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Diseases Due to Environmental Moulds
Fungi in general, and moulds in particular, can cause disease of people and animals in three ways [82]:
- Fungi can produce an actual infection of the host. This involves growth on or in the person or animal. It is quite uncommon for environmental moulds to produce this sort of disease unless one has a very severe reduction in the function of the immune system (e.g., is undergoing intensive therapy for cancer or is taking high doses of corticosteroids for prolonged periods of time.) We discuss these types of diseases on our
human and veterinary mycoses pages.
- Fungi can produce allergic reactions. This usually involves inhalation of mould particles. This type of problem can occur whether or not the fungus is still alive.
- Fungi can produce toxins that make people or animals sick. Although some toxins can be inhaled,the toxin is most often introduced into the person or animal by ingestion of mould-contaminated foods. Some of the toxins are very powerful.
This pages discusses the second and third forms of fungus-related disease. The Sick Building Syndrome is often NOT due to fungi. But, when it is, it may involve elements of both of the final two forms of fungus-related disease. We discuss it separately.
Fungi and fungal particles can clearly induce an allergic response in susceptible individuals. Typical symptoms are wheezing, cough, rhinorrhea, itchy nose, sore throat, sinus congestion, and so forth [90, 92]. These are well described and quite familiar. Dead fungi are able to produce symptoms just as well as live fungi [1964]. Thus, elimination of this form of reaction to requires reduction in the amount of fungi in the environment, not just disinfection of the environment.
Whereas allergic reactions to fungi (a) require prior exposure to fungi and (b) can occur upon re-exposure to small amounts of fungal antigens, Organic Dust Toxic Syndrome (ODTS) follows a single exposure to large amounts of fungus-contaminated dust. ODTS also differs in that it is often associated with flu-like symptoms. It differs from hypersensitivity pneumonitis in that it is not directly immune-mediated. Rather, it is direct toxicity of the acute fungal burden. ODTS is principally an occupational disease among people who perform renovations or fungal remediation [90, 92].
In somewhat related vein, fungi also make a series of volatile organic compounds (VOCs) that appear to be responsible for both the smell we associate with some fungal infestations along with (perhaps) some of the complaints associated with the presence of indoor fungal infestations [59, 82]. For example, the fungal metabolite 2-octen-1-ol has a strong musty odor. The degree to which VOCs contribute to human health issues is currently poorly understood.
Fungi are not the only causes of these syndromes. Bacterial and avian (bird) products can produce similar syndromes [1964]. Thus, before one blames a fungus for that sneeze or wheeze, one should consider the entire environment. One of the best references in this regard is the EPA's The Inside Story: A Guide to Indoor Air Quality.
Diagnostic strategies for all these forms of fungus-related illness are similar. Basically, the symptoms should remit when one is away from the fungus and recur when one returns to the fungus-contaminated area [1964]. Challenge tests such as skin-prick testing with fungal antigens are simply a variation on this concept. The EPA publication entitled Indoor Air Pollution: An Introduction for Health Professionals is a guide for physicians that specifically addresses the issues of evaluating building-related symptoms, and one of its sections discusses the issues of allergic reactions to biological pollutants such as mould antigens.
Far less common but far more feared are the diseases due to fungal toxins. These diseases provoke significant anxiety due to their potential to cause dramatic consequences. However, there is currently a great deal of overblown fear and legal attention to environmental fungal toxins. The American College of Occupational and Environmental Medicine (ACOEM) has an excellent fact-based position statement on this topic [82].
For excellent reviews on this topic, consult Kuhn and Ghannoum [1261] or Bennett [223]. Almost all real episodes human illness due to fungal toxins have followed ingestion of the toxin. Perhaps the best known of the ingestion syndromes is ergotism, a syndrome known for hundreds of years. It may present with limb gangrene, hallucinations, and death and thus can be quite dramatic. It is a vasospastic disorder caused by ingestion of rye products contaminated with ergot alkaloids produced by the mould Claviceps purpurea. (This fungus and its toxins may even have been the cause of the peculiar behavior of the individuals involved in the Salem witch trials. See Tom Volk's discussion of this on his website as well as a detailed article by L. R. Caporael that was published in Science in 1976.) In 1960, a disease known as Turkey X caused the deaths of 100,000 turkeys following their ingestion of peanut meal contaminated with aflatoxins produced by the mould Aspergillus flavus. Zearalenone, an estrogen-like steroid, is produced by mould Fusarium graminearum. Upon ingestion, estrogenic-effects may follow and have been associated with episodes of precocious puberty! The range of effects of these toxins is impressive and well reviewed elsewhere [340, 1804, 1805]. We also have a bit more detailed discussion on mycotoxins on our Stachybotrys-specific page. These types of discoveries have motivated significant interest into the investigation of fungal mycotoxins.
Despite this list of impressive effects in some settings, the vast majority of the time it has been difficult to link a particular fungal toxin to a particular effect or complaint. The toxins are generally present in low quantities and only occasionally will enough toxin be present acutely to cause a dramatic and clearly linked syndrome. Mycotoxins are also relatively large and non-volatile molecules (that is, they do not readily release into the air) [82]. Thus, very direct contact with the mycotoxin is required.
And, the ubiquitous presence of fungi in the environment can further confuse matters--if multiple toxins are present in small quantities, it can be difficult to tell which (if any) is causing the observed effect. Finally, even though a known mycotoxin-forming fungus is present, it might not even be making mycotoxins in that environment!
The Stachybotrys Story: A Case In Point
(For a guide to the literature on this topic, see our resources page.)
The great Stachybotrys episode is an excellent demonstration of the perils and pitfalls associated with assigning a disease to a fungus and its toxins. Prior to about 1993, Stachybotrys chartarum (previously known as both S. atra and S. alternans) was known for its ability to produce trichothecene mycotoxins and a syndrome in animals known as stachybotrytoxicosis [97, 1046]. In this syndrome, leukopenia (reduced white blood cell count) and hemorrhage (bleeding) are prominent and may lead to death [1046].
Then, during the period January 1993 to November 1994, a group of infants in Cleveland died with an unexplained hemorrhagic lung process of acute onset that was subsequently given the label acute idiopathic pulmonary hemosiderosis (AIPH) [81, 101, 102]. A case-control study found that the majority of the affected infants lived in water-damaged homes [1561], thus raising the possibility of a fungus-related disease. A microbiological investigation then suggested that affected infants were more likely to have toxin-producing S. chartarum in their homes than were control infants [694].
Initially, this all seemed pretty clear cut. But then, as time went by, some inconsistencies were noted. First and foremost, the clinical syndrome that had been observed was simply not that similar to veterinary stachybotrytoxicosis. Second, other infants that were heavily exposed to S. chartarum failed to develop similar symptoms [97, 102]. Third, investigation of a similar-appearing cluster of cases of AIPH in Chicago did not find the same linkage to S. chartarum.
Because of the implications for public health, all the data were again reviewed. Upon closer inspection, a number of assumptions made during the original investigation were challenged and reconsidered. While the discussion of the issues with the analysis is long and somewhat technical [97, 102], the bottom line is that an equally (or perhaps more) plausible re-analysis of the data found no meaningful statistical linkage between S. charatrum and the cases of AIPH. Other factors such as cigarette smoke exposure emerged as potentially relevant. The CDC has since published a statement effectively retracting the conclusions of the original investigation [102].
However, the damage was done and the horse was out of the barn. Recommendations based on the original investigation had been published by prominent authorities [100]. Numerous articles in the lay press further served to spread the faulty message [102].
Thus, while it is clear that S. chartarum produces toxins [2321] and that at least some strains can cause disease in animals [1046, 1648], it is simply not at all clear whether it is able to produce these symptoms in humans [1538]. And, as S. chartarum is among the least common of the fungi found in the home environment [745], the potential role of toxins made by other fungi must certainly be addressed. The amount of exposure required to produce S. chartarum-related disease has been estimated to be at least 1,000-fold higher than amounts reported in most environmental surveys [82].
What lessons can be learned here?
First, it is indeed clear that mycotoxins are real and that they can produce dramatic symptoms. However, clear linkage of a toxin to a disease is difficult. Second, given the broad range of fungi that produce mycotoxins [340], it seems reasonable to treat ALL fungi with substantial respect [96]. Thus, the goal in interior environments should be to maintain them in a clean, dry, and mould-free state. Identifying the specific fungus that is infesting a wall is less important than getting rid of it and preventing its return.
Is there a way to specifically diagnose mycotoxin-related diseases?
We're not aware of any specific such methods. While it is possible to do assays for many different mycotoxins, demonstrating their mere presence is not enough to prove that they are causing a disease. There really are not at present ANY recognized and reliable approaches to making this diagnosis.
How do I get rid of mycotoxins?
We do not know of any specific recommendations in this regard, nor do special steps appear necessary. Mycotoxins are simply chemical compounds released by fungi onto the surface where the fungus is growing. Cleaning procedures that are able to remove other surface contaminants would seem very likely to remove any relevant amounts of mycotoxins. As we state elsewhere, you are done with mould cleanup when (a) there is no visible mould, (b) there are no mould odors, and (c) you have fixed the moisture/water problem so that it will not recur [95]. We are very often asked about cleaning of colonized porous materials such as clothing. As stated so nicely in the ACOEM's position statement [82], "Colonized porous materials, e.g., clothing or upholstery, can be cleaned using appropriate routine methods, e.g., washing or dry cleaning clothing, and need not be discarded unless cleaning fails to restore an acceptable appearance."
Finally, not all mycotoxins are bad!
And lastly and if all this is not already confusing enough, let us point out that not all mycotoxins are bad! Remember that a mycotoxin is really just a toxic compound produced by a fungus, although that target of the compound is not necessarily humanity. Indeed, fungi probably generally make these compounds in order to harm the mites, insects, bacteria, and other fungi that might live in the same ecological niche. As a case in point, consider griseofulvin. Griseofulvin is produced naturally by Penicillium griseofulvum and Penicillium janczewskii and has the effect of killing other fungi in the soil. Hence it can be considered a mycotoxin. It was named in 1936 and was originally used as systemic fungicide in plant pathology beginning in 1957. In 1958, it was used orally in humans and animals to treat dermatophyte infections and is still used for that purpose (see our discussion of its medicinal use). It is currently used as a standard in thin layer chromatograpy when testing for the presence of various types of mycotoxins in agricultural commodities!
We provide specific literature references on most of our pages. However, we also have a separate page devoted just to a critical summary of the mould-related literature that is readily found on the web. Check it out!
About These Pages
The material and ideas here are drawn from many sources, including our own experience. However, this is an area with few guidelines and even fewer hard facts. So, you must always apply common sense in choosing how to adapt the ideas presented here to your own situation. When in doubt, please consult with a professional. At times, there is simply no substitute for experience and personal knowledge.
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References
59. Ammann, H. A. 1999. Microbial volatile organic compounds, p. 26-1 to 26-17. In J. Macher, H. A. Ammann, H. A. Burge, D. K. Milton, and P. R. Morey (ed.), Bioaerosols: Assessment and Control. American Conference of Governmental Industrial Hygienists (www.acgih.org), Cincinnati, OH.
81. Anonymous. 1994. Acute pulmonary hemorrhage/hemosiderosis among infants--Cleveland, January 1993-November 1994. MMWR Morb Mortal Wkly Rep. 43:881-3.
82. Anonymous. 2002. Adverse human health effects associated with molds in the indoor environment. American College of Occupational and Environmental Medicine (www.acoem.org), Arlington Heights,IL.
90. Anonymous. November 2000. Guidelines on Assessment and Remediation of Fungi in Indoor Environments. New York City Department of Health, Bureau of Environmental & Occupational Disease Epidemiology (www.ci.nyc.ny.us/html/doh/html/epi/moldrpt1.php), New York City, NY.
92. Anonymous. April 1998. Indoor Air Pollution: An Introduction for Health Professionals. United States Environmental Protection Agency (www.epa.gov), Washington, DC.
95. Anonymous. March 2001. Mold Remediation in Schools and Commercial Buildings, EPA 402-K-01-001. United States Environmental Protection Agency (www.epa.gov/iaq), Washington, DC.
96. Anonymous. March 2000. Questions and Answers on Stachybotrys chartarum and other molds. Centers for Disease Control and Prevention (http://www.cdc.gov/nceh/asthma/factsheets/molds/default.php), Atlanta, GA.
97. Anonymous. 1999. Report of the CDC Working Group on Pulmonary Hemorrhage/Hemosiderosis. Published online at http://www.cdc.gov/od/ads/pulhem_inf.php.
100. Anonymous. 1998. Toxic effects of indoor molds. American Academy of Pediatrics. Committee on Environmental Health. Pediatrics. 101:712-4.
101. Anonymous. 1997. Update: pulmonary hemorrhage/hemosiderosis among infants--Cleveland, Ohio, 1993-1996. MMWR Morb Mortal Wkly Rep. 46:33-5.
102. Anonymous. 2000. Update: pulmonary hemorrhage/hemosiderosis among infants--Cleveland, Ohio, 1993-1996. MMWR Morb Mortal Wkly Rep. 49:180-4.
223. Bennett, J. W., and M. Klich. 2003. Mycotoxins. Clin Microbiol Rev. 16:497-516.
340. Burge, H. A., and H. A. Ammann. 1999. Fungal toxins and beta-(1-3)-D-glucans, p. 24-1 to 24-13. In J. Macher, H. A. Ammann, H. A. Burge, D. K. Milton, and P. R. Morey (ed.), Bioaerosols: Assessment and Control. American Conference of Governmental Industrial Hygienists (www.acgih.org), Cincinnati, OH.
694. Etzel, R. A., E. Montana, W. G. Sorenson, G. J. Kullman, T. M. Allan, D. G. Dearborn, D. R. Olson, B. B. Jarvis, and J. D. Miller. 1998. Acute pulmonary hemorrhage in infants associated with exposure to Stachybotrys atra and other fungi. Arch Pediatr Adolesc Med. 152:757-62.
745. Flappan, S. M., J. Portnoy, P. Jones, and C. Barnes. 1999. Infant pulmonary hemorrhage in a suburban home with water damage and mold (Stachybotrys atra). Environ Health Perspect. 107:927-30.
1046. Hintikka, E.-L. 1977. Stachybotryotoxicosis as a veterinary problem, p. 277-284. In J. V. Rodricks, D. W. Hesseltine, and M. A. Mehlman (ed.), Mycotoxins in Human and Animal Health. Pathotox Publishers, Park Forest South, Illinois.
1261. Kuhn, D. M., and M. A. Ghannoum. 2003. Indoor mold, toxigenic fungi, and Stachybotrys chartarum: Infectious disease perspective. Clin Microbiol Rev. 16:144-72.
1538. Miller, J. D., T. G. Rand, and B. B. Jarvis. 2003. Stachybotrys chartarum: cause of human disease or media darling? Med Mycol. 41:271-291.
1561. Montana, E., R. A. Etzel, T. Allan, T. E. Horgan, and D. G. Dearborn. 1997. Environmental risk factors associated with pediatric idiopathic pulmonary hemorrhage and hemosiderosis in a Cleveland community. Pediatrics. 99:E5.
1648. Nikulin, M., K. Reijula, B. B. Jarvis, and E. L. Hintikka. 1996. Experimental lung mycotoxicosis in mice induced by Stachybotrys atra. Int J Exp Pathol. 77:213-8.
1804. Pitt, J. I. 2000. Toxigenic fungi: which are important? Med Mycol. 38:17-22.
1805. Pitt, J. I., J. C. Basilico, M. L. Abarca, and C. Lopez. 2000. Mycotoxins and toxigenic fungi. Med Mycol. 38:41-46.
1964. Rose, C. S. 1999. Antigens, p. 25-1 to 25-11. In J. Macher, H. A. Ammann, H. A. Burge, D. K. Milton, and P. R. Morey (ed.), Bioaerosols: Assessment and Control. American Conference of Governmental Industrial Hygienists (www.acgih.org), Cincinnati, OH.
2321. Vesper, S. J., M. L. Magnuson, D. G. Dearborn, I. Yike, and R. A. Haugland. 2001. Initial characterization of the hemolysin stachylysin from Stachybotrys chartarum. Infect Immun. 69:912-916.
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