Mold and Mycotoxins – More Common Than You Think!
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Mold and Mycotoxins – More Common Than You Think!
by Dr. Miles Nichols and Dr. Diane Mueller
Mycotoxins are byproducts of fungal metabolism have been deemed to cause illness and death to humans and animals. Most residential buildings are home to thousands of organisms, including fungi and bacteria. This is because of water damage as a result of construction flaws including: faulty design of crawl space and basements, flat roofs, and ignoring water leaks (Venge, et al, 2001). Toxins that attack crops also find their way to our diets due to bioaccumulation. This article is the first of a two-part series that tackles mycotoxins.
Common Types of Mycotoxins
Today, we discuss the main types of mycotoxins that you are likely to encounter, the molds that produce them, effects of exposure and remedies. These include: Aflatoxins, Ochratoxins, Citrinin, trichothecenes, gliotoxins and Ergot alkaloids.
The most common of all mycotoxins, this is a group of toxic and carcinogenic chemicals produced by Aspergillus molds (Eaton and Groopman, 2013). The mold species include Aspergillus flavus and Aspergillus parasiticus, which inhabit the soil, decomposing vegetation, hay and tropical grains. They mostly grow on improperly stored foods such as cassava, corn, cotton seed, rice, sorghum, wheat, peanuts and tree nuts.
Exposure to aflatoxins results in liver damage (and liver cancer), stunted growth and delayed development in children. It is highly carcinogenic and, since aflatoxins are metabolized in the liver, a major cause of hepatic necrosis, liver failure and cancer. Metabolic byproducts of aflatoxins are known to cause programmed cell death, resulting in various forms of cancer. Some types of aflatoxins lead to suppression of the immune system.
To reduce the effects of exposure, you are advised to include apiaceous vegetables, such as carrots, celery, parsley and parsnips in your diet. There is no cure for aflatoxin intoxication, which is instead managed symptomatically, using active Vitamin K, Vitamin B and a controlled quality protein diet combined with sufficient starch.
These are mycotoxins mainly produced by the Penicillium species, mainly P. carbonarius and P. verrucosum. It is also present in the spores of a few Aspergillus species such as A. ochraceus and A. niger industrial strains (Petzinger & Weidenbach, 2002). There are three kinds of Ochratoxins: Ochratoxin A, Ochratoxin B and Ochratoxin C. Ochratoxin is the most severe and significant toxin of the group, and is abundant in cereals, coffee, red wine and fruits. It accumulates in animal flesh, and thus meat products get contaminated with Ochratoxin. Diet exposure could cause acute kidney poisoning.
Traces of the toxin have been found in animal tissues such as milk and blood. Ochratoxins also arise from water damaged houses and faulty heating ducts. Ochratoxin can permeate through the skin. Laboratory studies have shown the toxin to be a slight carcinogen and mutagen. It is also a known neurotoxin with a high affinity for the cerebellum and hippocampus. Chronic exposure could result in Alzheimer’s and Parkinson’s diseases. Ochratoxin also causes mammalian immunosuppression.
Ochratoxin exposure manifests itself as anemia, anorexia, cell death, fatigue, headache, delayed clotting, blood stains in urine and yellow palms. Acute exposure to Ochratoxin A could be managed by administering activated carbon (Charcoal), which is known to bind strongly to most mycotoxins. Anion exchange resins, such as Cholestyramine, can be used to lower plasma concentrations of Ochratoxin A and aid its excretion. Methods to reduce exposure through diet include use of microorganisms that detoxify Ochratoxin A, use of adsorbents that bind to the toxin in the gut, and various strategies to prevent food from getting contaminated while in storage.
This mycotoxin is mainly secreted by Penicillium molds including Penicillium citrinium. Some members of the Aspergillus species also secrete this toxin. Some fungi responsible for this toxin are used to make food for human consumption, including cheese, miso and soy sauce (Pedersen, et al, 1973). Citrinin rarely occurs on its own, occurring in combination with aflatoxins and ochratoxins. Interaction with Ochratoxin A is of particular interest as the two together are highly nephrotoxic. The two compounds together are also responsible for the pathogenesis of Balkan Endemic Nephropathy, a kidney disease. This is aggravated by the fact that Citrinin is produced by the same mold species that produce Ochratoxins.
There are various paths of exposure; inhalation, skin contact and orally mainly by the intake of grains. The contaminant mainly attacks the renal system. Citrinin also targets the mitochondrial respiratory system. The chemical causes oxidative stress to cells it acts upon. Citrinin poisoning could be handled by gastric lavage, activated charcoal, dilution and dermal decontamination. While not proven carcinogenic, the chemical results in kidney failure.
They are produced by the fungi Claviceps. Ergot poisoning in humans results in hallucination, itchy skin, gangrene and death. Ergotamine, an ergot, is a major building block of lysergic acid diethylamide (LSD) and is being explored for use in treating migraines, to induce labor and control post-natal bleeding (Schardl, et al, 2006). Use of ergot-based prescriptions commonly results in symptoms of ergot intoxication.
It affects the reproductive organs of grasses and cereals in warm, damp weather. Economically significant victims of the fungus include: pearl millet, buffel grass, sorghum, rye, oats, barley and wheat. Ergot intoxication is known as ergotism. Ergotism is characterized by in neurotropic activities that result in hallucinations, seizures, fever, nausea, muscle atrophy, irrational behavior, convulsions, loss of consciousness and even death. In the middle ages, ergotism, then referred to as ‘Saint Anthony’s Fire’, was common due to a large consumption of rye.
To prevent ergot poisoning from infected grains, the produce is placed in a brine solution; healthy grains sink while ergots are left floating. Deeply plowing infected fields prevent the mold from releasing its spores into the air. Ergot exposure is treated symptomatically, with refrain from all ergot-containing substances being the top priority.
This is a large family of about 60 sesquiterpene compounds mainly produced by various species of Fusarium that infect grains such as wheat, oats and corn. Trichothecenes are also produced by other mold species such as Trichoderma, Stachybotrys, Myrotheciu and Cephalosporium. Some are found in moist indoor environments, which then become airborne and affect residents. These are mostly trichothecenes we produced by mold of the Stachybotrys species (Sudakin, 2003). These mycotoxins could also be found in poisonous mushrooms especially in Asian regions.
This group of compounds mostly inhibit protein synthesis by reacting with components of the ribosomes. Most tissues are susceptible to this inhibition, but area with active and rapid cell growth are affected the most. Symptoms of exposure to trichothecenes include: dry eyes, fatigue, vomiting, diarrhea, mental impairment, abdominal discomfort, bleeding and rashes. Trichothecenes are some of the most potent types of known mycotoxins, are resistant to UV light, are not water-soluble and remain actively toxic for years.
T-2 trichothecenes have been used in biological warfare. Since they can withstand heat, are highly stable in the atmosphere and cannot be killed by UV radiation, and can be absorbed in the through the skin, they are perfect for mass killings. They are cheap and easy to produce yet toxic and have no corresponding vaccines or antidotes. It was used in the Vietnam and Afghan wars and are believed to be the cause of the Gulf War Syndrome during the desert storm.
These are mycotoxins produced mainly by marine fungi. They are also produced by human pathogens, such as Aspergillus, Trichoderma and Penicillium. They have also reportedly been produced by yeasts of the genus candida.
Gliotoxins mainly cause immunosuppression, resulting in the death of various cells of the immune system. Some properties of Gliotoxins have given it use in developing anti-inflammatory, antibacterial and antiviral drugs (Jones & Hancock, 1998). Gliotoxins also prevent thrombosis so as to quickly reach areas of interest, this could be explored for use in patients with circulatory problems.
We could be exposed to Gliotoxins through ingestion, inhalation or skin contact. It irritates mucous membranes and the anterior respiratory tract. It also irritates the eye, skin and entire breathing system. If you suspect exposure, get the victim out to fresh air and administer artificial respiration or Oxygen. Seek medical attention immediately. Treatment is by flushing the site of irritation with a lot of water.
We have seen six of the common mycotoxins you are likely to encounter. These are aflatoxins, ochratoxins, citrinin trichothecenes, gliotoxins and ergot alkaloids. In our next post, we shall explore the signs to watch out for if you suspect mycotoxin exposure. We will also discuss the various remedies to mold and water damage.
- Wålinder, R., Wieslander, G., Norbäck, D., Wessen, B., & Venge, P. (2001). Nasal lavage biomarkers: effects of water damage and microbial growth in an office building. Archives of Environmental Health: An International Journal, 56(1), 30-36.
- Eaton, D. L., & Groopman, J. D. (Eds.). (2013). The toxicology of aflatoxins: human health, veterinary, and agricultural significance.
- Petzinger, E., & Weidenbach, A. (2002). Mycotoxins in the food chain: the role of ochratoxins. Livestock Production Science, 76(3), 245-250.
- Krogh, P., Hald, B., & Pedersen, E. J. (1973). Occurrence of Ochratoxin A and citrinin in cereals associated with mycotoxic porcine nephropathy. APMIS, 81(6), 689-695.
- Schardl, C. L., Panaccione, D. G., & Tudzynski, P. (2006). Ergot alkaloids–biology and molecular biology. The alkaloids: chemistry and biology, 63, 45-86.
- Sudakin, D. L. (2003). Trichothecenes in the environment: relevance to human health. Toxicology letters, 143(2), 97-107.
- Jones, R. W., & Hancock, J. G. (1988). Mechanism of gliotoxin action and factors mediating Gliotoxins sensitivity. Microbiology, 134(7), 2067-2075.
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