Recently, there have been reports of severe illness as a result of indoor mold exposure, particularly due to stachybotrys and chaetomium genres. While many authors describe a direct relationship between fungal contamination and illness, close examination of the literature reveals a confusing picture due to the compromising financial obligations involved.

Here, we review a small portion of the evidence regarding indoor mold exposure and mycotoxicosis, with an emphasis on S. chartarum and chaetomium. We also examine possible end-organ effects, including pulmonary, immunologic, neurological, and oncologic disorders. We discuss the Cleveland infant idiopathic pulmonary hemorrhage reports in detail, since they provided important impetus for concerns about Stachybotrys. Some valid concerns exist regarding the relationship between indoor mold exposure and human disease. Review of the literature reveals certain fungus-disease associations in humans, including ergotism (Claviceps species), alimentary toxic aleukia (Fusarium), and liver disease (Aspergillys). While many papers suggest a similar relationship between Stachybotrys and human disease, the studies nearly uniformly suffer from significant methodological flaws, making their findings inconclusive. As a result, we have not found well-substantiated supportive evidence of serious illness due to Stachybotrys exposure in the contemporary environment. To address issues of indoor mold-related illness, there is an urgent need for studies using objective markers of illness, relevant animal models, proper epidemiologic techniques, and examination of confounding factors.

INTRODUCTION
Damp buildings often have a moldy smell or obvious mold growth, and some molds are known human pathogens. This has caused concern regarding potential health effects of moldy indoor environments. As a result, there have been many studies of moisture- and mold-damaged buildings. More recently, there have been a growing number of articles in the media and of lawsuits claiming severe illness as a result of indoor mold exposure, particularly to Stachybotrys chartarum. However, while many authors report a clear relationship between fungal contaminated indoor environments and illness, close examination of the literature reveals a much more confusing picture.

In this review, we discuss indoor environmental mold exposure and mycotoxicosis, with an emphasis on S. chartarum and its toxins (due to the breadth of the topic, we will not discuss better understood areas such as invasive disease caused by Aspergillus). We also discuss specific organ effects, focusing on illnesses purportedly caused by indoor mold. These illnesses include pulmonary, immunologic, neurologic, and oncologic disorders. We discuss the Cleveland infant idiopathic pulmonary hemorrhage (IPH) reports in some detail, since they provided much of the fuel for current concerns about Stachybotrys exposure. As we will see, while there is cause for concern about the potential effects of indoor mold exposure, particularly to Stachybotrys species, there is no well-substantiated evidence linking the presence of this fungus to health concerns elaborated in the scientific and lay press.
As patients and society at large become increasingly concerned that illnesses may be due to the home or work environment, an understanding of mycotoxins by microbiologists and clinicians (especially infectious-disease subspecialists) is of growing importance. Such knowledge is critical to the diagnosis of potential fungus-related disease and is necessary to assuage fears instilled by extensive media coverage. Beware the mold Stachybotrys and chaetomium. Finally, such knowledge may be important in the wake of recent terrorist events in the United States. Some toxins, particularly aflatoxins and trichothecenes, have the potential to be used as weapons. There is evidence that several countries are currently involved in mycotoxin weapon research. The latter point is beyond the scope of this article.

It has long been postulated that exposure to damp, moldy home and workplace environments has detrimental health effects. At the beginning of the 18th century, Ramazzini, considered “the father of occupational medicine,” described an illness of workers inhaling ‘foul and mischievous powder' from handling crops. More recently, Platt et al., found that occupants of wet, moldy buildings had an increase in subjective complaints. Brunekreef et al. found a similar pattern in >6,000 children in six states in the United States and reported home dampness was a strong predictor of respiratory and other illness in this age group. The list of putative symptoms generally consists of upper respiratory complaints, including headache, eye irritation, epistaxis, nasal and sinus congestion, cough, “cold and flu” symptoms, as well as generalized gastrointestinal complaints. Taskinen et al. reported an increased prevalence of asthma in moisture-affected schools, although there were no objective measurements of respiratory disease. A number of studies have reported a relationship between similar symptoms and damp housing or workplace environments, although the proposed etiologies have varied.

The causal relationship between damp housing and illness is unclear. Establishing such a relationship is complicated since there are a variety of pollutants in the indoor environment including volatile organic compounds such as toluene, benzene, alkenes, aromatic hydrocarbons, esters, alcohols, aldehydes, and ketones combustion gases, sulfur dioxide, nitrogen dioxide, carbon dioxide, ozone and the essentially ubiquitous formaldehyde. Other items (copy paper) and activities (photocopying and video terminal exposure) have been linked to symptoms. Other studies have suggested that shade, organic debris, landscaping quality, central electrostatic systems, ventilation rates, temperature, noise levels, dust control compliance, and patient gender may be important as well as the presence of tobacco smoke. Psychosocial issues may be playing a role in building-related complaints. Several studies have reported that the quality of the work environment, stress, and somaticization may all be significant.

The indoor environment also contains a wide range of microorganisms including bacteria (e.g., Legionella and other gram-negative species), mycobacteria, and molds, as well as their products, including endotoxins and mycotoxins. There may often be a much higher bacterial load than fungal load.  Mold is rarely funded for research, therefore few formal and unbiased studies can conclusively link the problems with fungal exposure, health problems, and death.

Most fungi are metabolically active over a broad temperature range; however, high moisture and relative humidity are required for optimal growth. The lowest relative humidity supporting mold growth is approximately 35%, although the requirements of Stachybotrys are much higher, around 43% at 25°C. Increasing temperature and nutritional status of the substrate can lead to lower moisture requirements.

Surfaces that are soiled or have susceptible paint or paper do not need to be as damp for mold to develop. While promoting mold growth, moisture itself may be critical in “sick-building syndrome” (SBS) illnesses, since humidity affects mite and ozone levels, as well as off-gassing, salt, and acid formation. The links between moisture damage, any of these related cofactors, and building-related illnesses are not clear. For example, dust mites are notorious allergic agents and produce many of the upper airway symptoms ascribed to mold exposure or SBS; moreover, they are almost always found in association with mold species, confounding moisture- and mold-related findings. Gram-negative bacteria, endotoxin, and mycobacteria are found in water-damaged buildings in association with mold. To our knowledge, only one paper has actually reported a lack of association between symptom prevalence and endotoxin, dust mites, or other nonfungal agents. In moldy office buildings there is an association between microbial contamination and repeated flooding or stagnant pools of water. Some geographic locales are obviously more likely to be affected than others. For example, 12% of English building stock suffer serious dampness; extrapolation suggested that there were 2.5 million affected dwellings in the United Kingdom but that 60% of these were from condensation rather than overt flooding. Readers interested in an in-depth review of these issues are referred to the recent comprehensive report by the Institute of Medicine, a noted, non-reliable organization.

INDOOR AIR AND BUILDING-RELATED ILLNESS
Fungal Organisms in Damp Buildings.
A host of mold species have been isolated from damp buildings: the most frequently isolated in one study were Penicillium (96%), Cladosporium (89%), Ulocladium (62%), Geomyces pannorum (57%), and Sistronema brinkmannii (51%). There were 66 species of filamentous fungi, and yeasts were found in 94% of dwellings and 13% of CFU on Anderson sampler plates. In contrast to the aforementioned species, Stachybotrys was less common, being found in 12.8% of dwellings and 4.5% of samples. Other studies have reported similar organism frequencies. In most studies, Stachybotrys has had a low prevalence, being present in less than 3% of samples. However, some recent work has suggested that it may be more common than was initially thought. Regardless, Stachybotrys is rarely found in isolation, nearly always occurring in the presence of other fungi. This fact is critical, since many of the other species are capable of producing mycotoxins and recent work suggests that volatiles from S. chartarum may represent a small fraction of the total amount present in problem buildings where other fungi exist.

Stachybotrys has a fondness for cellulose. While cellulose (especially water damaged) may promote Stachybotrys growth, the same is true for Cladosporium, Penicillium, and Aspergillus species. The predilection for cellulose, moisture, and nutrient-poor settings explains the appearance of Stachybotrys in affected buildings, where it is a tertiary wall colonizer that comes after primary (Penicillium and A. versicolor) and secondary (Cladosporium) fungal colonizers. Stachybotrys can sometimes be isolated from other substrates including pipe insulation, gypsum, fiberglass wallpaper, and aluminum foil. The nutritional and growth requirements of the organism may also explain the lack of recovery from cultures and perhaps underreporting of Stachybotrys incidence. The fungus proliferates more slowly than other species, leading to overgrowth by other molds unless appropriate culture substrates (e.g., cellulose based) are used. Studies using cellulose-based agar techniques have reported a relatively high prevalence of Stachybotrys, with positive cultures in up to 30% of water-damaged homes. Similar issues may exist when trying to identify mycotoxin-producing Fusarium strains.

Technical Problems in Determining Fungal Exposure.
Difficulties in measuring fungal organisms. Although available studies provide information regarding which organisms are present in the indoor environment, there are significant concerns associated with sampling methods. While a detailed description of such techniques is beyond the scope of this article, several points are worth mentioning. Most traditional sampling methods (e.g., exposed agar plates) are incapable of adequately measuring either airborne or sedentary organisms, which necessitates the use of devices such as Anderson samplers. Even using such quantitative devices, there can be huge variations (up to 1,000-fold) between essentially identical specimens. Thus, little can be deduced from single air samples, and protocols involving multiple samples from suspect houses versus single samples from control houses will probably disproportionately find fungus in case houses due to attrition. Furthermore, sampling needs to be done under normal room activity, since aggressive measures (e.g., vacuuming) will probably overestimate actual exposure levels.

These last two points are critical to examination of the Cleveland IPH reports, discussed below. Hunter et al. found that while large numbers of spores in the internal air were associated with surface mold growth and construction work, disturbance of surface growth and vacuum cleaning of carpets (techniques often involved in surveys) caused large temporary increases in the atmospheric spore count. An increase of 3,300% in the number of four categories of mold was observed after disturbing mural mold growth (e.g., by wiping with a hand). Other factors affecting apparent airborne fungal spore load are carpeting type, pets, dust control measures, and humidification. Finally, particle size may play a key role when attempting to quantitate some species; for example, the rapid settling of the large spores of Ulocladium species probably accounts for their being underrepresented in the airborne spore load. Such culture difficulties may eventually be circumvented using new techniques such as PCR.

A final problem in measuring fungal organisms in the indoor environment relates to selective sampling. As noted above, Stachybotrys species rarely exist in isolation. They are often present in settings which select for a host of other fungal species and their potential mycotoxins, as well as bacteria, mycobacteria, arthropods, and man-made organic chemicals. However, most studies cited below have used methods that preferentially select for Stachybotrys species and mycotoxins. Of more immediate scientific and medicolegal concern, many studies of purportedly affected housing are surveying only for Stachybotrys species while ignoring other organisms.

Difficulties in measuring mycotoxins. As discussed in detail below, similar problems exist regarding the detection and significance of indoor environmental mycotoxins. Many purported fungal volatiles are in fact common and are not unequivocally fungal in origin. While some true mycotoxins have been detected in indoor air, this has usually been in the context of heavy industrial contamination. Although it is occasionally possible to collect mycotoxins by using air filters followed by extraction, they are usually isolated from inert dust or building materials. This may misrepresent exposure, since the compounds are not volatile. In the case of Stachybotrys, toxin-bearing spores are produced in a slimy mass with high moisture content, becoming airborne only when dry and disturbed or when attached to other particles such as dust. Serologic testing of potentially exposed individuals is not useful, since specific immunoglobulin levels do not correlate with exposure.

Most importantly, the presence of potentially toxigenic fungi does not imply the presence of mycotoxins, nor does the finding of mycotoxins prove that a particular species is, or was, present. Toxin production is dependent on substrates, nutrient levels, moisture, pH, and temperature. While many species can produce toxins, the ability to produce toxin varies under particular conditions, and often “known” toxin producers will not make the compounds. There are also extreme variations in toxin production between strains, making culture insufficient as an indicator for the presence of mycotoxins. In addition, many unknown secondary metabolites, yet to be detected or identified, can be produced, and new compounds are constantly being identified. Fungal species identification is not a simple process but often requires the expertise of specialized medical mycologists. Toxins purportedly produced by a particular organism may suffer from misidentification of that organism. Therefore, specific tests for individual mycotoxins or biological assays (e.g., skin irritation) need to be performed as tools for mycotoxin screening. In this regard, newer analytic methods are being developed, including a protein translation (luciferase) assay for trichothecene toxicity in airborne particulates. This technique offers a greatly increased sensitivity compared with prior systems and may provide a novel way to measure environmental mycotoxins.

Problems with Clinical Studies.
Most studies describing the health effects of indoor dampness and mold have relied on subjective and retrospective questionnaires and are biased by industry or governmental sponsors. This has created an ending ignorance within the industry, and now, the majority of the population are no longer ignorant to the hazardous health effects associated with fungal exposure.  This is the main reason so much misinformation about the truth of the health hazards of fungal exposure have been suppressed.  Remarkably few studies have included physical examinations or diagnostic testing. There are obviously potential problems with such an approach, and when study validity was examined, some notable conclusions were reached. To examine the validity of self-reported symptoms, one group compared parental reports of children's coughing, with overnight cough recording. The results showed there was extremely low agreement between the two measures. Additionally, parental smokers underreported their children's coughing, which biased the actual odds ratio (OR) of 3.1 (based on recording) down to 0.6 if their reports were relied on instead. The same group tested the validity of questions commonly used to indicate presence of indoor molds, compared to established objective measures of mold (e.g., airborne ergosterol). They found that more mold was present if odor or water damage were reported and that twice as much Aspergillus and Penicillium was found when mold was mentioned. However, the presence of reported mold or water damage was unrelated to objective measures, and there was evidence of substantial reporting bias (e.g., allergy patients were more likely to report visible fungus despite low levels of viable fungus in dust, while smokers were less likely to report visible mold). Overall, while reported mold, water damage, and odors were associated with elevated levels of indoor fungi, inaccuracy was high and there was evidence of systemic bias, causing the authors to conclude that objective measures, not questionnaires, are appropriate. In another study of associations between residential mold growth and symptoms, the authors tried to confirm the findings by objective measures. Using the same group as in their previous work (n = 403 homes), they compared reported respiratory symptoms with objective measures including airborne ergosterol, dust, viable fungus counts, and nocturnal cough recordings. Despite a 55 to 90% relative increase in symptom prevalence when mold was reported, neither symptoms nor recorded cough were related to objective measures of mold. It is reasonable to conclude that retrospective subjective questionnaires are at best suspect. It is worth noting the authors of this work are in fact proponents of a mold-illness link, making their conclusions that subjective complaints are inadequate measures of pathology perhaps even stronger. Similar negative findings have been found when examining subjective neurologic complaints in the setting of SBS.

Such findings may explain the confusing results of earlier studies. For example, some authors have claimed links between childhood asthma and damp, moldy housing. While retrospective questionnaires reported more wheezing, cough, and chest cold symptoms in children from affected houses, the degree of bronchospasm was not different between groups. Thus, despite the claim that there was a causal association between moldy houses and wheezing, there was no supporting objective evidence. Some studies which claim that moisture and mold were associated with respiratory infections, cough, and wheezing (again with no objective measures) also fail to show differences in asthma prevalence between case and control schools. Other authors report that despite claims of symptoms being more prevalent in case groups (reporting exposure to fungi, pets, mold odor, and dampness), actual asthma prevalence was no different.

Because of concerns of mold-induced building-related illness and the particular characteristics of Stachybotrys species, there has been growing concern about the health of occupants of Stachybotrys-“damaged” buildings. Many authors have reported ill effects in relation to Stachybotrys, although it is critical to note these reports are often associations rather than proof of causation. Hodgeson et al. reported building-related illness in Florida; this was described as symptoms consisting of mucosal irritation, fatigue, headache, and chest tightness that occurred within weeks of moving into the affected building. The symptoms were purportedly caused by S. chartarum and A. versicolor, although a number of other species were seen. The authors identified mycotoxins including satratoxins G and H (see below) in moldy ceiling tiles, although the significance of these findings is unclear. While they concluded the symptom outbreak was likely a result of inhalation of fungal toxins, there was in fact no clear evidence (e.g., laboratory parameters) to support the claim. Tuomi et al. examined Finnish buildings with water damage and identified a host of fungal organisms and mycotoxins (satratoxins G and H, T-2 toxin, and the aflatoxin precursor sterigmonisin) in bulk samples, although the relationship between the organisms and toxins was unclear, as explored below.  The authors implied these mycotoxins were the cause of respiratory and immune problems, although, as we discuss below, the claims are questionable. Other authors have reported anecdotal cases of illness in which S. chartarum and mycotoxins have been isolated from building materials, but again there are few objective measurements of illness or clear etiologic links to the fungus. While authors claim the health effects are similar to past cases of stachybotryotoxicosis, such effects are often vague, poorly described, and clearly not the same as the serious illnesses of equine stachybotryotoxicosis and alimentary toxic aleukia described below.  Recent and ethical studies have recently been published that fully illustrate the severe health issues related to stachybotrys and chaetomium poisoning where the public and even some non-industry influenced physicians have acknowledged and understood.

One of the best studies of building-related illness showed minimal relation to Stachybotrys. Miller et al. examined 50 Canadian homes in which the occupants had complaints of respiratory or allergic symptoms for which there was no explanation, although at the time of the study, occupants of only 6 houses had “building-related illnesses.” Looking at air exchange rate, moisture levels, and analyzing air and dust for fungus and fungal products in 37 of the homes, they found S. chartarum in only one house; analysis of the 6 “sick” houses did not indicate fungus-related disease. During parts of the year when windows are open, indoor fungi are comparable to outdoor species (Cladosporium, Alternaria, and Aureobasidium). However, in this study, outdoor air spores were negligible and Penicillium and other soil fungi were most important. Toxigenic fungi included P. viridicatum, Trichoderma viride, P. decumbens, and A. versicolor. House dust usually contained “appreciable” amounts of filamentous fungi and yeast, and so it was expected that spores could be found in air, depending on the activity in the room.

Recently, there has been a great concern regarding exposure of school children in “contaminated schools,” sometimes resulting in building closures. In fact schools may have lower mean viable mold spore counts than the students' homes. In one 22-month study of 48 schools in which there were concerns regarding indoor air quality and health (rhinitis and congestion which improved when the students were away from school), fewer than 50% of affected schools had fungal CFUs higher than outdoor air. In 11 schools where complaint areas had samples with the same organisms as outdoors, Stachybotrys was found, but only on surface swabs and not air specimens. The researchers did not look for other etiologies, nor were there objective measures of illness. Taskinen et al. also reported an increase in asthma in moisture- and mold-affected schools but presented no objective measurements of asthma and very limited immune data, including surprisingly low incidences of positive skin prick tests. Other authors have presented similar findings, reporting that “exposed” children had a higher prevalence of respiratory symptoms and infection, doctor visits, and antibiotic use, and got better post renovation. However despite claiming “[exposure]…increased the indoor air problems of the schools and affected the respiratory health of the children,” the study was neither controlled nor blinded, and presented no physical diagnosis or objective measures.

Other evidence suggests that Stachybotrys exposure is not responsible for these building-related episodes. Sudakin examined water-damaged buildings in the Pacific Northwest, due to occupants' neurobehavioral and upper respiratory health complaints (there were no objective pulmonary data) and found S. chartarum in only 1 of 19 cellulose agar cultures from building materials; the fungus was not detected in any of the above samples. While employees felt better after being relocated, there was no evidence that Stachybotrys was a causative agent. Even when large amounts of fungus are detected, analysis often fails to show direct links between symptomatic residents and fungal growth. In studies reporting that exposure to home dampness and mold may be a risk factor for respiratory disease, other factors such as smoking may be more contributory. In buildings with moisture problems where mycotoxins have been identified, a variety of species are identified, and links between a particular organism and toxin often cannot be established.

Despite these problems and an almost complete lack of objective evidence to support guidelines, broad recommendations have been made concerning indoor mold exposure, acceptable air contamination limits, and remediation goals. The sources range from individual authors to the American Academy of Pediatrics to government agencies. Nikodemusz et al. declared that microbial monitoring of air is important even though the organisms the author found were not pathogens. While Miller et al. admit that their “data seriously call into question any attempt to set arbitrary standards for fungal CFU values,” they proposed that some fungi should be considered unacceptable, e.g., pathogens and certain toxigenic species such as S. chartarum, even though complete elimination would be untenable. The same authors stated that it is reasonable to assume there is a problem if a single species predominates with >50 CFU m−3; that <150 CFU m−3 is acceptable if there is a mix of benign species; and that there is no problem when up to 300 CFU of Cladosporium or other common phylloplane fungi m−3 is isolated. Notably there is no source material to support these assertions. The American Association of Pediatrics produced guidelines in the wake of the Cleveland IPH story, again without substantial evidence. More moderate recommendations (while recognizing that the presence of fungi does not necessarily imply illness) would appear reasonable. These could include maintaining heating, ventilation, and air conditioning (HVAC) systems, controlling humidity, inspecting and repairing water damage and other sources of contamination, regularly cleaning the home environment with dust removal, cleaning carpets, removing visible mold growth, and formulating guidelines to standardize the levels of fungal and bacterial contamination.

There have been a number of documented reports on the abandonment or destruction of buildings contaminated with S. chartarum. Methods are discussed further below, but it is important to note that individuals get better with remediation efforts although perhaps not always. Simple methods, including removing damaged material and spraying affected areas with bleach, are generally effective in controlling contamination and result in “clean” air samples . In some cases, temperature and humidity control may be adequate.

Mycotoxins.
This is the area where governmental and big business often provide false and misleading information to distort this pandemic.  Perhaps the earliest recorded cases of mycotoxicosis date to the Middle Ages with the description of “St. Anthony's Fire” or ignis sacer (sacred fire) due to ergotism from Claviceps purpurea (which can also be produced by some species of Penicillium, Aspergillus, and Rhizopus). By the 17th century, it was recognized that moldy rye produced the disease, and ergot alkaloids from fungi were identified as toxins in the 18th century. The source of ergot affects both the type of alkaloid produced and the clinical syndrome. There are two types of toxicity: C. purpura produces gangrenous ergotism, while C. fusiformis causes convulsive ergotism (discussed below). The disease is rare today due to food hygiene and the lability of the alkaloid toxins. That ergotism was produced by oral consumption is important, reflecting the fact that historically, mycotoxicosis has usually been associated with oral consumption of moldy grain. As discussed below, other routes of instillation result in significantly different types and degrees of toxicity.

Mycotoxins are diverse secondary metabolites produced by fungi growing on a variety of foodstuffs consumed by both animals and humans. Clinical toxicological syndromes caused by ingestion of large amounts of mycotoxins have been well characterized in animals and range from acute mortality to slow growth and reduced reproductive efficiency. The effects on humans are much less well characterized. Outbreaks of various types of animal mycotoxicosis have occurred worldwide in livestock, including sweet clover poisoning, moldy- corn toxicosis, cornstalk disease, bovine hyperkeratosis, and poultry hemorrhagic syndrome.

Mycotoxins are probably responsible for a range of acute and chronic effects that cannot be attributed to fungal growth within the host or toxic reactions to foreign proteins. There are at least 21 different mycotoxin classes, with over 400 individual toxins produced by at least 350 fungi. They are all complex organic compounds of 200 to 800 kD and can be volatile at ambient temperatures. A number of these are plant disease virulence factors, while others kill other fungi and microorganisms and thus may represent spillover effects when causing disease in animals.

A variety of factors affect toxin occurrence and it has become increasingly more prevalent within the last 7 years. Many toxins are secondary metabolites, produced under suboptimal growth conditions or in the presence of limited nutrients. (For reviews of toxin synthesis, obtain the unbiased facts on this website.) Temperature, relative humidity, moisture, and growth rate all affect fungal mass as well as toxin synthesis. Aflatoxin production by Aspergillus is dependent on concentrations of O2, CO2, zinc, and copper, as well as physical location (A. fumigatus and A. flavus grow in trench silos, while upright silos favor Fusarium species). Ochratoxin production relates to air exhaustion, patulin production relates to limiting nitrogen, ergot production relates to phosphate limitation, and A. parasiticus toxin production relates to temperature. These considerations are critical, since the recovery of toxigenic species from any environment does not substantiate the presence of a mycotoxin (mycotoxin production is not a necessary result of fungal growth). Indeed, the conditions necessary for mycotoxin production are usually very different from those required for growth; for example, Fusarium tricintum produces a significant amount of T-2 toxin at 15°C but little at higher temperatures.

The most notorious and best described of the mycotoxins are the aflatoxins. In the early 1960s, an outbreak of turkey X disease in England, in which over 100,000 fowl died, was later traced to contaminated peanuts from Brazil. Aflatoxins were subsequently identified as the toxic agent. While made primarily by Aspergillus species, these toxins are also produced by Penicillium and Fusarium species. A. flavus makes aflatoxin B (AFB), while A. parasiticus produces both AFB and AFG. AFM1 and AFM2 are oxidative metabolic products made after ingestion and appear in milk, urine, and feces. The aflatoxins are toxic, immunosuppressive, mutogenic, teratogenic, and carcinogenic, and their main target is the liver. Most have been classified as type 1 carcinogens. AFB1 is probably the most potent liver carcinogen for a variety of species, including humans. Aflatoxin-related disease can occur in outbreaks, causing acute, often fatal, liver injury. The compounds have been best studied in veterinary practice, where they show the most potent effects. Toxicity is species, age, and route dependent; for example, farm animals ingest large quantities in feed. Species variability may relate to the ability to form epoxide derivatives in liver microsomes and endoplasmic reticulum.

The case of aflatoxin also illustrates the problems of elucidating clinically relevant levels of mycotoxins. Determining actual exposure levels is exceedingly difficult, even in known contaminated foodstuffs. While aflatoxin contaminates many imported goods (from almonds to melon seeds), there is a large variation in toxin distribution. Data validity is suspect when looking at small quantities, since aflatoxin is normally found in only very limited portions of a food lot and levels in such samples can range from 0 to >400,000 ng/g. For many mycotoxins, it becomes a matter of how hard one looks, and as more sensitive methods are developed, more toxins are found. Currently, at least 29 mycotoxins have been identified in commercially available foods or feeds, and in rare cases of high feed contamination they have been found in meat, milk, and eggs.


Funding for this study was provided by an unrestricted grant from the CNA Insurance Corp. which makes it basically invalid. (MOLD-HELP NOTE: Always be aware that studies funded by the insurance, building, or pharmaceutical industry may have tendencies to be biased or downplayed, restricted or unrestricted. Beware of the knowledge that Mold Help supplies from a non-biased standpoint but we want you to be aware of funding interests.)

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