Environment, Their Health Effects and the Moulds Producing Them

Growth of commonly occurring moulds in foods and building materials may result in production of toxic complex secondary metabolic by-products referred to as mycotoxins. Moulds that produce mycotoxins are said to be toxigenic (or incorrectly toxic moulds). According to experts, five kinds of mycotoxins are important in human health: aflatoxins, ochratoxin A, fumonisins, certain trichothecenes and zearalenone. It is believed the effect of mycotoxins as a cause of human mortality is underestimated. They can elicit a wide range of toxic responses including acute and chronic systemic effects in humans and animals that cannot be attributed to mould growth within the host or allergic reactions to foreign proteins. Exposure to mycotoxins can occur through ingestion, contact or inhalation of airborne particulates containing mycotoxins, including dust and mould components such as spores and mycelial fragments. In agricultural settings, mycotoxicoses (mycotoxin poisoning) in both farm animals and humans can result from oral, dermal, or exposure through inhalation of mycotoxin-contaminated grain or dust. The most widely known mycotoxins are the aflatoxins whose toxic effects were first realized in England in the 1960s when an outbreak of the so called turkey X disease killed over 100,000 fowls following consumption of contaminated peanuts. Aflatoxins are still a problem in developing countries. In mid 2004 more than 100 people died in an East African country after consuming grains contaminated with aflatoxins. Aflatoxins are mainly produced by two species of Aspergillus, Aspergillus flavus and A. parasiticus, in several agricultural commodities, including corn and nuts. Two structural types of aflatoxins are known (B and G types), of which aflatoxin B1 is a class 1 carcinogen and is considered the most toxic. In laboratory mammals, symptoms associated with mycotoxins can be induced by systemic, oral, dermal, subcutaneous, or exposure through inhalation. In experimental animals, exposure through breathing has been shown in some cases being several orders of magnitude more toxic than dermal or even systemic administration. Levels of mycotoxins in air in indoor environment have not well been established and neither the contribution of airborne mycotoxins to sick-building syndrome.

What Factors Favour Mycotoxin Production?

Mycotoxins are produced by a few strains of moulds at some point during their growth under suboptimal growth conditions or limited nutrients. Production occurs preferentially on materials that both allow toxigenic moulds to grow and provide the conditions for mycotoxin production. From the many studies of the production of mycotoxins by mould isolates derived from agricultural environments, a great deal is known about the mould species that are capable of producing known mycotoxins and about the growth media and conditions that induce production. Conditions that favour production of one type of mycotoxins may not be favourable for production of another type. For example, aflatoxin production by Aspergillus is dependent on concentrations of O2, CO2, zinc, and copper, as well as physical location while ochratoxin production relates to air exhaustion. Understanding the conditions under which mycotoxins are produced is important since presence of toxigenic moulds in any environment does not prove the presence of a mycotoxin.

What do we know about mycotoxins in indoor environment and their health effects?

Frequently, toxigenic moulds have been isolated from building materials and air samples in buildings where residents have suffered from non-specific symptoms possibly related to mycotoxin production, such as cough; irritation of eyes, skin, and respiratory tract; joint ache; headache; and fatigue. It is only recently that the presence of some mycotoxins has been confirmed in crude building materials. Most mycotoxins have yet to be extracted from either air samples or bulk material derived from indoor environments. Also, very few studies have been conducted to show correlation between mycotoxin exposure and building-related illnesses.

ABOUT THE AUTHOR:

Dr. Jackson Kung’u is a Microbiologist who has specialised in the field of mycology (the study of moulds and yeasts). He is a member of the Mycological Society of America. He graduated from the University of Kent at Canterbury, UK, with a Masters degree in Fungal Technology and a PhD in Microbiology. He has published several research papers in international scientific journals. Dr. Kung’u has analysed thousands of mould samples from across Canada. Dr. Kung’u helped one of the labs in Ontario to obtain AIHA accreditation. Dr. Kung’u provides how-to advice on indoor mould and bacteria issues. Get more information about indoor mould and bacteria at http://www.moldbacteria.com. Become a subscriber - FREE- for original reviews on mould and bacteria issues.
 
See:   http://www.oehc.uchc.edu/clinser/MOLD%20GUIDE.pdf    for an indepth booklet including check lists.

An excerpt from the above published booklet.  A very lengthy list of references is provided, many of which link to i/n articles.

Summary and Conclusions on Effects of Mycotoxins

There is abundant evidence for a role of ingested mycotoxins in human disease, and there is significant clinical evidence of a role for fungal spores and toxins by the respiratory route in military and agricultural settings following massive exposures. Laboratory studies in animals and at the cellular level provide supporting evidence for direct toxicity of fungal spores and mycotoxins in mammalian lungs. However, for humans residing or working in water-damaged buildings, the role of airborne fungal spores and toxins in the etiology of non-allergic disease remains controversial. Epidemiologic and clinical evidence raise the additional question of potential synergy between mycotoxin effects and environmental tobacco smoke. Recent reviews have concluded that scientific proof of the notion that the presence of fungal mycotoxins in indoor environments can lead to disease in humans is lacking (Robbins et al. 2000, Burge 2001, Terr 2001, Assouline-Dayan et al. 2002, Shum 2002, Kuhn and Ghannoum 2003, Miller et al. 2003). But there certainly is sufficient evidence available in the literature in support of this hypothesis to say that it also cannot be excluded. If we follow the usual framework for risk assessment in environmental toxicology, the identification of a hazardous agent depends on converging lines of evidence from three or four areas of investigation: epidemiology, in vivo (whole animal) toxicology, in vitro testing (in isolated cell systems or cell-free systems), and structure-activity analyses (Faustman and Omenn 1996). In general, our knowledge of the chemistry of mycotoxins has only begun to advance to the point where structure-activity relations can contribute, and the epidemiology supporting this hypothesis has often been judged as weak. But the available toxicology data would appear to grant significant support for the biologic plausibility of the hypothesis. (These data come from studies of isolated cell and whole animal models, as well as extensive observations in human pathology after rather massive inhalation or contact exposures to mycotoxinB–laden materials, including frequent reports of upper respiratory hemorrhages.) In addition, the available case-control studies from the Cleveland outbreak cannot be dismissed, especially in view of the case reports associating acute pulmonary hemorrhage/hemosiderosis syndrome with indoor toxigenic mold exposures that have now been published by independent sources. In addition, there is the continued experience in Cleveland, where over 30 cases have occurred, 90 percent of them from environments containing Stachybotrys (Dearborn et al. 2002). Clinical and basic scientific research continues to explore the hypothesis that fungal exposure in indoor air of water-damaged buildings can cause pulmonary hemorrhage in infants and children, as well as other diseases in adults. Ongoing work in toxicology and epidemiology will shed further light on these issues in the future (Etzel 2003a). Acknowledging that scientific uncertainty centers on how occupants are exposed to mycotoxins while living or working in contaminated indoor environments, reviews and guidance still advocate for addressing indoor environments contaminated with mold or water damage because of possible toxic effects as well as other, less controversial, effects of mold (concern for asthmatic patients and other allergic effects) (Ammann 2000, Burge 2001, US EPA 2001, CDC 2002, ACOEM 2002). The American Academy of Pediatrics recommends that pediatricians inquire about mold and water damage in the home when treating infants with pulmonary hemorrhage and, when mold is present, encourage parents to try to find and eliminate sources of moisture (American Academy of Pediatrics 1998). Avoidance of exposure to environmental tobacco smoke is always recommended, but has additional urgency in the presence of a case of pulmonary hemorrhage.

While methods under development to better characterize biological effects of and exposure to mycotoxins will aid our understanding, it should be useful to remember the words of Bennion and David-Bajar, which appear in their discussion of the use of trichothecene toxins in biological warfare:
The diagnosis of mycotoxin-related disease will be a challenge for medical personnel. The specific signs and symptoms that result from exposure depend on a large number of variables including the specific mycotoxin or mycotoxins involved, the method of delivery, the dose received, the specific vehicle used, the portal of entry into the body, climatic conditions, the use of protective gear, and the nutritional status and general health of the casualty. Because of the large number of variables determining the clinical presentation, the spectrum of disease resulting from exposure to mycotoxins will likely be very broad. (Bennion and David-Bajar 1994, 20) These, or even more complicated, considerations revolve around the situation that obtains during exposures to a “wet building�?with chronic mold growth and low-level exposures to fungal allergens, volatile organic compounds, and mycotoxins, with resultant occupational diseases or residential “building-related disease.�?In these cases, the patient may suffer chronic exposures to mycotoxins, combined with other co-factors, one or more of which may be at dose levels at or fluctuating around the threshold for adverse effects.