There are no FDA regulations or guidelines restricting the presence of lectins in food, but the FDA does provide recommended cooking practices prior to consuming legumes.
Concentrations of PHA and other lectins are higher in uncooked than cooked beans. A raw, red kidney bean can contain up to 70, hemagluttinating units hau. Most lectins are reduced by moist, but not dry heat. Therefore, steaming or boiling causes a significant reduction in concentrations of lectins in beans. Boiling for at least ten minutes has been shown to reduce hau in beans by fold. Substances that act on the availability of vitamins are commonly referred to as antivitamins.
These include materials that can cause a deficiency of vitamins by competing with vitamins in various metabolic reactions as the result of similar chemical structure or destroying or decreasing the effects of a vitamin by modifying the molecular conformation or by forming a complex [ 67 ].
Thiaminase cleaves thiamine vitamin B1 at the methylene linkage, rendering it biologically inactive. Activity of thiaminase requires a cosubstrate—usually an amine or sulfhydryl-containing protein such as proline or cysteine.
Thiaminase is found in fish, crab, clams and in some fruits and vegetables such as blueberries, black currants, red beets, Brussels sprouts and red cabbage [ 67 ]. Thiamine is an essential vitamin involved in energy production.
Thiamine deficiency is associated with impaired pyruvate utilization, resulting in a shortage of cellular ATP. In humans, thiamine deficiency may lead to weakness and weight loss. Cooking destroys thiaminases in fish and other sources.
There are no FDA regulations or guidelines specific to the presence of thiaminase in food. Herbs such as comfrey root and leaf Symphytum spp. Figure 2 , coltsfoot leaf and flower Tussilago farfara and borage leaf Borago officinale , and several species of Eupatorium typically contain high levels of PAs. Humans are exposed to PAs through the accidental contamination of foodstuffs and intentional ingestion of PA-containing vegetables and herbal medicines.
Serious incidences of illness have been reported in people consuming cereal grains that are contaminated with the seeds of PA-containing plants [ 81 ]. PAs are also present in milk from cows and goats and in honey [ 82 ].
Comfrey Symphytum officianale L. The pyrrolizidine structure is based on two fused, five-membered rings that share a bridgehead nitrogen atom, forming a tertiary alkaloid. The rings contain a hydroxymethylene group at the C-1 position and a hydroxyl group at the C-7 position, forming a necine base.
Toxicity is thought to be due to enzymatic conversion of PAs to pyrroles, which act as alkylating agents [ 67 ]. Pyrroles formed in the liver can travel to the lungs, causing thickening of the pulmonary vasculature and pulmonary hypertension [ 82 ].
The sale of comfrey products for internal use has been banned in the United States and Canada [ 82 ]. However, comfrey tea is still widely available.
It is estimated that consumers of comfrey tea could be ingesting up to 5 mg of PAs per day Speijers and Egmond, as cited in Deshpande b [ 81 ], p. The range of toxic doses in humans is thought to be 0.
Oxalic acid oxalate is generally found in rhubarb 0. Oxalic acid is an organic acid that can bind calcium and other minerals, making them insoluble and decreasing their bioavailability. Ingestion of foods containing high concentrations of oxalates may cause decreased bone growth, kidney stones, renal toxicity, vomiting, diarrhea, convulsions, coma and impaired blood clotting [ 73 ].
Because approximately 4. Because cooking does not remove oxalate, and mineral complexes with oxalate are insoluble in water, oxalates are somewhat difficult to remove from foods. Therefore, diets rich in oxalate-containing foods should be supplemented with minerals such as calcium or potassium to prevent deficiencies. Limits on oxalic acid have been cited in ferric ammonium ferrocyanide and ferric ferrocyanide when used as color additives 21 CFR Members of the Cucurbitacea family zucchini, cucumbers, pumpkins, squash, melons and gourds produce cucurbitacins oxygenated tetracyclic terpenes that act as movement arresters and compulsive feeding stimulants for Diabriticine beetles corn rootworms and cucumber beetles.
Cucurbitacins are among the most bitter compounds known, and in nanogram quantities they deter most non-Diabrotic herbivores [ 87 ]. Because cucurbitacins act as feeding stimulants, they are added to insecticidal baits to increase efficacy [ 88 ]. Therefore, dietary exposure to cucurbitacins could occur through ingesting plants that normally contain them or by ingesting plants to which cucurbitacin-containing pesticides have been applied. Under normal circumstances, cucubitacins are produced at low enough concentrations that are not perceived as being bitter by humans.
In response to stresses such as high temperatures, drought, low soil fertility and low soil pH, concentrations in fruits such as cucumbers may increase and cause the fruits to have a bitter taste [ 89 ].
Occasional cases of stomach cramps and diarrhea have occurred in people ingesting bitter zucchini. Twenty—two cases of human poisoning from ingestion of as little as 3 grams of bitter zucchini were reported in Australia from to , and in Alabama and California in There are no FDA regulations or guidelines specific to the presence of cucurbitacins in food.
Coumarin 2Hbenzopyranone is found in herb teas made from tonka beans Dipteryx odorata , melilot Melilotus officinalis or Melilotus arvensis and woodruff Asperula odorata , the flavoring oil of bergamot from Citrus bergamia and the spice cassia Cinnamomum cassia ; sometimes sold as cinnamon [ 91 ]. Coumarin is liberated from the glycoside melilotoside an ether of glucose bonded with an ester bond to coumarin on drying coumarin-containing herb material.
Molds present in spoiled sweet Melilotus clover and other hay products can metabolize coumarin to dicoumarol, which is similar in structure to vitamin K [ 92 ]. Vitamin K is necessary to activate prothrombin, which is converted to the blood clotting substance thrombin.
By inhibiting vitamin K, dicoumarol promotes bleeding. The addition of coumarin to food in the United States was banned in , based on reports of hepatoxicity in rats. However, because a number of foods contain coumarin, humans ingest approximately 0. The chronic administration of high doses of coumarin causes liver tumors in the rat and liver and lung tumors in the mouse. Overall, available data indicate that coumarin is not genotoxic.
It is thought that the carcinogenicity of coumarin is caused by metabolism to toxic epoxides. Because doses of coumarin that cause toxicity and carcinogenicity in the lung and liver of experimental animals are more than times the maximum human intake, exposure to coumarin from food poses no health risk to humans [ 93 ].
The addition of coumarin is prohibited in 21 CFR The regulation notes that coumarin is found in tonka beans and extract of tonka beans, among other natural sources, and is also synthesized.
It has been used as a flavoring compound, therefore addressing not just natural products which would include buffalo grass or sweetgrass Hierochloe odorata used in flavoring vodka and other natural sources see above , as well as synthesized coumarin. Phytic acid also referred to as phytate is found in bran and germ of many plant seeds and in grains, legumes and nuts.
Phytic acid is a simple sugar myo-inositol containing six phosphate sidechains, and as such, is a dietary source of phosphorus and an effective chelator of divalent cations such as zinc, copper, iron, magnesium and calcium [ 67 , 94 ]. Studies indicate that phytate-mineral complexes are insoluble in the intestinal tract, reducing mineral bioavailability [ 73 ].
Therefore, ingestion of foods containing high amounts of phytate could theoretically cause mineral deficiencies or decreased protein and starch digestibility. Vegetarians that consume large amounts of tofu and bean curd are particularly at risk of mineral deficiencies due to phytate consumption.
Because phytate-rich foods are digested at a slower rate and produce lower blood glucose responses than foods that do not contain phytate, it has been hypothesized that phytate could have a therapeutic role in management of diabetes [ 67 ].
It also may have utility as an antioxidant [ 95 ]. However, because the beneficial effects of phytate are outweighed by its ability to cause essential mineral deficiencies, consumption of a diet containing high amounts of phytate is not recommended.
Food manufacturers are developing methods to reduce phytate in foods, such as addition of the microbial phytase, which releases phosphates from the inositol backbone of phytate [ 96 ]. Phytate is fairly heat stable, but can be removed by soaking or fermentation [ 67 ]. The soybean has one of the highest phytate levels of any grain or legume, and requires a long period of fermentation for reduction [ 94 ].
In people who consume large amounts of soy products, mineral deficiencies can be prevented by consumption of meat or dairy products or use of supplemental vitamins.
There are no FDA regulations or guidelines restricting the presence of phytates in food. Ackee Blighia sapida ; Figure 3 is the national fruit of Jamaica and is also found in other Caribbean nations, Central America, South American and southern Florida [ 97 ]. Levels of HGA in the opened, ripe fruit are undetectable, making opened fruit safe for consumption [ 98 ].
The hypoglycin toxin L-methylenecyclopropylalanine inactivates several flavoprotein acyl-CoA dehydrogenases, causing disturbances of the oxidation of fatty acids and amino acids [ 99 ]. This leads to a secondary inhibition of gluconeogenesis which can precipitate an extreme, dangerous drop in blood-glucose levels hypoglycemia that can be fatal.
Symptoms of poisoning from unripe ackee fruit occur within 6 to 48 hours of ingestion and include drowsiness, repeated vomiting, thirst, delirium, fever or loose bowels. Exhaustion of the muscular and nervous systems, collapse, coma, and death may ensue [ , ]. Unripe Ackee Fruit left panel and ripe Ackee Fruit right panel [ ].
Dietary exposure to hypoglycin in Jamaicans ranges from 1. The importation of canned ackee fruit into the United States is restricted to certain manufacturers to insure that only properly ripened ackees are used for canning [ ], and the FDA routinely analyzes incoming shipments of ackee for hypoglycin levels that could be a health concern, having issued a recall of canned ackee fruit for this very reason in If hypoglycin poisoning is expected, glucose, fluids and electrolytes should be administered.
Antiemetics may be used to control vomiting and benzodiazepines to control seizures. Endotracheal intubation should be performed in people exhibiting seizures or coma [ 97 ]. Safrole 1-allyl-3,4-methylenedioxybenzene is found in aromatic oils of nutmeg Myristica fragrans , cinnamon Cinnamomum verum and camphor Cinnamomum camphora and is a major constituent of oil of sassafras Sassafras albidum [ ].
Prior to being banned as a food additive in the United States in , safrole was commonly used to flavor root beer and other foods. Based on sufficient evidence of carcinogenicity in experimental animals, safrole is reasonably anticipated to be a human carcinogen [ ]. Despite the FDA ban, sassafras is still a popular ingredient in herb teas and preparations [ 73 ]. This may be exceeded by ingesting sassafras tea, which has been estimated by Segelman and Bisset as cited in Burfield [ ], p.
Myristicin Figure 4 is a naturally occurring insecticide and acaracide that is found in nutmeg and mace Myristica spp. It is also present in black pepper, carrot, celery parsley and dill [ 67 ]. Myristicin is a weak inhibitor of monoamine oxidase, and is structurally related to mescaline. Unpleasant symptoms, such as nausea, tremor, tachycardia, anxiety and fear have also been reported in humans ingesting this dose. Although the metabolism of myristicin resembles that of safrole, there is no evidence to suggest that myristicin is carcinogenic [ ].
There are no FDA regulations or guidelines specific to the presence of myristicin in food. At the concentrations normally present in spices or food, the likelihood of toxicity arising from myristicin is low. Tomatine is toxic to a number of different fungi, thereby acting as a natural fungicide. It has been hypothesized that the toxic effects of tomatine on fungi are due to the ability of tomatine to complex with membrane sterols, causing membrane disruption [ ].
Currently, there is no evidence to suggest that tomatine is a substance of concern. There are no reports of acute toxicity in humans due to ingestion of green tomatoes and there are no FDA regulations or guidelines specific to the presence of tomatine in food.
Ingestion of a rare variety of ripe tomato Lycopersicon esculentum var. Concentrations of tomatine decrease as tomatoes ripen, and ripe fruit contains approximately 36 mg per a gram tomato [ 73 ]. Microwaving or frying does not reduce content of tomatine, and delayed-ripening varieties of tomatoes contain similar concentrations of tomatine as other tomatoes [ ]. At this time, there is no evidence to suggest that a diet high in green tomatoes would be injurious to human health. Tomatine forms strong, insoluble complexes with cholesterol in vitro , and has been shown to lower plasma LDL cholesterol in hamsters [ ], suggesting that it may have beneficial effects on blood lipids of humans.
Chinese star anise Illicium verum is a common source of anethole, a popular flavoring ingredient. On the other hand, Japanese star anise Illicium anisatum is scientifically recognized as highly poisonous and not fit for human consumption.
Japanese star anise contains the potent neurotoxins anisatin and neoanisatin, as well as the neurotoxic sesquiterpene lactone veranisatins that are normally found in other kinds of star anise, including Chinese star anise [ ].
The illnesses ranged from serious neurological effects, such as seizures, to vomiting, jitteriness and rapid eye movement. Although glycoalkaloids are found throughout the potato tuber, the greatest concentrations are in the sprouts, peels and sun-greened areas [ 74 ]. Under current FDA regulations, 20 milligrams of solanine per grams a small potato can render it unfit to eat.
Exposure of potatoes to light in the field or marketplace can lead to glycoalkaloid concentrations that are unsafe for human consumption. Concentrations of solanine in green or blighted potatoes have been shown to increase by seven fold [ 73 ]. Symptoms of glycoalkaloid toxicity in humans include drowsiness, itchiness in the neck region, increased sensitivity hyperesthesia , labored breathing and gastrointestinal symptoms abdominal pain, nausea, vomiting and diarrhea [ 74 ].
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. 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 [ ].
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 [ , ].
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.
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. 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 [ ]. 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 [ ]. 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. 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.
In food, biogenic amines are mainly formed from microbial decarboxylation of amino acids. They are commonly found in fermented meat, beverages and dairy products, sauerkraut, and spoiled fish. The main biogenic amines in food are histamine, tyramine cadaverine, putrescine, spermidine and spermine. The two biogenic amines that have been associated with acute toxicity are histamine and tyramine. Putresine, spermine, sperimidine and cadaverine are not toxic in and of themselves, but may react with nitrite or nitrate to form nitrosamines see Section 4.
Scombrotoxicosis is a common seafood-borne disease associated with the consumption of toxic levels of histamine in spoiled scombroid fish such as tuna Thunnus spp. Red wine may also contain relatively high levels of histamine. Symptoms of histamine intoxication from food are similar to allergies to other substances and include sneezing, nose congestion, breathing difficulties and urticaria [ ].
Consumption of tyramine may precipitate migraine headache or a hypertensive crisis. The most serious case reports of tyramine toxicity have occurred in people consuming aged cheese. Because monoamine oxidase inhibitor MAOI drugs inhibit metabolism of amines, people taking these drugs may be particularly susceptible to tyramine toxicity.
Whereas — mg of dietary tyramine induces only a mild rise in blood pressure in unmedicated adults, 10—25 mg may produce a serious adverse event in those taking MAOI drugs.
Other potentiating factors for tyramine toxicity include alcohol consumption, gastrointestinal distress and exposure to other amines [ ]. Efforts taken by food manufacturers to reduce biogenic amine concentrations in fermented foods include using amine-negative starter cultures, adding probiotic bacterial strains alone or in combination with starter cultures, high pressure processing or low-dose gamma radiation [ ].
Consumption of seafood contaminated with algal toxins results in five different syndromes, paralytic, neurotoxic, amnesic, or diarrhetic shellfish poisoning and ciguatera fish poisoning [ ]. Paralytic shellfish poisoning PSP is caused by the consumption of molluscan shellfish contaminated with heterocyclic guanidines called saxitoxins. Currently, over 21 known saxitoxins are produced by dinoflagellate species from three genera: Alexandrium , Gymnodium and Pyrodinium.
Toxicity is caused by binding of saxitoxins to voltage-dependent sodium channels, which blocks neuronal activity. The primary site of action in humans is the peripheral nervous system.
Symptoms of toxicity include tingling and numbness of the perioral area and extremities, loss of motor control, drowsiness, and incoherence. Ingestion of 1—4 mg saxitoxin has resulted in death from respiratory paralysis [ ]. Outbreaks of PSP have occurred worldwide, due to the fact that saxitoxin-producing species of dinoflagellates can live in either temperate or tropical waters. Saxitoxins are not inactivated by cooking, and must be mitigated at their source to prevent ingestion.
PSP is prevented by large-scale, proactive monitoring programs and rapid closures of harvest in areas containing dinoflagellate algal blooms [ ]. The dinoflagellate Karenia brevis produces brevetoxins that are lethal to fish, but not to mollusks such as oysters, clams and mussels. Consequently, they can accumulate in healthy-appearing mollusks to concentrations that are toxic to humans who ingest them. Karenia brevis brevitoxins cause the syndrome known as neurotoxic shellfish poisoning NSP , which affects sodium transport in the autonomic nervous system and causes inhibition of neuromuscular transmission in skeletal muscle.
NSP is usually a relatively mild illness and should not be confused with the more serious condition of PSP. Dilated pupils, bradycardia and convulsions may occur in cases of severe poisoning [ ]. Blooms along the west coast of Florida occur regularly [ ]. Biotoxin control plans that are implemented during period of red tide are generally effective in preventing NSP, but have not eliminated NSP entirely.
The FDA has established an action level of 0. Amnesic shellfish poisoning ASP is caused by domoic acid produced by diatoms of the genus Pseudo - nitzchia Figure 7 , which are consumed by mussels, scallops, clams and crabs. Domoic acid is a water-soluble, tricarboxylic amino acid that is a structural analog of the neurotransmitter glutamate and is a glutamate receptor agonist.
Persistent activation of the kainite glutamate receptor causes an increase in intracellular calcium, which can cause neuronal cell death and lesions of the brain where glutamineric pathways are concentrated. Areas of the brain involved in learning and memory processing are particularly susceptible [ ]. The symptoms of ASP are gastroenteritis, dizziness, disorientation, lethargy, seizures and loss of short term memory.
Respiratory difficulty, coma and death may ensue [ ]. Pseudo - nitzchia [ ]. In , approximately people became ill and died in Prince Edward Island, Canada, after eating contaminated mussels.
In , domoic acid poisoning caused the deaths of numerous pelicans and cormorants in Monterey Bay that ingested sardines and anchovies. Domoic acid also was responsible for a massive sea lion kill in Monterey Bay in [ ]. Pseudo - nitzchia and domoic acid are now closely monitored throughout the world [ ].
The FDA has established an action level of 20 ppm for domoic acid, except in the viscera of Dungeness crab, where 30 ppm is permitted [ ]. Regulatory guidance has been effective in preventing ASP in humans, since no human outbreaks of ASP have occurred since Diarrhetic shellfish poisoning DSP is caused by the production of okadaic acid and dinophysistoxins in the dinoflagellates Dinophysis fortii or Prorocentrum lima , which are consumed by mollusks.
Compared to other types of shellfish poisoning, symptoms of DSP are relatively mild, and generally consist of diarrhea, abdominal cramps, nausea, chills or vomiting within 30 minutes to a few hours after consumption of DSP toxins.
Symptoms generally resolve within 2—3 days, with or without medical treatment [ ]. Diarrhea is most likely due to the hyperphosphorylation of proteins including ion channels in the intestinal epithelia, resulting in impaired water balance and fluid loss. The long term consequences of low level exposure to DSP toxins may be more serious, as they have been shown to be tumor promoters [ ]. Ciguatera fish poisoning CFP is caused by the dinoflagellate Gambierdiscus toxicus , which grows on filamentous macroalgae associated with coral reefs.
The lipophilic precursors to ciguatoxin are biotransformed to ciguatoxins in herbivorous fish and invertebrates that consume the macroalgae, and bioaccumulate in large carnivorous fishes associated with coral reefs. High ciguatoxin concentrations may be found in barracuda, snapper, grouper and jacks [ ]. Ciguatoxins are structurally related to the brevetoxins and compete with brevetoxin for binding to the same site on the voltage-dependent sodium channel.
However, because ciguatoxin has a higher binding affinity for the site than brevetoxin, the toxic potency of ciguatoxin is higher than that of brevetoxin. The threshold level for toxicity in humans is estimated to be 0. CFP is estimated to affect over 50, people worldwide each year. In rare cases, CFP is fatal [ ]. Inasmuch as ciguatoxin is produced by organisms that live beneath the surface and is not routinely monitored for concentration in seafood, the only way to prevent consumption is to completely abstain from ingesting tropical reef fish, as the occurrence of toxic fish is sporadic, and not all fish of a given species or from a given locality will be toxic [ ].
Currently, there are no FDA regulations limiting levels of ciguatoxins in fish, although a recent publication suggests an advisory level of 0. There are naturally occurring toxins in some species that do not involve marine algae.
Ingestion of fish containing wax esters in large amounts, coupled with their indigestibility and low melting point, results in diarrhea [ ].
No tolerances have been established, and the FDA recommends avoidance of these fish [ ]. Juvenile Oilfish Ruvettus pretiosus [ ]. Tetramine is a toxin found in the salivary glands of Buccinum , Busycon or Neptunia spp. Whelk are associated with a heat-stable neurotoxin, tetramine, which upon ingestion produces, among other symptoms, eyeball pain, headache, dizziness, abdominal pain, ataxia, tingling in the fingers, nausea and diarrhea [ , ]. Power et al. Reid et al. Because the whelk is a predator of bivalves, it is assumed the toxin is used for food procurement [ ].
Although the FDA recommends removal of the salivary gland to avoid possible intoxication [ ], tetramine is present in other tissues, albeit at lesser concentrations [ ]. The meat of the Greenland shark Somniosus microcephalus and the related member of the dogfish family, the pacific sleeper shark Somniosus pacificus , is known to be poisonous to both man and dogs. The causative agent is trimethylamine oxide, which breaks down to trimethylamine in the gut, probably by enteric bacteria.
The result is absorption of trimethylamine, which acts as a neurotoxin, producing ataxia in both man and dogs. However, the flesh may be consumed if boiled several times with changes of water, or as the Inuit prepares it, by burying it in the ground and allowing the meat to go through several freezing and thawing cycles [ , , ].
Rhododendrons and azaleas Rhododendron spp. Although not all rhododendrons produce grayanotoxins also known as oleander toxin, andromedotoxin, acetylandromedol or rhodotoxin , several species growing in the US are known to produce grayanotoxins and include Rhododendron occidentale , Rhododendron macrophyllum and Rhododendron albiflorum , all in the western US.
Grayanotoxin is also found in the eastern US, within the botanical family Ericaceae, to which rhododendrons belong and are probably the most important sources of the toxin [ ]. Grayanotoxins [ ]. Grayanotoxin consists of a series of cardiac glycosides: thevetin, convallarin, steroidal, helleborein, ouabain, and digitoxin. At first, sympathetic nerves are paralyzed; the cardiotoxin stimulates the heart muscles similar to the action of digitalis, and gastric distress ensues.
Symptoms start out as nausea, vomiting, abdominal pain and diarrhea; followed by tremor, drowsiness and ataxia. In severe cases, ectopic beats occur which may be followed by ventricular tachycardia and fibrillation.
The origin of toxicity may be honey made from the nectar of the flowers , milk from a cow having eaten the foliage and meat e. The pooling of large quantities of grayanotoxin-containing honey or milk during commercial processing typically dilutes grayanotoxin to nontoxic levels.
There are no FDA regulations specific to grayanotoxin levels in foods. In humans, milk sickness is characterized by loss of appetite, listlessness, weakness, vague pains, muscle stiffness, vomiting, abdominal discomfort, constipation, foul breath and finally, coma. For many years the origin of milk sickness was unknown, because there was nothing comparable in Europe origin of most of the pioneers and the outbreaks were sporadic.
The sporadic nature of outbreaks became clear when it was realized that cattle would consume these plants in over-grazed pasture or in years of drought; additionally, the toxin levels in plants can vary considerably, making identification of the source of poisonings difficult.
Tremetol or tremetone is the toxic agent and consists of a mixture of sterols and derivatives of methyl ketone benzofuran. The three major benzofuran ketones are tremetone, dehydrotremetone and 3-oxyangeloyl-tremetone [ , , , , ].
Currently, there is no USDA guidance specific to tremetol levels in dairy products. At normal levels of food consumption, there is little potential for toxicity from natural food toxins. Nevertheless, there is always the possibility of an idiosyncratic response or undetected contamination. National Center for Biotechnology Information , U. However, there are a few ingredients that may be harmful, particularly when consumed in large amounts.
Refined vegetable and seed oils include corn, sunflower, safflower, soybean, and cottonseed oils. Unlike oils that come from naturally oily foods — such as coconut oil, olive oil, and avocado oil — these oils must be extracted through a complicated process that involves using chemical compounds such as hexane to extract and purify them 1.
Oils are also high in calories and fat. This is not generally an issue, because fat is a macronutrient that provides the body with energy. However, some oils are particularly high in omega-6 polyunsaturated fatty acids 2. Still, new guidelines recommend replacing saturated fats with unsaturated fats such as omega-6s.
Finally, when these oils are heated, they can produce potentially cancer-causing aldehydes. The highest emissions can occur during deep-frying, while lower emissions occur from gentle cooking methods such as stir-frying.
You can reduce production of aldehydes by opting for oils low in unsaturated fatty acids, such as rapeseed oil 6. Unlike oils from naturally oily foods, like coconut oil and olive oil, vegetable and seed oils may be refined. They can also produce potentially cancer-causing aldehydes, especially during deep-frying, but other cooking methods can reduce those emissions. Bisphenol A BPA is a chemical that used to be found in the plastic containers of many common foods and beverages and in the lining inside metal cans for instance, those used for canned tomatoes.
However, studies have shown that BPA can leach out of these containers and into the food or beverage inside 7. BPA is believed to mimic estrogen by binding to the receptor sites meant for the hormone.
This can disrupt typical hormone function 7. Some observational studies have also found that high BPA levels are associated with insulin resistance, type 2 diabetes, and obesity 10 , However, while animal studies have found an association between BPA and weight gain and insulin resistance, few human studies have studied the association between markers of BPA exposure and diabetes 10 , Fortunately, most plastics and cans are now BPA-free.
However, BPA has been replaced in many products with very similar compounds such as bisphenol S, which may have similar effects To reduce your exposure to these potentially harmful compounds, avoid plastic dishware as much as possible — including bottled water. Use glass and stainless steel drinkware instead of plastic, and look for foods that are packaged in glass rather than aluminum cans.
BPA was once commonly found in plastic and the lining of aluminum cans, but it has since been mostly phased out because of links to negative health effects.
However, replacements such as BPS may have similar drawbacks. Artificial trans fats are made by pumping hydrogen into unsaturated oils such as soybean and corn oils to turn them into solid fats. They used to be in many processed foods, such as margarine, snack foods, and packaged baked goods. However, animal and observational studies have repeatedly shown that trans fat consumption causes inflammation and has negative effects on heart health 13 , 14 , For this reason, the use of artificial trans fats has been fully banned in the United States since January Artificial trans fats are highly inflammatory and may contribute to heart disease.
They are now banned from being used in food in the United States, but if a serving of food contains less than 0. Below we examine some of the most prevalent contaminants in dry, plant-based foods and ingredients.
Because sesame seeds are a common ingredient in dry foods with long shelf lives, as of February , further reports of contamination had been issued across the EU, resulting in thousands of product recalls to date. Mycotoxins are a naturally occurring type of toxins when certain fungi grow on crops and harvested foods.
And now climate change is giving rise to new challenges. Although hundreds of mycotoxins exist and are screened for regularly, aflatoxins and ochratoxin A in particular, are considered some of the most prevalent in dry foods and ingredients. Aflatoxins are a type of mould that occur before harvest in hot and humid environments or during storage when exposed to poor conditions. Aflatoxins not only pose a risk to those consuming foods but also those handling them.
Read more about aflatoxins here on our blog. OTA is one of the most toxic and common natural contaminants in foods. Numerous studies have found that it specifically targets the kidneys and liver. Coumarin is a natural and fragrant compound that occurs in high levels of cassia cinnamon.
It is also present in trace amounts in Ceylon cinnamon as well as a handful of other plants. Today, many manufacturers opt to utilise cassia cinnamon as a spice over Ceylon cinnamon because of its more distinct flavour and lower price point. In , the EFSA established that it is safe to consume up to 0. Cadmium is present in the environment naturally but can also enter the environment industrially through industrial or agricultural processes.
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