Moldy Food Overview

Is Government Protecting You From Mold and Mycotoxins

A worldwide survey of more than 19,000 grain and oilseed samples found that 72% were contaminated with one or more mycotoxins. These mycotoxins were aflatoxins, deoxynivalenol, ochratoxin A, fumonisins and zearalenone. Other studies have had similar findings. It seems that countries would simply make regulations around set limits for mycotoxins, but first they have to be able to identify known mycotoxins and then know what level is dangerous and then know how to measure it in the foods. Next there is the issue that some areas have higher levels of mycotoxins than others and when people have to choose between eating nothing or eating food with mycotoxins, guess what the government decides. You might decide the same if you are hungry.  Moldy food is better than starving. Then there is the issue with masked mycotoxins. Sometimes a mycotoxin has been identified but its metabolic degradation products may not be and the plant may have broken it down into these metabolic products already, so they won't be identified as being there. (Yes plants have detox systems too.) There are a lot of things I think the government over-regulates or should not regulate at all, but poisons in the food supply seems like a logical area to regulate. However, the fact is that you can't regulate what you can't find or measure. Some of the mycotoxins that can be found and we can kind of measure and know are hazardous, in the U.S.A. where I live, are largely not regulated either. Only patulin and aflatoxins have legal limits on them. There are some suggested limits for other mycotoxins, but they are only suggested. Of course if the farmer is selling their product over-seas, they may have to test for certain mycotoins depending on the country it is going to.  It is much harder for a farmer to sell moldy food in the European Union than it is here. There they have limits on many mycotoxins. Here we have mostly suggestions on limits for a handful of mycotoxins and then the farmer and manufacturer are told to use good agricultural and manufacturing practices and have food safety plans, which if they do this will indeed limit growth and sale of moldy products. Unfortunately, many moldy products end up being fed to farm animals.

What is really needed currently is more research. We need to identify masked mycotoxins and learn more about how these mycotoxins affect us. We also need more studies examining how to prevent mycotoxin damage to food and buildings and how to remove mycotoxins from food as well as animals, people and our buildings.

 

What Are Food Mycotoxins

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 Phase II processes that we use to biotransform toxins. It might interest the reader to know that they rely heavily on glutathione as we do in this process. "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 biotransforming these mycotoxins creates plant derived mycotoxin metabolites. So, in reality we really have two categories of plant related mycotoxins 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 original 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. (Pestka J, Zhou)

How Mycotoxins Grow On Food

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.

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. A review of studies proved that current evidence does not show conventional or organic practices to be any better or worse as far as growing mycotoxins on the food. There was much inconsistancy. We do know that the application of nitrogen fertilizer enhances the liklihood of growth of mold on mold prone crops. Conventional growers will usually use fungicides if they are using the nitrogen fertilizer. 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 or who are more genetically capable to withstand 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.  A study on barley showed that high levels of nitrogen fertilizer used on the grain as well as the application of fungicides and growth regulators stimulated fungal growth of fusarium.

Weather conditions  also place the fungal population under stress, they produce mycotoxins as part of their response to the stress. Most people think of moisture causing fungal growth, but droughts often place the plants under stress and can result in high mycotoxin levels.

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. To keep mold from growing in grains you are storing it is necessary that the moisture content stay under 0.7. 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 by someone else, you will also decrease the chances of mold growth.

Link to Research Abstracts on Specific Foods That Have Mold Issues

Plant Factors That Increase Toxin Production

• moisture content of plant
• plant type and nutrient composition of plant

Environmental Factors That Increase Toxin Production

• humidity
• temperature
• air flow

Processing Factors That Increase Toxin Production

• harvesting
• drying
• storage
• blending
• addition of preservatives
• handling of the food
• transport
• packaging

Which Mycotoxins Are The Most Concern On Food

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.
• Fumonisins are reported as neurotoxic and possible carcinogens and are associated with several mycotoxicoses, including equine leukoencephalomalacia, porcine pulmonary edema, and experimental kidney and liver cancer in rats.
• Trichothecenes are immunotoxic compounds produced by various species of Fusarium; they act as potent protein synthesis inhibitors and cause multi-organ effects including vomiting and diarrhea, weight loss, nervous disorders, cardiovascular alterations, immunosupression, hemostatic derrangements, skin toxicity, decreased reproductive capacity, and bone marrow damage. At least one of them is known to be a potent endocrine disrupter.
• Ochratoxin A, a toxin produced by A. ochraceus, A. carbonarius and Penicillium verrucosum, is one of the most abundant food-contaminating mycotoxin in the world. It is a kidney toxin, liver toxin, immunosuppressant, and possibly carcinogenic for humans and associated to Balkan Endemic Nephropathy.

It is also expected that combination of mycotoxins would have at least an additive, if not synergistic relevant effect. These toxins are the primary sources of both yield losses and increase of management costs worldwide. You can see this full European report on this PDF: http://www.doiserbia.nb.rs/img/doi/0352-4906/2012/0352-49061222007F.pdf

Testing Food For Mycotoxins

This website has a listing of labs that test for mycotoxins: http://www.omafra.gov.on.ca/english/livestock/swine/facts/mycolabs.htm

For information on the types of testing that is available for testing food, check out this Biomin blog.

There are 3 major mold groups found in food that are considered to effect human health.

• Aspergillus spp.
• Fusarium spp.
• Penicillium spp.

These 3 groups of molds produce 5 mycotoxin groups of significance. The mycotoxins are Patulin, Fumonisins, Aflatoxisn, Ochratoxins, Zearalanone, Tricothecenes.

Examples of fungi known to produce mycotoxins harmful to humans/animals.

Aspergillus Genus

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.

I have written up extensive data on aflatoxins and you can find it here. I am currently working on data for the oher mycotoxins listed below.

Aspergillus makes Ochratoxin too. (Also made by some penicillium species.)

Ochratoxin

Ochratoxin (OTA) is an other mycotoxin produced by Aspergillus spp. It is also produced by Penicillium spp. It is present in a large variety of foods due to  it being produced by several fungal strains of the Penicillium spp. and Aspergillus spp. 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 meat products and milk of animals. 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 World Health Organization 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.

 

Fusarium Genus

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 families of trichothecenes, and fumonisins.

The trichothecenes are a large family of chemically related toxins and include T-2 toxin(T-2), HT-2 toxin (HT-2), deoxynivalenol (DON), Diacetoxyscirpenol (DAS), Fusarenone-X (FUS-X), Nivalenol (NIV), diacetylnivalenol (DAS), neosolaniol and Zearalenone (ZEA or also called ZEN) . 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 or ZEN . Zearalenone  is a nonsteroidal, estrogenic mycotoxin and has been shown to be able to bind competitively to estrogen receptors. It is known as a serious endrocrine disruptor. The black mold Stachybotrys chartarum is also known to produce trichothecenes such as Satratoxin-G (SG).

Toxins from Fusarium in food largely depends on environmental conditions, such as temperature and humidity. This means Fusarium caused toxin contamination can not be avoided completely. Therefore, exposure to toxins from this mold is a permanent health risk for both humans and farm animals.

As a side note: Fusarium has been noted in some research papers to grow like crazy after application of glyphosate (RoundUp). See research here.

Trichothecenes

These mycotoxins are produced by several different types of molds. In addition to Fusarium (the main culprit), there is also Myrothecium, Stachybotrys, Trichoderma, and Trichothecium that produce trichothecenes.

Trichothecenes are sesquiterpenoid mycotoxins with a 12,13-epoxy-trichothec-9-ene skeleton.

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) - type of trichothecene

Where you might come in contact with Deoxynivalenol

The Fusarium toxin DON is one of the most prevalent and hazardous food-associated mycotoxins, particularly in cereals and cereal-derived products. Deoxynivalenol 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 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,  animal derivatives of DON may be present in food originated from animal tissues and blood or  milk, however there is little reserach on this. It appears that it is in the milk of dairy animals but at low concentrations generally. 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 its absorption and toxicity.

The Badness Of DON

Deoxynivalenol 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.) DON has also 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.

Deoxynivalenol 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. Deoxynivalenol  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.
(Awad , Bohm , Zentek, 2010)

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.

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.

For More Data on DON treatment, check out the Trichothecene Article.

 

T-2 Toxin- type of trichothecene

T-2 toxin is known to be one of the most toxic trichothecene mycotoxins.

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. Although there are no studies on this that I know of, getting first hand information from people like this is very useful.

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. If you have read much research on mycotoxins, you will already know that immunotoxicity is common amongst mycotoxins.

 

Zearalenone - type of trichothecene

The same fungus (Fusarium graminearum) that makes the trichothecene called DON also makes another mycotoxin called Zearalenone.

This mycotoxin is a known endocrine disruptor.

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 due to it's estrogenic effect. It is quite disheartening that this mycotoxin would actually be fed to animals and then to make it even worse, people eat the meat from those animals.

Where you might come in contact with zearalenone

Zearalenone has been found in corn, moldy hay and small grains. High humidity and low temperatures support the production of zearalenone by F. graminearum in maize.

 

Fumonisins - Not A trichothecene

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  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 Genus

Penicillium creates the mycotoxin Patulin that is found on damaged fruit. Several Penicillium species also create Ochratoxin (See ochratoxin information under Aspergillus above, 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% while 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.

Ergot Alkaloids

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.

Acute Toxicity

I have been giving mostly data on chronic toxicity of these mycotoxins and thought I would list the acute toxicty known.

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

 

Toxicity In Animals

Farm animals have been the test subjects for mycotoxin poisoning as well as methods to reduce toxicity from mycotoxins. This is because farm animals are oten fed moldy food.  This means they naturally end up with reactions to mycotoxins simply due to the low quality feed given to them.

In farm animals, mycotoxins can cause many diverse symtpoms. What is largely noticed is a decreased performance, feed refusal, poor feed conversion into meat or milk, diminished body weight gain, immune suppression and reproductive disorders. The progression and diversity of symptoms are confusing and diagnosis is difficult  when an animal has acute or chronic mycotoxicosis. Similar to the situation with himans, the diagnosis is complicated by a lack of research, by nonspecific symptoms and by interactions with other stress factors. Mycotoxin effects are also moderated by a number of factors, such as animal species, gender, age, diet, and duration of exposure. Many mycotoxigenic fungi can grow and produce their toxic metabolites under similar conditions. This means they often have more than one mycotoxin affecting them. We don't know if mycotoxins interact with each other, but it is likely they may have synergistic affects.

Testing For These Mycotoxins In Your Body

There are some tests available to test urine and blood. The urine tests are the most commonly available.

 

Prevent Mold Poisoning From Food

• Inspect whole grains (especially corn, sorghum, wheat, rice), dried figs and nuts such as peanuts, pistachio, almond, walnut, coconut, Brazil nuts and hazelnuts which are all regularly contaminated with aflatoxins for evidence of mold, and discard any that look moldy, discolored, or shriveled. I have actually looked at grains  with a magnifying glass when I noted a slight odd smell and found mold starting to grow on them. Toss anything that smells or looks odd. Start a compost pile if you feel wasteful throwing it out. Everyone should have a compost pile any way.
• Avoid damage of grains before and during drying, and in storage, as damaged grain is more prone to invasion of molds and therefore mycotoxin contamination.
• Buy grains and nuts as fresh as possible.
• Make sure that foods are stored properly – kept free of insects, dry, in the dark and not too warm.
• Do not keep foods for extended periods of time before being used, and eat a diverse diet – this not only helps to reduce mycotoxins exposure, but also improves nutrition.

 

Research On Moldy Food

For research abstracts on Mold and food click here.

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