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53 Seiten, Note: 1
2.0 LITERATURE REVIEW
2.1 Historical Overview
2.2 Acrylamide Formation in Foods
2.2.1 Major Acrylamide Formation Pathway
2.2.2 Minor Acrylamide Formation Pathway
2.3 Potential Acrylamide Precursors in Foodstuffs
2.4 Range of Products Associated with Acrylamide
2.5 Effects of Acrylamide Consumption
2.6 Acrylamide in Potatoes
2.6.1 Formation of Acrylamide in Potatoes
2.6.2 Acrylamide Levels in Potato Products
2.7 Aspects Affecting Acrylamide Formation in Fried Potato Products
3.0 ACRYLAMIDE REGULATIONS
3.1 International Regulations
3.2 EU Regulations
3.3 Acceptable Acrylamide Levels in Saudi Arabia and the EU
3.4 ACRYLAMIDE RISK MANAGEMENT
3.4.1 Evolution of Acrylamide Risk Management
3.5 ACRYLAMIDE RISK ASSESSMENT
3.5.1 Hazard Identification
3.5.2 Hazard Characterization
3.6 EXPOSURE ASSESSMENT
3.6.1 Methods Used To Assess Human Dietary Acrylamide Intake
18.104.22.168 Food Frequency Questionnaire (FFQ) Method
3.7 ACRYLAMIDE MITIGATION IN POTATO PRODUCTS
3.7.1 Acrylamide Mitigation Methods
22.214.171.124 Biological methods for Acrylamide mitigation in Potato products
126.96.36.199 Physical methods for Acrylamide Mitigation in Potato Product
188.8.131.52 Chemical Methods for Acrylamide Reduction in Potato Products
3.8 Industry and Consumer Based Guidelines
3.8.1 WHO/FAO acrylamide reduction Guidelines
3.8.2 US Draft Industry Guidelines
3.8.3 EU Guidelines on Acrylamide Reduction
3.8.4 Saudi Arabia mitigation Approaches
Appendix 1: Regulatory Documentation
Appendix 2: Amount of asparagine in cereals
Acrylamide has been found to be a biodegradable compound that exhibits high mobility in groundwater and soil. These characteristics are attributable to its physical and chemical characteristics including its high solubility in water and organic solvents such as ethanol and acetone. Clinical studies indicate that acrylamide forms glycidamide as the principal metabolite in animals. In humans, acrylamide and glycidamide are known to form adducts with most proteins including glutathione, and they are eliminated from the body through the renal system which serves as the primary route of acrylamide excretion. In the past decade, acrylamide has attracted immense attention from food agencies after it was found to be formed naturally in most carbohydrate-rich foods; thus, raising health concerns. The results obtained from epidemiological studies show that dietary acrylamide causes toxicity, and it is a potent carcinogen. Therefore, mitigation approaches have been designed including the reduction of acrylamide precursors in potatoes and controlling processing conditions.
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Illustration 1: Illustration showing the formation of Schiff Base
Illustration 2: Flow diagram showing pathways of acrylamide formation
Figure 1: Contribution of foods to mean acrylamide exposure
Figure 2: Time-Temperature Relationship in acrylamide formation (μg/kg)
Acrylamide is a crystalline solid which is colourless and odourless, and it is known to have a low molecular weight which is usually formed after the hydration of acrylonitrite. It has a number of chemical and physical properties like any other chemical compound. Acrylamide has been found to be a biodegradable compound that exhibits high mobility in groundwater and soil. These characteristics are attributable to its physical and chemical characteristics including its high solubility in water and organic solvents such as ethanol and acetone. In addition, acrylamide exhibits a melting point of 84.5 0C. Its chemical properties allow the compound to form cross-linked polymers such as polyacrylamide gel and other polyacrylamides which are used in industrial and laboratory research (Arvanitoyannis & Dionisopoulou 2014, p. 708). On the other hand, acrylamide is not known to constitute a significant burden to the environment owing to its biodegradable property. However, it is worth noting that high environmental contamination with acrylamide is caused by the plastic industries.
Clinical studies indicate that acrylamide forms glycidamide as the principal metabolite in animals. In humans, acrylamide and glycidamide are known to form adducts with most proteins including glutathione, and they are eliminated from the body through the renal system which serves as the primary route of acrylamide excretion (Riboldi, Vinhas & Moreira 2014, p. 311).
In the past decade, acrylamide has attracted immense attention from food agencies after it was found to be formed naturally in most carbohydrate-rich foods; thus, raising health concerns. Therefore, this dissertation focuses on acrylamide in potatoes and its mitigation measures.
It is reported that acrylamide contamination was considered as a significant scare in 1997 when caused death of cattle in southern Sweden. In this case, cows in Bjare peninsula showed alarming symptoms which led to death of the affected animals. This led to epidemiological investigation which revealed that the affected animals had been drinking acrylamide contaminated water from a stream. The stream had its tributaries from a mountain where polyacrylamide was being used in drilling works as a crack sealant.
In 2002, researchers in Sweden released their findings which revealed that acrylamide is formed in some types of foods that are cooked at high temperatures. As a result, the Swedish National Food Administration (SNFA) alerted international authorities about the health risk associated to acrylamide exposure. This alert prompted international such as WHO and Food and FAO, and regional authorities to carry out extensive findings to identify specific food products in which acrylamide is formed. In the studies which investigated raw foods, results showed that acrylamide was not present in raw foods. In addition, most foods which are known for food poisoning such as fish, chicken, fish, and infant formula were not found to have traces of acrylamide. In other studies, results showed that boiled foods did not contain acrylamide, even those which are rich in carbohydrates (Arvanitoyannis & Dionisopoulou 2014, p. 708). On the other hand, studies indicated that some baked and fried foods contained acrylamide levels which are higher than the levels permitted by the World Health Organization (Lofstedt 2003, p. 430).
In the recent years, efforts to control acrylamide formation in food products have focused on the mechanism of formation, in order to design reliable food safety approaches. Therefore, there is consistency in all the studies which have investigated the mechanism of acrylamide formation in food products. Two principal pathways have so far been identified: the asparagine route is considered as the major acrylamide formation pathway, whereas the minor pathway involves lipids and protein metabolism.
Over the past 7 decades, Maillard reaction has been investigated to demystify the mechanism of the browning reaction which is known to be non-enzymatic. This reaction has been found to influence some qualities of heat processed foods. For instance, food flavour, aroma and colour formation qualities of most foods are attributable to Maillard reaction although some of the underlying mechanisms have not yet been unrevealed. Mass spectral studies indicate that acrylamide bears some components of asparagines especially the amide nitrogen atom and the three carbon atoms which constitute the side chain. This implies that asparagine, an amino acid, can release acrylamide through deamination and decarboxylation reactions under high thermal conditions. It is also believed that reducing sugars create favourable conditions for the formation of acrylamide in heat processed foods. Therefore, the asparagines route has been identified as the major pathway for the formation of acrylamide in most food products (Vinci, Mestdagh & Meulenaer 2012, p. 1138).
In this pathway, asparagine is usually converted to acrylamide through thermal deamination and decarboxylation. Evidence shows that this reaction requires a carboxyl compound; thus, reducing sugars serve as the principal sources of the required components. However, it is worth noting that some reducing sugars have different influence on acrylamide formation. For instance, fructose which comprises of two α-hydroxy carbonyl groups has been found to increase the rate of acrylamide formation by two-folds compared with glucose and other reducing sugars which comprise of one α-hydroxy carbonyl group (Eriksson 2005, p. 43). The rationale for this phenomenon can be explained the number of the α-hydroxy carbonyl groups which form the reducing sugars. Glucose exists as a monosaccharide with one α-hydroxy carbonyl group whereas fructose is a monosaccharide, comprising of two α-hydroxy carbonyl groups. Therefore, it is apparent that glucose produces one α-hydroxy carbonyl group for the formation of acrylamide during the Maillard reaction. In this case, fructose produces two α-hydroxy carbonyl groups, one from each of the two carbonyl groups forming the monosaccharide.
Therefore, the reaction between a reducing sugar and asparagine involves the formation of a decarboxylated Schiff base. Ordinarily, N-glycosylasparagine, a Schiff base, decomposes to form an imine and acrylamide as the end-products of the Maillard reaction.
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Illustration 1: Illustration showing the formation of Schiff Base (Brunton, Gormley & Murray 2005, p. 6)
It is also reported that enzymatic reactions involving decarboxylases generate biogenic amine from asparagine. This biogenic amine undergoes deamination under high thermal conditions to generate acrylamide. This process does not require the presence of reducing sugars; thus, it serves as an alternative process for the formation of acrylamide via the Maillard reaction. In addition, the formation of acrylamide in foods through the Maillard reaction can occur through the Strecker aldehyde route. In the Strecker aldehyde route, reactive di-carbonyl compounds form acrylamide during the degradation of amino acids such as methionine and asparagine through the formation of different intermediates which enter into the Maillard reaction as the main pathway (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 2). Therefore, the degradation of amino acids through the Strecker aldehyde route is considered as another significant alternative for the formation of acrylamide through the Maillard reaction.
Several studies show that there are other pathways through which acrylamide is formed in foods, although the Maillard reaction serves as the main pathway. One of these minor pathways of acrylamide formation in foods is the lipid pathway. In this pathway, lipids produce acrylic acid, a three-carbon unit compound, at elevated temperatures. Other compounds such as acrolein and ammonia are also believed to be formed during lipid degradation. Therefore, acrylamide formation in lipid rich foods has been proposed to occur through the lipids route in which asparagine is not involved in the reaction. Ordinarily, the three-carbon unit compounds: acrolein and acrylic acid are formed from the oxidative degradation of lipids (Eriksson 2005, p. 44). For instance, glycerol is degraded into acrylic acid, which reacts with ammonia to produce acrylamide. In this pathway, ammonia serves as the principal source of the amine groups of acrylamide in the absence of asparagine. Evidence shows that lipids play significant roles in the formation of acrylamide in some foods. However, it is worth noting that this pathway does not occur in fried potatoes, but it is common in lipid-rich foods (Vinci, Mestdagh & Meulenaer 2012, p. 1139).
In addition, protein metabolism has also been proposed to be a significant pathway for the formation of acrylamide in foods. Studies indicate that protein metabolism leads to the generation of acrylic acid and acrolein which are some of the significant intermediates of acrylamide formation in foods (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 3). For instance, protein pyrolysis is responsible for acrylamide formation in dry-heated wheat products (Vinci, Mestdagh & Meulenaer 2012, p. 1139). This process involves the degradation of gluten, the principal protein in wheat which constitutes the elasticity of dough. It is also proposed that the decarboxylation of organic acids such as citric acid, lactic acid and malic acid generate acrylic acid and acrolein which are converted to acrylamide (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 3). Therefore, it is apparent that there are different minor pathways for acrylamide formation in foods although consistency in some findings on the minor pathways in different foods is lacking. However, there is a consensus on the Maillard reaction as the main route for acrylamide formation in virtually all potato products (Vinci, Mestdagh & Meulenaer 2012, p. 1139).
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Illustration 2: Flow diagram showing pathways of acrylamide formation; (A) Major pathway, (B) Minor pathway (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 3)
Evidence studies indicate that acrylamide formation in foodstuffs is enhanced by the presence of endogenous factors which serve as acrylamide precursors. Some of these precursors are present in the raw materials for food processing in which high thermal conditions increase their influence in acrylamide formation. Currently, two main precursors for acrylamide formation in foods have been identified. These precursors include amino acids and carbohydrates, primarily glucose and fructose (Brunton, Gormley & Murray 2005, p. 5). Amino acids are usually present in most foods because they form significant components of proteins which serve as dietary requirements for the human body. However, it is worth noting that some amino acids are not involved in acrylamide formation in foods. Evidence indicates that free asparagine is one of the most significant precursors for acrylamide formation. This is so because asparagine has been found to form N-glycosylasparagine Schiff base during the Maillard reaction. Other amino acids which have been found to be significant precursors for acrylamide formation include alanine, methionine, arginine, cysteine, aspartic acid, and valine. In addition, glutamine and threonine have been identified as some of the principal precursors for acrylamide formation in heat-processed foods (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 3).
On the other hand, monosaccharides such as fructose and glucose which are reducing sugars serve as significant precursors for acrylamide formation. In addition, sucrose which is a non-reducing sugar has been found to be the principal disaccharide involved in acrylamide formation in some foodstuffs (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 3). Ordinarily, sucrose comprises of two glucose molecules which are held together by glycosidic bonds. This implies that sucrose has α-hydroxy carbonyl groups which are necessary for acrylamide formation through the asparagine route. Evidence shows that these carbohydrates provide α-hydroxy carbonyl groups which facilitate the Maillard reaction (Eriksson 2005, p. 43). Therefore, foods prepared from raw materials which are rich in reducing sugars such as fructose and glucose, and non-reducing sugar sucrose are likely to form acrylamide during heat processing.
Over the years, Maillard products have been in use as dietary sources. Therefore, the discovery of acrylamide formation in these products has led to a significant health scare. Acrylamide has been identified as a toxic compound which can cause an array of health risks. As such, it bears potential implications on public health although the amounts of acrylamide in different food products have not yet been determined. It is suggested that some foods contain low amounts of acrylamide, whereas others contain high amounts. However, scientists agree that the method of food processing serves as the principal determinant of the amounts of acrylamide which are formed in different foodstuffs during food preparation. Arvanitoyannis and Dionisopoulou (2014, p. 711) report that the application of high temperatures during food processing enhances the acrylamide levels formed in the foods. However, there is a consensus that some foods contain compounds which facilitate acrylamide formation. For instance, carbohydrate and lipid-rich foods have been found to contain high levels of acrylamide compared to those which have low levels of acrylamide precursors. Currently, a number of foods where acrylamide is formed have been identified. Some of these foods include cereals, flours, bread, almonds, meat, coffee, and tea. In addition, water has also been found to have significant amounts of acrylamide.
It is reported that breakfast cereals contain high amounts of acrylamide, yet they form a significant component of diet for people in the western countries. As such, it is apparent that the daily intake of acrylamide which is derived from food among western communities comes from breakfast cereals. Evidence indicates that breakfast cereals contain an average of 292 lg/kg acrylamide content in which the daily acrylamide intake from breakfast cereals is estimated to be 2.68 lg AA/person (Arvanitoyannis & Dionisopoulou 2014, p. 714). In most studies, wheat-based cereals have been found to contain high acrylamide levels the same as food samples with high protein or fibre content.
On the other hand, flours such as rye, wheat and whole-wheat flours contain precursors of acrylamide formation. Evidence shows that these flours contain high amounts of asparagine. For instance, wheat germ has been found to contain the highest amount of free asparagine which ranges from 55.5-57.4 g/kg. Rye flour contains 1.07 g/kg, whereas maize flour which constitutes of starch contains 0.59-1.07 g/kg (Arvanitoyannis & Dionisopoulou 2014, p. 716). This amino acid plays significant roles in the Maillard reaction which is responsible for the formation of acrylamide at elevated temperatures. In most cases, cooking wheat cake and rye at 180 0C and beyond has been found to enhance the levels of acrylamide formation.
Bread is also considered as one of the foods where acrylamide is formed. Ordinarily, dough contains high levels of free asparagine and glycine. These amino acids serve as precursors for acrylamide formation in breads during bread toasting. However, glycine has been found to enhance the colour intensity in bread than acrylamide formation. This is contrary to the influence of asparagine because it increases acrylamide formation. Therefore, it is apparent that the content of acrylamide in bread is determined by the amount of free asparagine in the dough. It is reported that bread accounts for 10% of the total acrylamide dietary exposure, whereas all bakery products account for 30% (Boon, DeMul, Voet, Donkersgoed, Brette & Klaveren 2005, p. 152).
On the other hand, almonds contain low levels of free asparagine as compared to other food products. Therefore, the content of acrylamide in roasted almonds is believed to be associated to the content of free asparagine in the raw materials. In some studies which investigated the effect of roasting in almonds regarding the formation of acrylamide, it was noted that the content of reducing sugars did not have significant influence on the amount of acrylamide formed in roasted almonds. However, the content of acrylamide formed varied in different almond products. Almond-containing baked products have been found to contain moderate acrylamide contents, whereas brown roasted almonds contain the highest contents of acrylamide (Arvanitoyannis & Dionisopoulou 2014, p. 718).
Meat has also been identified as one of the foods where acrylamide is formed. This is so because meat products contain unsaturated animal fats and oils. In addition, animal products contain high levels of free asparagine. Therefore, the degree of acrylamide formation in meat products depends on the content of lipids and asparagine. For instance, acrylamide contents in breaded chicken products ranges from 0.00091-0.00097 mg/kg.
Beverages such as coffee and tea have also been found to contain acrylamide. Roasted coffee is usually prepared through the application of high temperatures which have been found to enhance acrylamide formation. Evidence shows that coffee blends with cereals contain acrylamide contents ranging from 200.8-229.4 μg/l. However, studies indicate that green coffee does not contain acrylamide. This implies that coffee roasting enhances acrylamide formation in roasted coffee products (Arvanitoyannis & Dionisopoulou 2014, p. 721). On the other hand, tea contains phenolic compounds which are suggested to be significant precursors of acrylamide formation. Ordinarily, the degradation of catechins generates intermediates which are converted to acrylamide during roasting, especially at temperatures beyond 160 0C. Acrylamide contents as high as 4.0 have been obtained from tea infusions roasted at 180 0C for a minimum of 15 minutes (Mizukami, Sawai & Yamaguchi 2008, p. 2157). Of all the foods containing acrylamide, potato products account for the largest proportion (Food Safety Authority of Ireland 2009, p. 3).
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Acrylamide is known as a toxic compound; thus, it causes adverse health effects in humans and other animals as it was the case in Sweden where cattle were reported to die after drinking from acrylamide contaminated stream. Therefore, recent epidemiological studies seem to be focused on the toxicity of acrylamide. Despite the controversy surrounding the toxicological mechanisms involved in acrylamide toxicity, different studies have investigated acrylamide induced carcinogenicity, neurotoxicity and genotoxicity (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 4). In addition, reproductive and developmental toxicity studies have been carried out in which their results suggest toxicity in laboratory animals although reproductive toxicity has not yet been confirmed.
Acrylamide carcinogenicity has attracted immense focus from scientists in toxicological studies. Evidence indicates that acrylamide exposure to laboratory animals acts as a multi-organ carcinogen (Morales, Jimenez, Garcia, Mendoza & Beristain 2014, p. 587).
Cesar Ignacio Beristain). Other studies indicate that acrylamide metabolites such as glycidamide are carcinogenic to both rats and mice. However, it is worth noting that there is no significant relationship between tumour formation and acrylamide exposure. This implies that acrylamide is not associated with cancers in humans although advanced epidemiological studies are ongoing to ascertain acrylamide’s carcinogenicity in humans. However, the risk of pancreatic cancer has been suggested to be enhanced by high acrylamide exposure in workers. Therefore, evidence indicates that the consumption of acrylamide in the normal diet does not cause significant carcinogenic potential in humans. As such, acrylamide is believed to have lower carcinogenic potential compared to other carcinogenic compounds such as mycotoxins including aflatoxin (Rice 2005, p. 17).
On the other hand, acrylamide has been confirmed to cause neurotoxic effects in humans. However, neurotoxicity is believed to occur after prolonged exposure to acrylamide, and it is reported in mine workers, construction industry workers, tunnel workers and floculator manufacture workers. In some workers, acrylamide has been reported to cause reversible peripheral neuropathy and cerebral dysfunction (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 4). Proteomic studies have demonstrated that acrylamide inactivates proteins in the pre-synaptic nerve terminals; thus, impairing neurotransmission. However, the mechanism for protein inactivation by acrylamide has not been identified, although it is hypothesized that neurotoxicity of acrylamide is attributable to the low levels of neurotransmitter and the inhibition of axonal transport.
Despite the intensive epidemiological investigations on the neurotoxic effects of acrylamide, low amounts of acrylamide from dietary sources have not been identified to cause cumulative effects in humans. However, it is suggested that low-chronic exposure to acrylamide can lead to neurotoxicity in humans. It is also believed that acrylamide binding with cysteine residues that cause disruption to the axonal transport and nerve terminal degeneration suggests that acrylamide is responsible for some neurodegenerative diseases (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 5).
Over the years, genotoxicity associated with acrylamide has been studied extensively, in order to demystify this phenomenon. Preliminary studies indicated that acrylamide, as well as glycidamide caused the induction of sister-chromatid exchanges and chromosomal aberrations. In one of the studies, glycidamide was found to produce specific glycidamide-DNA adducts such as N3-(2-carbamoyl-2-hydroxyethyl) adenine and N7-(2-carbamoyl-2-hydroxyethyl) guanine. These studies indicated that acrylamide is responsible for the production of depurinating DNA adducts in animals. In humans acrylamide has been found to cause similar effects in human lymphocytes in which it influences metaphase reactions. Further studies indicate that acrylamide and its metabolites affect blood leucocytes by increasing DNA damage (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 4). Therefore, genotoxicity associated with acrylamide has been confirmed in which two mechanisms explain the occurrence of genotoxic effects.
The first mechanism involves acrylamide metabolism in which it is converted into glycidamide which, in turn causes gene mutation at HPRT locus. Secondly, acrylamide exerts its genotoxicity through forming adducts with hydroxyl, amino or thiol groups. It also forms adducts with the nucleophilic centres in the DNA molecule (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 4).
From a clinical perspective, the genotoxic characteristics of acrylamide are relatively different from those exhibited by its metabolites, primarily glycidamide. In human cells, as well as, other mammalian cells, cytochrome P4502E1 plays the most significant role in the metabolism of acrylamide. This protein converts acrylamide into glycidamide which has been identified to be a strong mutagen owing to its high reactivity to mammalian DNA (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 4). In recent studies, glycidamide has been shown to cause impairment in cell proliferation kinetics and induction of micronuclei. These studies have provided evidence that acrylamide metabolites such as glycidamide are potent toxicants to human mammary cells because exposure to glycidamide has been found to cause a significant decrease in cell viability, especially at high concentrations. However, it is worth noting that the observed decrease in cell viability is not associated with oxidative stress, and this implies there is a different mechanism involved which has not yet been discovered.
On the other hand, acrylamide exerts weak mutagenic effects as compared with glycidamide. Instead, it causes chromosomal aberrations by acting as a clastogen. Hogervorst, Baars, Schouten, Konings, Goldbohm & Brandt (2010, p. 508) reaffirms the role of acrylamide on cancer. They report that acrylamide depletes glutathione, one of the most significant anti-oxidants involved in the removal of reactive oxidative species from the body. Evidence shows that active radicals are responsible for the onset of different cancers because they cause gene mutations in humans. Therefore, the depletion of glutathione by acrylamide reduces the ability of the body to remove active radicals; thus, increasing the risk of cancer. In addition, acrylamide has been found to influence hormone levels through inducing gene expression during the production of sex hormones (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 4). Evidence shows that the increased gene expression in human colorectal and breast cells increases the risk of some cancers such as prostate cancer which is caused by hormonal imbalance.
Acrylamide consumption has also been found to cause developmental and reproductive toxicity. Laboratory investigations indicate that acrylamide toxicity results into reduced fertility rates, disrupted mating and high rate of foetus resorptions. In male mammals such as rats and mice, acrylamide leads to the production of abnormal sperms accompanied by a significant decrease in sperm count. It is apparent that the molecular mechanisms involved in reproductive toxicity are attributable to DNA damage, depletion of glutathione hormone and chromosomal damage (Xu, Cui, Ran, Liu, Chen, Kai et al. 2014, p. 5).
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