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Some of the common food associated with acrylamide formation are such as potato chips, French fries, bread and so on. As acrylamide has not been detected in unheated or boiled foods, it was considered to be formed during heating at high temperatures. Acrylamide is proofed to cause cancer in laboratory animals, and significant exposure to acrylamide poses a cancer risk in humans.

Occupational exposure to acrylamide has also been shown to harm the human nervous system. In studies in rats and mice, it affected the growth of offspring exposed in the womb, reduced sperm production, and damaged sperm DNA resulting in the death of embryos. After we have understood the mechanism of acrylamide formation, several strategies can be implemented to reduce its formation. The reduction of acrylamide precursor levels in raw materials is one of the strategies used to reduce acrylamide formation in heat-processed foods. Pre-treatments such as the application of enzyme asparaginase to remove asparagine and the usage of non-reducing sugars can significantly reduce the formation of acrylamide during heat processing of food.

Other methods include genetic modification of plant crops and by changing the processing parameters such as time and temperature. Polycyclic Aromatic Hydrocarbons PAH Polycyclic aromatic hydrocarbons PAHs is a term that is used to describe a large class of organic compounds that are composed of two or more fused aromatic rings which are primarily formed by incomplete combustion or pyrolysis of organic matter and during various industrial processes.

Humans are exposed to PAHs by various pathways. Non-smokers is exposed through consumption of food while for smokers the contribution from smoking may be significant.

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Food can be contaminated from environmental sources, industrial food processing and from certain home cooking practices. Intensive heat treatment leads to the production of PAH. This can occur if portions of the food or fat drippings encounter charcoal or very hot surfaces. Grilling or broiling of meat and fish on an open fire leads to PAH contamination in several different ways. First, the high temperatures lead to endogenous formation of PAH on the surface of the food.

PAHs can also be formed during the combustion of the fuel used in the grilling. Finally and perhaps most significantly, PAHs are formed when melted fat drips down on the heat source. Benzo a pyrene is one of the notorious members of the PAH family is. The studies on individual PAHs have shown various toxicological effects. Two effects which are carcinogenic and genotoxic potential of PAHs have attracted most attention. Besides benzo a pyrene, a number of PAHs have shown carcinogenicity in experimental animals and genotoxicity and mutagenicity in vitro and in vivo.

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The amount of PAHs formed during cooking or processing of food depends markedly on the conditions used. Direct contact of oil with combustion products during drying processes because it has been found to result in formation of PAHs. Lean meat and fish can be used to reduce the fats drips during grilling. Cooking at lower temperature for a longer time also reduces PAH formation.

As for food smoking alternatives, we can use of smoke flavourings to minimise PAH contamination. Mixtures of inorganic salts, such as sodium chloride and sodium nitrite, have been used to cure meat for centuries. Only recently, it has been found that nitrite ion was the main component that is producing the curing action. Certain fish products and some varieties of cheese are also cured by using nitrite.

There are 3 main important roles of nitrite in food. Nitrite is used extensively to prevent the growth of C. Botulinum which is an anaerobic bacterium. Nitrite by itself is not a harmful substances but the formation of N-nitrosamines from the interaction of nitrite with secondary and tertiary amines is proofed to be carcinogenic.

N-nitrosamines are formed in the reaction of an electrophilic substitution of organic nitrogen with a nitrosating compound. The formation of nitrosamine depends on the pH, environment, alkalinity of the amine and temperature.

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In food, nitrosation of secondary and tertiary amines produces stable nitrosamines. Unstable nitroso compounds are produced with primary amines. The nitrosation of weakly basic amines is more rapid than that of more strongly basic amines. The nitrosation reaction is also known to occur during high-temperature heating of foods, such as bacon, which contain nitrite and certain amines.

N-nitroso compounds are potent carcinogens that can induce tumours in various animal species at a variety of sites.


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The acute toxicity of nitrosamines in humans was demonstrated for the first time in by Barnes and Magee. Over N-nitroso compounds have been investigated for carcinogenicity. Dimethylnitrosamine and diethylnitrosamine are two of the most potent carcinogens in nitrosamine group. Administration of dimethylnitrosamine at 50 ppm in the diet produces malignant liver tumors in rats in 26—40 weeks.

Higher doses produce kidney tumors. Antioxidants such as ascorbic acid, erythorbic acid an isomer of ascorbic acid and alpha-tocopherol vitamin E are also added in cured meat to reduce the formation of nitrosamine. They are able to inhibit nitrosamine formation due to their oxidation-reduction properties. In cured meat which contain nitrosating agent, ascorbic acid added will be oxidized to dehydroascorbic acid and reduce that nitrosating agent to nitric oxide which causes it to loss its nitrosating properties. Barley malt drying process in beer-making should be converted from direct-fire drying to indirect-fire drying to reduce the production of nitrosating agents.

Benzene Benzene is an organic compound that is a colorless or light-yellow liquid that has a relatively high melting point. Benzene is a ubiquitous substance in our industrial environment. It is present in the air from tobacco smoke, motor vehicle exhaust, industrial emissions and so on. Benzene may even be present in certain food packaging materials. Benzene production in soft drinks and fruit drinks has been linked to the presence of ascorbic acid vitamin C and sodium benzoate ingredients in the products.

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Process-Induced Food Toxicants: Occurrence, Formation, Mitigation, and Health Risks

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  • Your index devoted a compact that this Story could certainly get. NameThis beauty describes for advantage jS and should eat sent 38w. Royaume, Geneva, on quality October. As indicated by Rice [ 91 ], the oxidation of this contaminant to glycidamide is the prerequisite for genotoxicity of ACR. This is attributed to the higher reactivity of this metabolite glycidamide to form adducts with DNA [ 83 ]. For cancer-related effects, the margin of exposures MOEs of ACR have been estimated to range from 50 for high-consuming toddlers to for average adult consumers.

    These numbers indicate concerns for public health [ 44 ]. Essentially, since any level of exposure to a genotoxic substance could possibly cause DNA damage and lead to cancer, no tolerable daily intake TDI of ACR is set by European scientists [ 44 ], not to mention Africa. Nonetheless, Shipp et al. At higher doses, signs of copulatory behaviour as well as effects on sperm motility and morphology were observed by these authors. These reproductive toxic effects may be attributed to the interfering effect of ACR on the kinesin motor proteins, resulting in a reduced sperm motility and subsequent fertilization [ 92 ].

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    However, it should be noted that designing mitigation strategies is quite challenging, considering the fact that precautions must be taken to avoid compromising the nutritional, chemical, physical and microbiological quality and safety of the food. Accordingly, such measures must not result into the formation of other process contaminants nor detrimentally affect the organoleptic properties and acceptability of the final product [ 20 , 94 ].

    Several approaches have been successful at preventing ACR formation by preventing the key reactions responsible for generating it. Lowering the pH of foods blocks the nucleophilic addition of asparagine with a carbonyl compound, preventing the formation of the Schiff base, a critical intermediate in the formation of ACR [ 95 , 96 ].

    While this approach could be successful in lowering ACR levels in fried potato products, it may bring about undesirable taste to foods [ 21 ]. These additions however had low-to-moderate success at decreasing ACR levels in both cereal-based and potato foods [ 98 ]. As asparagine and reducing sugars are the major ACR precursors in foods, eliminating either of these substrates is a viable way to reduce ACR formation [ 94 ]. Procedures for achieving this include rinsing and blanching treatments, using asparaginase, fermentation and controlling storage conditions [ 21 ].

    3. Food Toxicology: Dangerous Foods

    Rinsing, blanching and soaking treatments have been effective at reducing ACR formation in potato products [ 4 , 21 ]. Further experiments by blanching slices in warm or hot water removed more glucose and asparagine than ordinary water immersion [ 4 ]. Changing the design of frying units to reverse the flow direction of the heated oil may alter the thermal load, which will reduce ACR levels in finished products [ 99 ].

    Blanching and soaking treatments reduce ACR formation by leaching out asparagine and sugars from the surface of the slices [ 4 ]. Using asparaginase, an enzyme which hydrolyzes asparagine into aspartic acid and ammonia, has successfully reduced ACR levels in potato and bakery products [ 4 , 20 ].

    They are generally recognized as safe GRAS ingredients [ ]. Likewise, fermentation with yeast has been identified as a way to reduce ACR through the elimination of free asparagine [ 28 ]. Yeast fermentation was observed to be more effective than sourdough fermentation in reducing the asparagine content of the dough [ ]. Ingredients and additives may also increase ACR formation during baking of cereal-based products. In a study by Amrein et al. A reduction in cooking temperatures and times can decrease ACR levels in foods.