This page contains educational material about moldy food and health problems that can be caused by moldy food. This information is for educational purposes only. Nothing in this text is intended to serve as medical advice. All medical decisions should be made only with the guidance of your own personal medical authority. I am doing my best to get this data up quickly and correctly. If you find errors in this data, please let me know.
For research abstracts on Mold and food click here.
Mold on food may or may not be harmful. Some molds are used to create cheese such as "blue cheese" which is made from penicillium. Mold is also used to create medications such as penicillin. However, mold can cause illness or even death if it is a mold that creates mycotoxins that are harmful to animals and humans when ingested.
Mycotoxins are secondary metabolites of fungus that are toxic to humans, animals and plants. They often grow on edible plants. This can lead to contamination of feed for animals or human food. Plants are often able to alter these mycotoxins in what appears to be methods of biotransformation or detoxification to protect themselves. These methods are very similar to our own Phase 1 and Pase II processes that we use to biotransform toxins. It might interest the reader to know that they rely heavily on glutathione as we do. "Apart from glycosylation, conjugation with reduced glutathione is the most important phase II detoxification mechanism in plants." (Dixon DP, 1998) The fact that they are biotransorming these mycotoxins creates plant derived mycotoxin metabolites. So, in reality we really have two categories of toxins from mold that are a threat. The original fungal generated mycotoxins and the altered mycotoxin metabolites.
The Plant altered mycotoxins which are categorized as 1) extractable conjugated or 2) non-extractable or bound mycotoxins. Both of these plant derived mycotoxin metabolite groups are present in the plant tissue. In a 2013 research article Franz Berthiller called them "masked mycotoxin." Extractable conjugated mycotoxins can be detected by appropriate analytical methods if their structure is known to researchers and analytical standards are available. Bound mycotoxins are not directly accessible and have to be removed from the matrix they are bound in, by chemical or enzymatic treatment prior to chemical analysis.
These altered metabolites from the mycotoxins are not screened for on plants. Only the origianl mold generated mycotoxins are presently screened for on plants. The masked mycotoxins are currently not routinely screened for in food. They are also not regulated by legislation. This is due to lack of screening procedures and lack of funds to support screening.
I suggest if you want to know more about masked mycotoxins you read this great research review article by Franz Berthiller.
I will discuss the commonly found mycotoxins in food below.
Some of the more common foods you should be suspicious of harboring mold mycotoxins are corn, wheat, barley, sorghum, rye, peanuts, coconut, wine, beer, old or damaged fruit. Farm animals fed moldy grains can build up mycotoxins in their tissues and you can get if from eating their meat. Mycotoxins can also be passed through their milk. This is why great care should be taken to harvest and store food for people and animals properly.
Research has shown that toxic molds can interact with toxic bacterias to create more inflammation and cell damage than either one of the two on their own. (see pestka J, Zhou HR Toll-like receptor priming sensitizes macrophages to proinflammatory cytokine gene induction by deoxynivalenol and other toxicants. Toxicological Science)
It is not normal to find mold growing on a healthy plant in the prime of its life. Plants have various means to resist fungal infections. These are structural, innate and induced resistance to mold. However, certain environmental factors such as heat, drought, excess/long periods of moisture and insect damage can weaken a plants resistance to fungal infection. The fungus growing on a plant may or may not produce toxins that are harmful to humans, animals and other plants. These toxins called mycotoxins are byproducts that the fungi makes in response to stress caused by environmental extremes, shortage of food, or competition from other microorganisms or application of chemicals by human.
The toxic effects of mycotoxins can be either acute or chronic in nature.
Control of mycotoxins in food has been attempted through control of farming practices, control of incoming food into warehouses, control of moisture,and pH. Some biotechnology companies and conventional farmers have claimed there is higher mycotoxin contamination from organic farming practices. Science however has shown that two conventional agricultural practices trigger mycotoxins. This is the application of nitrogen fertilizer and use of fungicides. Fungicides are particularly frightening. They will not kill all the target fungi. Those that are left are placed under stress and one of their defense mechanisms brought on by stress is to make mycotoxins. Additionally, other species of fungi that are not targeted by the chemicals will now have less competition and they will grow to fill in the empty space. Sometimes this is a fungi that will produce dangerous mycotoxins. Studies have shown that high levels of nitrogen fertilizer used on conventional wheat stimulates fungal growth. If the weather conditions place the fungal population under stress, they produce mycotoxins as part of their response to the stress.
Farmers and food warehousers attempt to keep mold out of our food. Still we find mycotoxins in our food supply. The United Nations has said that 25% of our worlds grain supply is contaminated with mycotoxins. If you really want control of your food, I suggest you grow as much of it yourself as you can and get the rest form local farmers that you can trust. Any time you cut down on transport and storage of a food, you will also decrease the chances of mold growth.
In Europe they have identified the top mycotoxins that concern them in the food chain as follows:
Aflatoxin B1 is produced by many species of Aspergillus, most notably A. flavus and A. parasiticus; it is a proven carcinogen for humans, immunotoxic, and it causes stunted growth in children and growth retardation in animals. High-level of aflatoxin exposure produces acute hepatic necrosis and later it can result in cirrhosis, and/or carcinoma of the liver.
There are 3 major mold groups found in food that are considered to effect human health.
Aspergillus spp. Fusarium spp., penicillium.
These 3 groups of molds produce 5 mycotoxin groups of significance. The mycotoxins are Patulin, Fumonisins, Aflatoxisn, Ochratoxins, Zearalanon, Tricothecenes.
Examples of fungi known to produce mycotoxins harmful to humans/animals.
The Aspergillus genus are found worldwide in the soil, forage products for animals, food products, in organic debris, in composting material, and in dust. They are considered to be weak plant pathogens. However two of the species, Aspergillus flavus and parasiticus are known to produce potent toxins called afflatoxins on certain crops.
Aflatoxin: Aspergillus produces the mycotoxin called Aflatoxin. It was discovered after 10,000 turkeys died from contaminated peanuts in England. Aflatoxin has been the cause of deaths in humans and animals as well as birds. They are known to be hepatotoxic (liver toxins), teratogenic (causes malformations of an embryo or fetus) and mutagenic (causes mutations in genetic material).
The food/forage crops that are known to be especially susceptible to Aspergillus flavus and parasiticus are peanuts, corn and cottonseed. A. flavus is more common on corn and cottonseed, while A. parasiticus is more common on peanuts. Those corns containing higher oil contents are at greater risk for aflotaxins than normal hybrids during the growing process.
Aflatoxins contaminate many crops including corn, peanuts, cottonseed, brazil nuts, pistachios dried coconut, dried figs, and spices. They are common in hot and humid regions of the world. Aflatoxin contamination is worse during drought years.
There are four main aflatoxins produced by A. flavus and A. parasiticus known as B1, B2, G1 and G2. "B" and "G" refer to the blue or green fluorescence observed upon exposure of the toxin to ultraviolet irradiation. In animals and humans metabolism and oxidation of B1 and B2 will change them into the metabolites M1 and M2 which will appear in milk, urine and feces. Since aflatoxin B1 is a strong carcinogen and is found on corn crops used as feed for animals and humans, contamination of corn is taken very seriously and there is much research on methods to lower contamination and/or bind the aflatoxins so they are not absorbed by animals or humans. AFB1 metabolites can be measured in urine if suspected as a toxin in people or animals. Chlorophyllin has been shown to protect against human AFB1 toxicity (Kensler and others 2004)
Carcinoma appears to be due to AFB1 being metabolized by the liver via cytochrome P450 enzyme system to a carcinogenic metabolite called AFB1-8,9-epoxide (AFBO). there are several pathways that AFBO can take, one resulting in cancer, another in toxicity, and others in AFBO excretion. Inhibition of AFBO formation (through disruption of the cytochrome P450 system) and/or adduct formation are important strategies for prevention of these damaging mutations. In animal models, metabolic detoxification of AFBO is facilitated by induction of glutathione S-transferase (GST). This enzyme catalyzes the reaction that binds glutathione to AFBO and renders AFBO noncarcinogenic.
The early observations that an epoxide of AFB1 created adducts with DNA led to the concept that mycotoxin-DNA adducts, such as AFB1-DNAs, initiate cancer—an observation which has been documented in vitro and in vivo.
People who have Hepatitis B and consume food with aflatoxin increase their risk of hepatocellular carcinoma much more than having one of these factors by themselves. It is implicated in hepatocellular carcinoma in humans and hepatic necrosis in horses. A cohort study of more than 18000 individuals in China clearly showed a relative risk (measure of how much a particular risk factor [for example, AFB1] influences the risk of a specified outcome [for example, HCC]) for HCC of 3.4 in subjects who showed AFB1 exposure (urinary AFB1-N7-guanine; due to AFB1 exposure, a person is 3.4 times more likely to develop HCC), whereas relative risk for subjects positive for hepatitis B antigen was 7.3; combination of hepatitis B and AFB1 exposure increased relative risk for HCC to 59 (Qian and others 1994). Additionally, workers who are processing corn or other grains with aflatoxins release particles of aflatoxin contaminated plant material into the air and are then exposing their lungs which can cause inflammation and eventually irreversible pulmonary interstitial fibrosis. (Scared lung tissue between the air sacs.)
aflatoxin can be reduced by some food processing methods. Roasting peanuts eradicates more aflatoxin than boiling them. Fermenting wheat flour reduces aflatoxin by 50%. Baking dough decreases it from0-25%. Alkaline processing or nixtamalization (the traditional process of cooking corn in lime water to produce nixtamal that is then ground to form masa) of corn also resulted in significant reductions of aflatoxin (Torres and others 2001). Alkaline processing or nixtamalization (the traditional process of cooking corn in lime water to produce nixtamal that is then ground to form masa) of corn also resulted in significant reductions of aflatoxin (Torres and others 2001). There are reports of reformation or reactivation of aflatoxins post process. For example, initial loss of detectable aflatoxin was followed by detection upon acidification of the masa flour. The researchers speculated that this acidification could happen after consumption of nixtamalized aflatoxin-contaminated corn (Mendez-Albores and others 2004b).
Aspergillus fumigatus is a common cause of avian pulmonary aspergillosis, although other species have also been implicated in aspergillosis. Environmental factors that cause this in birds are heavy contamination of feed with Aspergillus and contaminated air, as well as stress or immunosupression. In chickens this is called "brooders pneumonia".
Of the 180 known species of Aspergillus, only four are known to be associated with invasive infection. They can cause infections in healthy individuals but are more commonly associated with invasive infections in immunocompromised people. These species are A. flavus, A fumigatus, A. terreus and A. niger. These species are worldwide and produce large amounts of spores that are dispersed into air currents where anyone around them will be exposed by contact with skin, eyes, ears and by inhalation. When inhaled they can lodge in the lung. In most people their innate immune system protects them from infection unless they enter a wound and the person is under some type of trauma or severe stress. When the immune system is weakened, the inhaled spores can germinate and produce hyphae that invade the surrounding lung tissue. This can cause invasive pulmonary aspergillosis.
In healthy people Aspergillus can cause infections in people. There is an Aspergillus induced shpenoid sinusitis and intracranial invasive aspergillosis. (Originates in sphenoid sinus.) Agricultural workers who injure their eyes have been known to develop Aspergillus corneal infections. Aspergillus has been known to infect ears in healthy individuals in both the external and middle ear. Additionally, aspergillus has infected postoperative cavities and then migrated into the ear.
A. fumigatus is more often found in areas with temperate climates while A. flavus is more common in hot, tropical climates. A. fumigatus is responsible for about 90% of the cases of pulmonary fungal infections. A. flavus is less common in pulmonary aspergillosis but does cause invasive disease at other sites. A. terreus also causes infections in immunocompromised individuals. One study implicated potted plants in a hospital setting as a source of A. terreus that caused infections in nine patients.
Aspergillus species cause four forms of respiratory hypersensitivity disorders; allergic bronchopulmonary aspergillosis, allergic Aspergillus sinusitis, IgE-mediated asthma and hypersensitivity pneumonitis. A. flavus has been known to cause allergic rhinosinusitis.
Where you might come in contact with A. species spores and/or toxins
Agricultural work (Dirt and handling plants with A. species) , Bakeries (Large amounts of grain flour is airborne.), farming communities. Remember, spores become airborne and are found all over the world. Some areas just have more than others.
AFB1 has animal research showing many dietary factors can modulate the formation fo AFB1-DNA adducts. Adducts(binding of mycotoxin to DNA) are the initial step of AFB1 carcinogenesis. Some of the substances that redue this binding are vitamin A, vitamin C, riboflavin. Restriction of carnitine, choline lead to more adducts being formed. Low fat, high carb diet increase adducts being formed. Carnitine, choline, copper, selenium, food restriction indole-3-carbinol, curcumin, garlic, green tea and coffee decrease adduct formation. Phenolic compounds appear to have protective effects against AFB1-induced mutagenicity.
Aspergillus makes Ochratoxin. (Also made by some penicillium species.)
Ochratoxin: Ochratoxin (OTA) is an other mycotoxin produced by Aspergillus. It is also produced by Penicillium. It is present in a large variety of foods because it is produced by several fungal strains of the Penicillium and Aspergillus species. It is most commonly found in wheat, corn and oats. Ochratoxin A is the most economically important form of ochratoxin; ochratoxins B and C are less toxic and less common. Ochratoxins may be transferred through milk, blood, and meat, so you will find it in dairy and meat products from animals that have consumed contaminated grains. It has been found on such food as dried and smoked fish, legumes, dried fruit and tree nuts. It has also been found on grapes and grape products such as wine, raisens, wine vinegars. The WHO in 2001 reported that the main sources are cereals, wine, grape juice, coffee and pork for human exposure at levels of 58%, 21%, 7%,5% and 3% of ochratoxin intake respectively. Red wines typically contain higher ochratoxin levels than white wines. Although coffee bean roasting lowers ochratoxin levels by 80% - 96%, it was shown to be fairly stable in processing of wheat and barley via dry milling and heat processing. Wet milling of corn resulted in reductions of corn grits and germ by 49% and 96 % respectively. Penicillium verrucosum is the leading cause of ochratoxin contamination of cereal grains in temperate climates. Grapes, raisins, and even wines may become contaminated with ochratoxins produced by Aspergillus carbonarius, the principal causal agent of grape black mold. A number of Aspergillus spp. may cause ochratoxin contamination in green and processed coffee, including A. ochraceus, A. carbonarius, and A. niger. Tree nuts and figs may be infested with A. ochraceus and A. melleus, the leading producers of ochratoxins in these commodities.
Ochratoxin is considered toxic to the kidneys, immune system, damages the growing fetus and is a possible carcinogen. Ochratoxin poisoning is thought to be the cause of a chronic kidney disease in humans known as Balkan endemic nephropathy. Recent studies have provided a link between ochratoxin exposure and human testicular cancer in Europe.
Interest in the mechanism of action of mycotoxins and especially OTA has increased with the availability of a Clinical Laboratory Improvement Amendments (CLIA) regulation-compliant registered laboratory test, which has identified OTA in the urine of humans with chronic illness . One of the clinical studies identified OTA in 83% of over 100 individuals tested with chronic illness and a history of water-damaged building exposure
The genus Fusarium is common in soil, marine and river environments as well as on plants all over the world. F. species are some of the most problematic molds known in the northern temperate regions of the world. They are responsible for many plant diseases and they can produce potent mycotoxins. Fusarium mycotoxins are commonly found on grains. Besides ingestion, fusarium mycotoxins can also gain access to the body by inhalation. The most important Fusarium food mycotoxins are the familys of trichothecenes, and fumonisins.
The trichothecenes are a large family of chemically related toxins and include T-2 toxinT-2, HT-2 toxin (HT-2), deoxynivalenol (DON), Diacetoxyscirpenol (DAS), Fusarenone-X (FUS-X), Nivalenol (NIV), diacetylnivalenol (DAS), neosolaniol and Zearalenone (ZEA . Mycotoxins of the Fusarium species are generally of two types: (1) the nonestrogenic trichothecenes such as DON, NIV, T-2, and DAS; (2) the mycoestrogens, including ZEA . ZEA is a nonsteroidal, estrogenic mycotoxin and has been shown to be able to bind competitively to estrogen receptors. The black mold Stachybotrys chartarum is also known to produce trichothecenes such as Satratoxin-G (SG).
Fusarium toxin production in food largely depends on environmental conditions, such as temperature and humidity. This means fusarium toxin contamination can not be avoided completely. Therefore, exposure to this toxin is a permanent health risk for both humans and farm animals.
Trichothecenes: These mycotoxins are produced by several species of Fusarium (the main culprit), Myrothecium, Stachybotrys, Trichoderma, and Trichothecium. and are sesquiterpenoid mycotoxins with a 12,13-epoxy-trichothec-9-ene skeleton.
Fusarium has been noted in some research papers to grow like crazy after application of glyphosate (RoundUp). See research here.
Where you might come in contact with Trichothecenes
Trichothecene is most common associated with wheat, barley, oats and maize.
Some trichothecenes are known to disrupt the endothelial cells in the brain and cause it to become more permeable (leaky). The same is true of the gut. Some trichothecenes can also cause a leaky gut by disruption of the endothelial cells in the small intestine.
There are around 180 trichothecenes, but only a few cause significant toxicity to humans. The most common trichothecene in food is deoxynivalenol (DON). Tricothecenes such as 3-acetyl DON, T-2 toxin, and nivalenol are also found in food.
Deoxynivalenol (DON): The fusarium toxin DON is one of the most prevalent and hazardous food-associated mycotoxins, particularly in cereals and cereal-derived products. DON is a common contaminant in wheat, barley and corn. In the US, 73% and 92% of wheat and corn samples, respectively, were found positive for DON [Canady R. & others, 2001] In Europe, a large-scale collaborative study conducted on more than 40,000 food samples has shown that DON was present in 57% of all samples, with a percentage of positive samples varying depending of the country. [Schothorst R.C., 2004] Fusarium graminearum (sexual stage Gibberella zeae) is the leading cause of DON contamination in maize and small grains in the United States. The fungus causes a disease of wheat and barley known as Fusarium head blight and a disease of corn known as Gibberella ear rot. Infected wheat spikelets exhibit premature bleaching as the pathogen progresses within the head and the developing grain becomes contaminated with DON. Maize ears infested with F. graminearum are often covered with a pinkish fungal mycelium as the maturing kernels become contaminated with DON. In addition, although theoretical, and no studies yet confirm it, animal derivatives of DON may be present in food originated from animal tissues and blood. The amount of DON metabolites has not been considered in the regulatory limits fixed by food agencies for DON due to the lack of data regarding their absorption and toxicity.
Inhibition of protein synthesis is thought to be the fundamental mechanism of trichothecene toxicity. The epoxide group is necessary for the inhibition of protein biosynthesis. Two mechanisms leading to destruction of the epoxide group of trichothecenes have been reported: reductive de-epoxidation leading to olefin and hydrolytic de-epoxidation generating two vicinal hydroxyls. The possibility of nucleophilic attack of the epoxide group by thiols in plants was suggested (Subramanian 2002) but not supported by data.
(DON) has been shown to enhance the inflammatory response to food-borne bacterial pathogens. The endotoxins from gram negative bacteria sensitize macrophages, amplifying the innate immune response. (see pestka J, Zhou HR Toll-like receptor priming sensitizes macrophages to proinflammatory cytokine gene induction by deoxynivalenol and other toxicants. Toxicological Science) Endotoxins from gram negative bacteria sensitize macrophages, amplifying the innate immune response. (See hymery n, leon k, carpentier fg, T-2 toxin inhibits the differentiation of human monocytes into dendritic cells and macrophages. Toxicol In Vitro 2009) DON has been shown to to be immunotoxic to animals.
The ingestion of DON has been associated with alterations of the intestinal, immune and nervous systems, thus leading, in cases of acute exposure, to illnesses characterized by vomiting, anorexia, abdominal pain, diarrhea, malnutrition, headache and dizziness.
In 1987 several thousand people in India were poisoned by tricothecenes. 97 reported feeling abdominal pain within 15 min to 1 hour after eating food made with bread that was later found to contain tricothecenes. Other symptoms included throat irritation (63%), diarrhea (39%), vomiting (7%), blood in stools (5%) and facial rash (2%). Increased respiratory tract infections were reported in children who ate the bread for more than a week. The illnesses disappeared when the flour was found to be contaminated and they stopped eating it. Samples of flours and wheat in the local markets contained DON (11/17 had toxin levels of 0.346 to 8.38 μg/g), nivalenol (2/19 had levels of 0.03 to 0.1 μg/g), T-2 toxin (4/19 had levels of 0.55 to 4 μg/g), and 3-acetyl DON (4/19 had levels of 0.6 to 2.4 μg/g), but were negative for aflatoxins and ergot alkaloids (Bhat and others 1989).
Chronic exposure to DON contaminated foods may damage the gut barrier and cause intestinal hyperpermeability which in turn can trigger a chronic inflammatory response at the level of the gut wall. (Serget t, parys m, Deoxynialenol transport across human intestinal Caco-2 cells and its effect on cellular metabolism at realistic intestinal concentrations. Toxicol letter 2006)
DON is resistant to high temperature (up to 350 °C), thereby making it stable during processing and cooking, leading to its persistence throughout the food chain. However DON is altered by gut microbes.
Grain crops are commonly contaminated with DON and animal diets consist mainly of grains in industrialized countries. It can be assumed that animals consuming grains are frequently exposed to DON-contaminated feeds. A variety of methods are used to decrease the toxic effects of DON. This includes pre-harvest, post-harvest and storage methods to decrease mold. However, additional approaches by the farmer can be taken. Farmers have tried adding adsorbent materials to the feed to bind the mycotoxins in the gastrointestinal tract and reduce absorption of the mycotoxin. Some research shows use of adsorbents can decrease many mycotoxins but generally the efficacy against trichothecenes is negligible. One method that has been shown to be beneficial is the use of gut bugs. These are also called beneficial micro-organisms or probiotics. DON has been completely transformed to de-epoxy DON by ruminal and intestinal microflora. Eubacterium BBSH 797 is one bacteria that has been shown to degrade DON and stop the effects of DON on animals.
Research has shown bacteria in the digestive system of animals are able to reduce the epoxide group of trichothecenes, generating 9,12-diene derivatives. The structure of the product of the de-epoxidation of DON was first examined in the 1980s. (Yoshizawa et al. 1983; King et al. 1984). Since then, the de-epoxidation of trichothecenes by mixed populations of ruminal and intestinal bacteria has been repetatively documented (Yoshizawa et al. 1985, Swanson et al. 1987a; Lake et al. 1987; Worrell et al. 1989, He et al. 1993; Kollarczik et al. 1994). Negative results reported by some authors (He et al. 1992; Swanson et al. 1987a, b; Munger et al. 1987) may be accounted for by the intestinal or ruminal microbes having not been previously exposed to trichothecenes and therefore having lacked the necessary adaptation. In support of this explanation, Hedman and Pettersson (1997) reported that neither DON nor nivalenol was detoxified in pig feces unless the pigs were fed with a diet containing trichothecenes. The experiments confirming this observation for chickens are described in a recent patent application by Zhou et al. (2010). Patents have been taken out on bacteria of the Bacillus spp. and Eubacterium sp for commercial use to lower DON in animal feed. Other genus's that de-epoxidize DON in research are Clostridiales, Anaerofilum sp., and Collinsella sp. For more data on DON and methods to alter and detoxify it I suggest this research article "Biological detoxification of the mycotoxin deoxynivalenol and its use in genetically engineered crops and feed additives".
Research shows that DON stimulates proinflammatory cytokines in the gut. IL-1B, IL-6, IL-8 TNF-alpha, IFN-gama, IL-10 is increased significantly.
Reproductive toxicity of animals induced by DON was shown to be inhibited by resveratrol in vitro.
In Europe, another trichothecene mycotoxin known as T-2 toxin may contaminate small grains. T-2 toxin has been implicated as part of the alleged chemical warfare agent ‘yellow rain’ in Southeast Asia. T-2 toxin causes a fatal disease of humans known as alimentary toxic aleukia (ATA); a disease that was particularly problematic in Russia in the 1940s. Symptoms of ATA in humans include skin pain, vomiting, diarrhea, complete degeneration of bone marrow, and eventually death. Broiler chickens fed low doses of T-2 toxin may demonstrate symptoms of weight loss, feather malformation, and yellowing of the beak and legs
People who live in areas with trichothecene produced by fusarium and have sensitivity to trichothecenes, feel like air filters can help remove it from the air and that below-freezing temperatures as well as snow may decrease its presence in the air.
T-2 Toxin: T-2 toxin is known to be one of the most toxic trichothecene mycotoxins.
T2 is produced predominantly by Fusarium sporotrichioïdes and F. langsethiae. Exposure to T-2 toxin is associated with low white blood cell counts and cell depletion in lymphoid organs as well as inhibition of red blood cell formation in bone marrow and the spleen. Furthermore, T-2 toxin reduces proliferation of the white blood cells called lymphocytes and it disturbs the maturation process of dendritic cells (an antigen presenting cell).
After hearing all these various ways that T2 depresses the immune system, it is no surprise that exposure to T-2 suppresses immune response to systemic bacterial infections such as Salmonella typhimurium, Listeria monocytogenes, Mycobacterium bovis, and Babesia microti. Respiratory immune defences are also compromised by T-2 exposure. T2 also has been shown to decrease viral resistance.
Zearalenone: The same fungus (Fusarium graminearum) that makes the trichothecene called DON also makes another mycotoxin called Zearalenone.
Where you might come in contact with Zearalenone
Zearalenone has been found in corn, moldy hay and small grains. Zearalenone is a mycotoxin that mimics the reproductive hormone estrogen. In animals it can induce an enlarged uterus, swelling of the vulva and vagina (known as vulvovaginitis), enlarged mammary glands, anestrus (periods of infertility), and abortion. Zearalenone has been shown to be passed to nursing piglets through the mother’s milk. A commercially available derivative of zearalenone (zeranol) has been used as a growth hormone to increase weight gain in beef cattle. High humidity and low temperatures support the production of zearalenone by F. graminearum in maize.
Fumonisins: The fumonisins are a group of mycotoxins produced primarily by Fusarium verticillioides and Fusarium proliferatum, although a few other Fusarium species also may produce them. There are at least 28 different forms of fumonisins. Fumonisin B1 is the most common and economically important form, followed by B2 and B3.
Where you might come in contact with Fumonisins
Corn is the most commonly contaminated crop, and fumonisins are the most common mycotoxins found in corn, although these toxins can occur in a few other crops as well.
Fumonisin-producing Fusarium fungi cause a disease in corn known as Fusarium ear rot. Fumonisins can contaminate grain used for human food or livestock feed, as well as silage. Infection is increased if the corn kernels are physically damaged, especially by insect feeding. Fungal growth and fumonisin production cease when grain is dried below about 19% moisture content, but the fumonisins remain alive, and the fungus can grow and produce additional fumonisins in storage if proper humidity conditions are not maintained. Fumonisins can be found in a few other crops, typically at low levels.
Fumonisins are classified as possible human carcinogens. They are known carcinogens in animals. Although, the research on human toxicity is needing to be undertaken, there is animal research. Horses that are poisoned with fumonisins may develop a fatal disease known as equine leukoencephalomalacia. Symptoms of this disease include drowsiness, blindness, staggering, and liquefaction of brain tissue. Pigs that are poisoned with fumonisins may experience reduced feed intake and weight gain, liver damage, and can develop pulmonary edema, in which the animals' lungs are filled with fluid. Fumonisins are carcinogenic to laboratory animals, and in humans, consumption of fumonisin-contaminated corn appears to possibly be associated with higher rates of esophageal cancer and neural tube birth defects although this is inconclusive.
Penicillium creates the mycotoxin Patulin that is found on damaged fruit. Several penicillium species also create Ochratoxin (See ochratoxin information under Aspergillus which is another mold that also make ochratoxin.)
Patulin: This mycotoxin has also be identified as other names such as clavacin, claviformin, expansin, mycoin c and penicidin.
The blue mold found in soft rot of apples, pears, cherries and other fruits is recognized as one of the most common causes of patulin contamination.
Where you might come in contact with Patulin
This mycotoxin is found in low acid fruit juices such as apple, grape, pear and fruit including, apple, grapes, cherries, pears, peaches, apricots, as well as olives and cereals. It is not found in intact fruit. It infects fruit that has had damage to the surface of the fruit. This makes it vulnerable to Penicillium infection that produces patulin.
Patulin is toxic to both plants and animals. It is thought to have genotoxicity but is not thought to cause cancer.
Methods to destroy Patulin: Filtration of apple juice has been shown to reduce it up to 40%. Fermentation of apple juice to apple cider helps destroy it. Some researchers claim it does not survive fermentation in cider products. 0.125% sulfur dioxide destroys it completely. Some researchers report it to be heat stable while others have reported 25% of it to be destroyed by pasteurization or evaporation temperatures of 70-100 centigrade.
Although this is not considered to be common nowadays, I want to mention ergot alkaloid mycotoxins which are produced by several species of fungi in the Claviceps genus. There are four main groups of ergot alkaloids: the clavines, the lysergic acids, the lysergic acid amides, and the ergopeptides.
Ergot poisoning is known in humans and animals. It can cause hallucinations, the feeling of itchy and burning skin, gangrene, loss of hands and feet, and even death. Ergotism is one of the oldest known toxic reactions to mycotoxins. In the Middle Ages, humans suffering from a disease called St. Anthony's fire that is thought to have been due to ergot poisoning. Ergotamine is one of the building blocks of the psychoactive drug lysergic acid diethylamide (LSD). Today, ergot alkaloids are used medicinally for treatment of migraines, inducing child birth, and the control of post-partum bleeding
For research abstracts on Mold and food click here.
For effect of mycotoxins on the gut click here.
Regarding acute toxicity, these toxins can be divided into three groups: (i) mycotoxins of low toxicity (oral LD50 lower than 100 mg/kg body weight in mice) including fumonisins, zearalenone, citrinin, penicillic acid, mycophenolic acid, sterigmatocystin, sporidesmin, tenuazonic acid, rubratoxins, (ii) mycotoxins of intermediate toxicity (oral LD50 between 20 and 100 mg/kg body weight in mice) including deoxynivalenol, ochratoxin A, patulin, gliotoxin, cyclopiazonic acid, verruculogen, and (iii) mycotoxins of high toxicity (oral LD50 lower than 10 mg/kg body weight in mice) including penitrem, aflatoxin B1, T-2 toxin, diacetoxyscirpenol and fusarenon X
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