Reviews in Food and Nutrition Toxicity, Volume 2 (Reviews in Food and Nutrition Toxicity)

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Teratogenic effects in mammals include central nervous system abnormalities e. Although one human case study reported a correlation between the severity of potato late-blight and the incidence of spina bifida, no other studies in humans have found a correlation between the consumption of potatoes and birth defects [ ].

In , the National Institute of Environmental Health Sciences determined that the average consumption of glycoalkaloids from potatoes was Ceska et al. Microbial infection of parsnip roots can result in a dramatic increase in furocoumarin levels. Furocoumarin concentrations the sum of five furocoumarins: angelicin, isopimpinellin, 5-MOP, 8-MOP and psoralen in freshly harvested parsnips are generally lower than 2.

1. Introduction

In celery, infection with fungal pathogens has been shown to produce timethylpsoralen which is absent from plants that are not infected and increased concentrations of 8-MOP. Fungal infection also has been shown to stimulate a fold increase in furocoumarin production by carrots Ceska et al. There are two major classes of heterocyclic aromatic amines HAAs. Pyrolytic HAAs are formed from the pyrolysis of amino acids or proteins at high temperature and aminoimidazoarenes AIAs are formed from creatine, free amino acids and monosaccharides, via the Maillard reaction.

HAAs are present in many protein-rich foods of animal origin including cooked meat, fish, poultry and gravies and sauces derived from pan residues and scrapings of cooked meats. The formation and yield of HAAs are dependent on cooking temperature and time concentrations increase with higher temperatures and longer cooking times , cooking technique and equipment concentrations of HAAs in meat are generally higher after grilling and panfrying than broiling or roasting , and the ability of HAA precursors to migrate to the surface [ ].

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The AIAs 2-aminomethylimidazo-[4,5-f]quinoline IQ , 2-amino-3,4-dimethylimidazo[4,5-f]quinoline MeIQ and 2-amino-3,8,dimethylimidazo[4,5-f]quinoxaline MeIQx are among the most potent mutagens ever tested in the Ames assay. Therefore, the potential for genotoxicity due to PhIP may be higher than that of more genotoxic HAAs in meat consumers [ ].

Several HAAs are carcinogenic in rodents after long-term dietary administration. Currently, no tolerable upper limit of exposure to HAAs has been established. Polycyclic aromatic hydrocarbons PAHs are known carcinogens that are formed from the incomplete combustion of fossil fuels such as wood, coal and oil. PAHs can enter the food chain from environmental contamination or from food processing.

Foods containing the highest concentrations of PAHs include cooked or smoked meat or fish, smoked or cured cheese, tea and roasted coffee. Grilling or broiling of meat, fish or other foods over intense heat or direct contact with flames promotes production of PAHs.

In general, concentrations of PAHs in meat are highest after charcoal grilling, followed by smoking, roasting and steaming. Concentrations of PAHs in smoked foods are influenced by temperature, type of wood, oxygen concentration and type of smoker. Concentrations of PAHs in tea dried over burning wood, oil or coal are generally higher than in tea dried over air, and coffee beans that are roasted over a direct fire contain higher concentrations than beans that do not come in contact with flames [ ]. Three of the four PAHs that have been tested for carcinogenicity in rats after oral exposure benz[a]anthracene, benzo[a]pyrene and dibenz[a,h]anthracene are carcinogenic.

The estimated high and safe levels of intake of the benchmark PAH benzo[a]pyrene are 0. It also is found in cocoa-based products and coffee. Acrylamide is formed via a Maillard reaction, a reaction between the carbonyl group of a reducing sugar and the nucleophilic group of an amino acid. Although a number of carbohydrates can be used as the source of the carbonyl group, the amino acid required for the formation of acrylamide is asparagine. Acrylamide is mutagenic and has been shown to be a neurotoxicant, reproductive toxicant and carcinogen in experimental animals and is classified by IARC as a probable human carcinogen.

The main metabolite, glycidamide an epoxide is thought to be responsible for genotoxicity [ ]. In humans, the only toxicological effect that has been linked to acrylamide is neurotoxicity in individuals occupationally exposed to high levels. Epidemiological studies have failed to show an increased risk of cancer from either occupational or dietary exposure to acrylamide and reproductive toxicity has not been reported in humans exposed to acrylamide [ ].

The residual acrylamide cannot be more than 0. Utilizing a benchmark dose of 0. Exposure to acrylamide can be reduced by avoiding deep-fried foods, soaking potato slices before cooking, cooking french fries at lower temperatures and to a lighter color, and toasting bread to a lighter color [ ]. Chloropropanols are formed in hydrolyzed vegetable proteins HVP produced by hydrochloric acid HCl hydrolysis of proteinaceous by-products from edible oil extraction, such as soybean meal, rapeseed meal and maize gluten [ , ].

Current Nutrition & Food Science

The chloropropanol most commonly found in food is 3-MCPD 3-monochloropropane-1,2-diol , although others may also be present, including 2-MCPD 2-monochloropropane-1,3-diol , 1,3-DCP 1,3-dichloropropanol , and 2,3-DCP 2,3-dichloropropanol [ ]. It is thought that 3-MCPD is formed as a result of a reaction between a source of chlorine chlorinated water or sodium chloride in a food or a food contact material and a lipid.

Two basic pathways have been proposed: thermally driven and enzyme-catalyzed generally lipase reactions. Direct precursors are thought to be glycerol and chloride. Recent work has also suggested glycidol 2,3-epoxypropanol as a precursor. Other foods that may contain 3-MCPD are cereal, toasted bread, coffee, cheese, licorice, baked goods, processed garlic, liquid smokes, malts, cured or smoked meat or fish or foods containing acid-HVP as a savory ingredient soups, prepared meals, savory snacks, gravy mixes and stick cubes [ , , , ].

Foods containing 1,3-DCP include raw meat and soy sauce produced using an acid hydrolysis process [ ]. In rats and mice, 3-MCPD is toxic to the kidney, producing renal tubule hyperplasia. It is also carcinogenic in rats when given in high doses over prolonged periods. Although 3-MCPD is genotoxic in vitro , it is not in vivo.

Therefore, 1,3-DCP is considered to be a potential carcinogen in humans. Furan Figure 6 is a by-product of high-energy and thermal treatment of carbohydrate. Meat and vegetable containing foods that are heat processed in cans and jars such as soups, pastas, sauces, gravy and baby food and brewed coffee, typically contain the highest concentrations. Although the mechanism of formation of furan in food is not completely understood, it can be synthesized from vitamin C, amino acids, reducing sugars, organic acids, carotenes and polyunsaturated fatty acids in the presence of heat [ ].

Furan is mutagenic and clastogenic in a number of in vitro mammalian cell assays, causes damage to chromosomes in mice, and is carcinogenic in both rats and mice after oral administration [ , , , ]. Furan is classified by IARC as possibly carcinogenic to humans [ ]. In the United States and Europe, exposure to furan from food is estimated to be a maximum of 1.

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Current Nutrition & Food Science, Volume 13 - Number 2

Mitigation of furan in foods is difficult because the mechanism for its formation in food is unclear. Due to the fact that furan is volatile, it is thought that concentrations can be reduced by heating food in open containers or leaving ready-to-eat foods open to air after preparation. However, the effectiveness of this strategy in reducing exposure to furan has yet to be demonstrated [ ].

Currently, there are no FDA regulations specific to the level of furan in food. Trans fatty acids also known as trans fat are the sum of all unsaturated fatty acids that contain one or more isolated double bonds in a trans configuration. Trans fatty acids more closely resemble saturated fatty acids than cis unsaturated fatty acids because their trans configuration makes them rigid. Trans fatty acids in the diet originate from two sources.

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The first is from bacterial hydrogenation in the forestomach of ruminants, which produces trans fatty acids that are found in beef and mutton fat, milk and butter. Trans fatty acids are also produced from the hydrogenation of liquid oils mainly of vegetable origin. This produces solid fats and partially hydrogenated oils such as margarines, spreads, shortenings and frying oil, which are more stable than liquid oils [ ].

Biochemically, trans-fatty acids act similarly to saturated fatty acids, raising low density lipoprotein LDL cholesterol and decreasing high-density lipoprotein HDL cholesterol levels [ ]. High intakes of trans fatty acids have been associated with an increased risk of coronary heart disease CHD independent of other risk factors in large epidemiological studies [ ].

A tolerable upper limit of trans fatty acids has not been set because any incremental increase in the intake of trans fatty acids increases the risk of coronary heart disease [ ]. In , the FDA estimated that the average daily intake of trans fat in the United States is about 5. Due to increased efforts by food manufacturers to reduce or eliminate the use of partially hydrogenated vegetable fat in food production, it is estimated that trans fatty acid content of processed foods has decreased over the last decade [ ].

Integrative Food, Nutrition and Metabolism

Nitrosamines are formed from the interaction of nitrites or other nitrosating agents with amines in food or in vivo , under acidic conditions. Nitrites may be directly added to food or can be formed from bacterial reduction of nitrate. Nitrites and nitrates may occur naturally in water or foods such as leafy vegetables due to the use of fertilizer, or may be added to foods to prevent growth of Clostridium botulinum , or to add color or flavor [ ].

Nitrosamines have been found in a variety of different foods such as cheese, soybean oil, canned fruit, meat products, cured or smoked meats, fish and fish products, spices used for meat curing, and beer and other alcoholic beverages [ ].

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Beer, meat products and fish are considered the main sources of exposure. Drying, kilning, salting, smoking or curing promotes formation of nitrosamines [ ]. Evidence from case-control studies supports an association between nitrosamine intake with gastric cancer, but not esophageal cancer in humans [ ]. Levels of nitrosamines have been declining during the past three decades, concurrent with a lowering of the nitrite used in food, use of inhibitors such as ascorbic acid and use of lower operating temperatures and indirect heating during food processing.

Based on an estimated exposure level of 3.


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Although current FDA regulations do not limit nitrosamine levels in foods, the FDA has provided an action level of 10 ppb for individual nitrosamines in both consumer and hospital rubber baby bottle nipples, while the FDA limits the approval of nitrites in curing mixes to the FDA-regulated food additive process 21 CFR Biogenic amines are normally formed in humans by normal cellular metabolism.