents of immature spermatocytes and multinucleated giant cells. The prostate glands and seminal vesicles showed cystic dilatation with less secretory materials, epithelial hyperplasia, necrosis and desquamation. Nearly similar scales of lesions were seen in the group administrated by ACR with low levels of GSO, while the lesions in the other group of administration by ACR with the high levels of GSO were of less scales. The conclusion from this microscopic evaluation was the occurrence of a less and leveldependent impact ameliorating effect of GSO supplementation against ACRinduced lesions in male genital organs of the adult rats.
Male Fisher albino rats of the F-344 strain were dosed with 5, 10, or 20 mg/kg of acrylamide in distilled water vehicle three times weekly for 13 weeks. Control animals were either not dosed or given 1 ml/100 g ml/100g distilled water vehicle. There were 10 animals per group. Neurobehavioral tests were administered during the week prior to dosing (week 0) and after 1, 4, 7, 10 and 13 weeks of dosing. At the end of the dosing period, 10 rats in the 10 mg/kg group, 5 rats in the 20 mg/kg group, and 5 rats in the distilled water group were sacrificed and assessed for histopathological evidence of acrylamide neurotoxicity. The remaining rats in the high dose group (N = 5) and distilled water control group (N = 5) were retested for neurobehavioral effects 1 and 5 weeks after cessation of dosing and then sacrificed for neuropathological examination. Those rats receiving 20 mg/kg of acrylamide had significantly lower body weights at 4-13 weeks of dosing. Significant decreases in hindlimb function were observed in these animals at 7-13 weeks of dosing, while motor activity was decreased at 10-13 weeks. Forelimb grip strength was not affected during the dosing period. In rats receiving 10 mg/kg of acrylamide, there was a significant decrease in body weight only at the 7 week test. Neurobehavioral measures were not affected at any time in animals dosed with 10 mg/kg. No effects of any sort were seen at 5 mg/kg. At the end of the 13 weeks of dosing, signs of early fiber degeneration were observed in the peripheral nerves of all animals receiving 10 mg/kg of acrylamide, while the rats in the high dose group were found to have signs of moderate to severe acrylamide neurotoxicity. One week after cessation of dosing, fore- and hindlimb scores, spontaneous motor activity, and body weights were significantly decreased in the high dose rats. Five weeks after cessation of dosing, the acrylamide-treated rats did not differ from controls on neurobehavioral measures. Neuropathological examination showed signs of regenerating and remyelinating fibers in the animals previously exposed to acrylamide.
Acrylamide (AM) and N-methylolacrylamide (NMA) are used in the formulation of grouting materials. AM undergoes metabolism to a reactive epoxide, glycidamide (GA). Both AM and GA react with hemoglobin to form adducts that can be related to exposure to AM. The objective of this study was to evaluate the extent to which NMA could form the same adducts as AM. N-(2-carbamoylethyl)valine (AAVal derived from AM) and N-(2carbamoyl-2-hydroxyethyl)valine (GAVal derived from GA) were measured following a single oral dose of AM (50 mg/kg) or NMA (71 mg/kg) in male F344 rats. AAVal and GAVal were measured by a modified Edman degradation to produce phenylthiohydantoin derivatives and liquid chromatography/tandem mass spectrometry. In AM-treated rats, AAVal was 21 1.7-pmol/mg globin (mean SD, n 4), and GAVal was 7.9 0.8 pmol/mg. In NMA-treated rats, AAVal was 41 4.9 pmol/mg, and GAVal was 1.4 0.1 pmol/mg. Whether AAVal was derived from reaction of NMA with globin followed by loss of the hydroxymethyl group, or loss of the hydroxymethyl group to form AM prior to reaction with globin, is not known. However, the higher ratio of AAVal:GAVal in NMA-treated rats (29 vs. 2.6 in AM-treated rats) suggests that reaction of NMA with globin is the predominant route to AAVal in NMA-treated rats. The detection of GAVal in NMA-treated rats indicates oxidation of NMA, either directly or following conversion to AM. The lower levels of GAVal on NMA administration suggest that a much lower level of epoxide was formed than compared with AM treatment.
High exposure to the acrylamide monomer has been associated with neuropathy and neurotoxic effects. Chronic lower exposure causes endocrine disruption associated with thyroid, testicular, and mammary tumors. To investigate mechanisms of endocrine disruption, short-term, low-level oral dosing studies were conducted. Weanling female Fischer 344 rats were acclimatized for two weeks before dosing. Controls were given distilled water by gavage and rats in other groups were given acrylamide at doses of 2 mg/kg/day and 15 mg/kg/day for 2 or 7 days by gavage. Twenty-four h after the last dose, the rats were killed by decapitation. Trunk blood was collected for hormone analyses and tissues for histopathological examination. There were no toxicity-related deaths, no clinical signs of toxicity, and no significant difference in the mean body weight of animal groups. Histopathological examination of select tissues showed no lesions of pathologic significance. Plasma thyroxine (T 4 ), thyroid stimulating hormone (TSH), prolactin (PRL), and pituitary TSH and PRL analyses did not reveal significant changes between control vs. treated rats. In the 7-day study, however, there was a slight dose-dependent increase in plasma T 4 and a slight dose-dependent decrease in plasma TSH. Thyroid gland morphometry showed a significant (p < 0.05) decrease in the colloid area and a significant increase (p < 0.05) in the follicular cell height of treated rats as compared to controls. The follicular area shrinkage was similar in both studies. These results show a very early endocrine response to very low levels of toxic insult and opens other venues to further investigate the mechanisms of endocrine disruption by acrylamide.
OBJECTIVE: The aim of this study was to examine possible exposure-related symptoms and neuropsychological changes among tunnel workers previously exposed to grout containing acrylamide and N-methylolacrylamide. METHODS: In a cross sectional study, 44 male tunnel workers previously exposed to acrylamide and N-methylolacrylamide during grouting operations were examined with neuropsychological tests, 2–10 years after last exposure. The control group consisted of 49 male tunnel workers with no history of acrylamide exposure. Questionnaires were used to assess retrospectively recalled symptoms during work and current symptoms at the time of the examination. RESULTS: The prevalence of paresthesia in hands and legs, and leg cramps during work periods were higher in the exposed than control group. Self-reported prevalence of skin irritation, peeling of skin on the hands, white-finger attacks, headache, and breathlessness was also higher among the exposed workers. The Q-16 questionnaire on current symptoms indicated higher symptom prevalence among the exposed of impaired memory and concentration, emotional change, sleep disturbances, tiredness, headache, and sensory or motor changes. In contrast, no association was found between neuropsychological test results and acrylamide exposure, adjusting for relevant confounders. However, selected motor symptoms were associated with the corresponding results on tests for motor function. CONCLUSIONS: Despite higher prevalences of self-reported current symptoms among the acrylamide-exposed compared to the control group, we did not find an association between occupational acrylamide exposure and health outcomes as measured by the chosen neuropsychological tests. Observed associations between chemical exposure and self-reported symptoms should be interpreted with great caution.
The present human intervention study investigated the relation between the intake of acrylamide (AA) in diets with minimized, low, and high AA contents and the levels of urinary exposure biomarkers. As biomarkers, the mercapturic acids, N-acetyl-S-(carbamoylethyl)-L-cysteine (AAMA), and N-acetyl-S-(1-carbamoyl-2-hydroxyethyl)-L-cysteine (GAMA) were monitored. The study was performed with 14 healthy male volunteers over a period of 9 days, under controlled conditions excluding any inadvertent AA exposure. Dietary exposure to AA was measured by determining AA contents in duplicates of all meals consumed by the volunteers. The study design included an initial washout period of 3 days on AA-minimized diet, resulting in dietary AA exposure not exceeding 41 ng/kg bw/d. Identical washout periods of 2 days each followed the AA exposure days (day 4, low exposure, and day 7, high exposure). At the respective AA intake days, volunteers ingested 0.6-0.8 (low exposure) or 1.3-1.8 (high exposure) μg AA/kg bw/d with their food. Both low and high AA intakes resulted in an AAMA output within 72 h corresponding to 58 % of the respective AA intake. At the end of the initial 3-day washout period, an AAMA baseline level of 93 ± 31 nmol/d was recorded, suggestive for an assumed net AA baseline exposure level of 0.2-0.3 μg AA/kg bw/d.
Berries are dietary plants with high antioxidant activity. The aim of this study is to investigate the protective effect of berries (strawberry, grape, and blueberry) against the acrylamide (AA)-induced general toxicity, genotoxicity, and reproductive toxicity in mice model, respectively. Mice were treated with 50 mg/kg b.w./day AA intraperitoneal injection for 5 d after feeding control diet or diet containing freeze-dried strawberry, grape, and blueberry powder. The results showed that AA induced a significant general toxicity, genotoxicity, and reproductive toxicity in mice. Compared with the control diet, the diets containing berries could reverse the AA-induced alterations in liver antioxidant enzymes activities (P < 0.05). Moreover, the AA-induced genotoxicity could be prevented by the diet containing berries. The DNA damage in the lymphocyte and liver cells and the micronucleus formation in bone marrow cell were significantly alleviated (P < 0.05). Meanwhile, the mice fed with diets containing berries showed a recovery in the sperm count, the sperm activity rate, sperm motility parameters, and the abnormal sperm rate (P < 0.05). Berry powders have remarkable intervention against the AA-induced general toxicity, genotoxicity, reproductive toxicity. Abundant phenolics, especially anthocyanins, may contribute to the intervention.
© 2015 Institute of Food Technologists®
Acrylamide is known to be a neurotoxic, genotoxic, and carcinogenic compound. Glycidamide has a close relationship to the toxic mechanism of acrylamide. In order to explore the toxic mechanism of acrylamide, we further discussed the effects of oral administration of allicin on glycidamide-induced toxicity by determining the hematological parameters like AST, ALT, LDH, BUN, creatinine, ROS, and 8-OHdG, and biochemical parameters such as MDA, MPO, SOD, GST and GSH in the kidney, liver, brain and lung of male and female mice for the first time. We found that the same dose of glycidamide had more toxic effects and damage effects to the mice compared to the previous study of acrylamide. It could markedly increase the level of AST, ALT, LDH, BUN, ROS, 8-OHdG, MDA, MPO while decrease the SOD, GST and GSH. However, our data showed the oral administered allicin with a concentration of 5, 10, and 20 mg/kg b.w./day could significantly decrease the damage indexes of AST, ALT, LDH, BUN, ROS, 8-OHdG, MDA, and MPO, while increase the antioxidant indicators of SOD, GST and GSH. Thus allicin could be used as an effective dietary supplement for the chemoprevention of glycidamide genotoxicity internally, and to prevent the tissue damage and toxicity induced by glycidamide.
Acrylamide (AA), a proven rodent carcinogen, is found in a variety of commonly consumed human foods, which has raised public health concerns. AA is largely oxidized to the chemically reactive epoxide, glycidamide (GA), by cytochrome P450 2E1. The genotoxic effects of AA and GA have been extensively evaluated. However, the results in mammalian gene mutation tests were inconsistent, especially the genotoxic effects at the HPRT gene and TK gene. In this article, the relevant mutations induced by AA and GA on both gene loci in various test systems involving in vivo and in vitro tests are reviewed. It is confirmed that AA acts directly as a clastogen and produces weakly mutagenic effects at the HPRT gene probably by metabolic conversion of AA to GA. On the other hand, GA is a strong mutagen with high reactivity to DNA, inducing predominantly point mutations. The molecular mutation spectra of AA and GA at the HPRT and TK genes are also compared and summarized here, for better clarifying the mechanisms of mutation induced by these two compounds. These data would help to understand the mutagenicity of AA and its contribution to human cancers.
Acrylamide (ACR) is an industrial chemical which induces neurotoxic effects in experimental animals and humans. The present study was carried out to investigate the hematological, biochemical, neurological and histopathological effects of ACR on immature male and female rats. Animals were divided into 2 main groups; immature male group and immature female group and all rats were treated for 28 consecutive days. Each main group subsequently was divided into 2 subgroups: (I) Untreated control group that received a daily oral administration of distilled water and (II) ACR treated rats which received a daily oral administration of ACR (15 mg/kg/body weight). The results obtained indicate that ACR administration induced some behavioral disorders in the movement of immature male and female rats as well as loss of body weight. ACR induced a significant decrease in hemoglobin (Hb), erythrocytes (RBCS), hematocrit (HCT) and lymphocyte levels of young female rats. ACR significantly increased serum glucose, total cholesterol and triglycerides concentrations of both immature male and female rats. While, significant increase in the total urea concentration was noticed only in the immature male rats following ACR administration. Moreover, ACR induced marked increase in the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the immature male and female rats. On the other hand, the activities of serum alkaline phosphatase (ALP) and acetylcholinesterase (AChE) were significantly decreased in both treated groups. ACR caused a significant increase in norepinephrin (NE), glutamate, aspartate and taurine, while it reduced dopamine (DA) and serotonin (5-HT) levels. In conclusion, the present study showed that, ACR induced hazardous effects on immature male and female rats. So, we recommended that children must avoid fast or junk foods.
Acrylamide, a neurotoxic and potential cancer-causing agent, was found in a range of fried and baked starchy foods and has caused worldwide concern. Ever since, it has been an urgent agenda to find out effective ways to limit acrylamide formation during processing. The aim of this work is to examine the effect of immersion in different solutions on the acrylamide content in potato slices after microwaving and frying. Acrylamide levels were analyzed by the HPLC method, which was confirmed by HPLC-MS/MS. The results showed that immersing potato slices in water reduced the amount of acrylamide by 8-40% after microwaving and 19-75% after frying, respectively. For microwave processing, immersion in a NaCl solution at a concentration of 0.5 g L−1 caused a considerable reduction of the acrylamide content by 96%, followed by a treatment with a CaCl2 solution of 2 g L−1 (80%) and a citric acid solution at a concentration of 1 g L−1 (58%) . For the frying process, the most effective method for acrylamide reduction was the immersion in a citric acid solution at a concentration of 1 g L−1 (77%), followed by a CaCl2 solution at a concentration of 2 g L−1 (72%) and a NaCl solution at a concentration of 0.5 g L−1 (64%). The optimal soaking treatments could effectively reduce the acrylamide content while reasonably retaining the sensory attributes of the crisps.