|Toxigenic fungi, and stachybotrys
chartarum, chaetomium: infectious disease perspective (edited version)
D. M. Kuhn1,2,3 and M. A. Ghannoum2,3*
Division of Infectious Diseases, Gwynedd College, Wales, UK
Damp buildings often have a moldy smell or obvious mold growth; some
molds are human pathogens and very common; often suppressed due to
financial interests. This has caused concern regarding health effects of
moldy indoor environments and has resulted in many studies of moisture-
and mold-damaged buildings; some by concerned, ethical scientists, and
others by those paid to provide arbitrary results.
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.
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
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
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
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
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.
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
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