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Adverse Human Health Effects Associated with Molds in
the Indoor Environment
by American College of Occupational and Environmental Medicine
Particular attention is given to the possible health effects of mycotoxins,
which give rise to much of the concern and controversy surrounding indoor molds.
Food-borne exposures, methods of exposure assessment, and mold remediation
procedures are beyond the scope of this paper.
The fungi are eukaryotic, unicellular, or multicellular organisms that, because
they lack chlorophyll, are dependent upon external food sources. Fungi are
ubiquitous in all environments and play a vital role in the Earth's ecology by
decomposing organic matter. Familiar fungi include yeasts, rusts, smuts,
mushrooms, puffballs, and bracket fungi. Many species of fungi live as commensal
organisms in or on the surface of the human body. "Mold" is the common term for
multicellular fungi that grow as a mat of intertwined microscopic filaments (hyphae).
Exposure to molds and other fungi and their spores is unavoidable except when
the most stringent of air filtration, isolation, and environmental sanitation
measures are observed, eg, in organ transplant isolation units.
Molds and other fungi may adversely affect human health through three processes:
1) allergy; 2) infection; and 3) toxicity. One can estimate that about 10% of
the population has allergic antibodies to fungal antigens. Only half of these,
or 5%, would be expected to show clinical illness. Furthermore, outdoor molds
are generally more abundant and important in airway allergic disease than indoor
molds — leaving the latter with an important, but minor overall role in allergic
airway disease. Allergic responses are most commonly experienced as allergic
asthma or allergic rhinitis ("hay fever"). A rare, but much more serious
immune-related condition, hypersensitivity pneumonitis (HP), may follow exposure
(usually occupational) to very high concentrations of fungal (and other
Most fungi generally are not pathogenic to healthy humans. A number of fungi
commonly cause superficial infections involving the feet (tinea pedis), groin (tinea
cruris), dry body skin (tinea corporus), or nails (tinea onchomycosis). A very
limited number of pathogenic fungi — such as Blastomyces, Coccidioides,
Cryptococcus, and Histoplasma — infect non-immunocompromised individuals. In
contrast, persons with severely impaired immune function, eg, cancer patients
receiving chemotherapy, organ transplant patients receiving immunosuppressive
drugs, AIDS patients, and patients with uncontrolled diabetes, are at
significant risk for more severe opportunistic fungal infection.
Some species of fungi, including some molds, are known to be capable of
producing secondary metabolites, or mycotoxins, some of which find a valuable
clinical use, eg, penicillin, cyclosporine. Serious veterinary and human
mycotoxicoses have been documented following ingestion of foods heavily
overgrown with molds. In agricultural settings, inhalation exposure to high
concentrations of mixed organic dusts — which include bacteria, fungi,
endotoxins, glucans, and mycotoxins — is associated with organic dust toxic
syndrome, an acute febrile illness. The present alarm over human exposure to
molds in the indoor environment derives from a belief that inhalation exposures
to mycotoxins cause numerous and varied, but generally nonspecific, symptoms.
Current scientific evidence does not support the proposition that human health
has been adversely affected by inhaled mycotoxins in the home, school, or office
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Allergy and other hypersensitivity reactions
Allergic and other hypersensitivity responses to indoor molds may be
immunoglobulin E (IgE) or immunoglobulin G (IgG) mediated, and both types of
response are associated with exposure to indoor molds. Uncommon allergic
syndromes, allergic bronchopulmonary aspergillosis (ABPA), and allergic fungal
sinusitus (AFS), are briefly discussed for completeness, although indoor mold
has not been suggested as a particular risk factor in the etiology of either.
1. Immediate hypersensitivity: The most common form of hypersensitivity to molds
is immediate type hypersensitivity or IgE-mediated "allergy" to fungal proteins.
This reactivity can lead to allergic asthma or allergic rhinitis that is
triggered by breathing in mold spores or hyphal fragments. Residential or office
fungal exposures may be a substantial factor in an individual's allergic airway
disease depending on the subject's profile of allergic sensitivity and the
levels of indoor exposures. Individuals with this type of mold allergy are
"atopic" individuals, ie, have allergic asthma, allergic rhinitis, or atopic
dermatitis and manifest allergic (IgE) antibodies to a wide range of
environmental proteins among which molds are only one participant. These
individuals generally will have allergic reactivity against other important
indoor and outdoor allergens such as animal dander, dust mites, and weed, tree,
and grass pollens. Among the fungi, the most important indoor allergenic molds
are Penicillium and Aspergillus species.1 Outdoor molds, eg, Cladosporium and
Alternaria, as well as pollens, can often be found at high levels indoors if
there is access for outdoor air (eg, open windows).
About 40% of the population are atopic and express high levels of allergic
antibodies to inhalant allergens. Of these, 25%, or 10% of the population, have
allergic antibodies to common inhalant molds.2 Since about half of persons with
allergic antibodies will express clinical disease from those antibodies, about
5% of the population is predicted to have, at some time, allergic symptoms from
molds. While indoor molds are well-recognized allergens, outdoor molds are more
A growing body of literature associates a variety of diagnosable respiratory
illnesses (asthma, wheezing, cough, phlegm, etc.), particularly in children,
with residence in damp or water-damaged homes (see reviews 3-5). Recent studies
have documented increased inflammatory mediators in the nasal fluids of persons
in damp buildings, but found that mold spores themselves were not responsible
for these changes.6,7 While dampness may indicate potential mold growth, it is
also a likely indicator of dust mite infestation and bacterial growth. The
relative contribution of each is unknown, but mold, bacteria, bacterial
endotoxins, and dust mites can all play a role in the reported spectrum of
illnesses, and can all be minimized by control of relative humidity and water
2. Hypersensitivity pneumonitis (HP): HP results from
exaggeration of the normal IgG immune response against inhaled foreign (fungal
or other) proteins and is characterized by: 1) very high serum levels of
specific IgG proteins (classically detected in precipitin tests performed as
double diffusion tests); and 2) inhalation exposure to very large quantities of
fungal (or other) proteins.8 The resulting interaction between the inhaled
fungal proteins and fungal-directed cell mediated and humoral (antibody) immune
reactivity leads to an intense local immune reaction recognized as HP. As
opposed to immediate hypersensitivity (IgE-mediated) reactions to mold proteins,
HP is not induced by normal or even modestly elevated levels of mold spores.
Most cases of HP result from occupational exposures, although cases have also
been attributed to pet birds, humidifiers, and heating, ventilating, and air
conditioning (HVAC) systems. The predominant organisms in the latter two
exposures are thermophilic Actinomyces, which are not molds but rather are
filamentous bacteria that grow at high temperatures (116°F).
The presence of high levels of a specific antibody — generally demonstrated as
the presence of precipitating antibodies — is required to initiate HP, but is
not diagnostic of HP.9 More than half of the people who have occupational
exposure to high levels of a specific protein have such precipitin antibodies,
but do not have clinical disease.8 Many laboratories now measure IgG to selected
antigens by using solid phase immunoassays, which are easier to perform and more
quantitative than precipitin (gel diffusion) assays. However, solid phase IgG
levels that are above the reference range do not carry the same discriminatory
power as do results of a precipitin test, which requires much greater levels of
antibody to be positive. Five percent of the normal population have levels above
the reference value for any one tested material. Consequently, a panel of tests
(eg, 10) has a high probability of producing a false-positive result. Screening
IgG antibody titers to a host of mold and other antigens is not justified unless
there is a reasonable clinical suspicion for HP and should not be used to screen
for mold exposure.10
3. Uncommon allergic syndromes: Allergic bronchopulmonary
aspergillosis (ABPA) and allergic fungal sinusitis (AFS).11 These conditions are
unusual variants of allergic (IgE-mediated) reactions in which fungi actually
grow within the patient's airway. ABPA is the classic form of this syndrome,
which occurs in allergic individuals who generally have airway damage from
previous illnesses leading to bronchial irregularities that impair normal
drainage, eg, bronchiectasis.12,13 Bronchial disease and old cavitary lung
disease are predisposing factors contributing to fungal colonization and the
formation of mycetomas. Aspergillus may colonize these areas without invading
adjacent tissues. Such fungal colonization is without adverse health consequence
unless the subject is allergic to the specific fungus that has taken up
residence, in which case there may be ongoing allergic reactivity to fungal
proteins released directly into the body. Specific criteria have been recognized
for some time for the diagnosis of ABPA.14,15 As fungi other than Aspergillus
may cause this condition, the term "allergic bronchopulmonary mycosis" has been
suggested. It has more recently become appreciated that a similar process may
affect the sinuses — allergic fungal sinusitis (AFS).16 This condition also
presents in subjects who have underlying allergic disease and in whom, because
of poor drainage, a fungus colonizes the sinus cavity. Aspergillus and
Curvularia are the most common forms, although the number of fungal organisms
involved continues to increase. As with ABPA, the diagnosis of AFS has specific
criteria that should be used to make this diagnosis.17-19
Individuals with allergic airway disease should take steps to minimize their
exposure to molds and other airborne allergens, eg, animal dander, dust mites,
pollens. For these individuals, it is prudent to take feasible steps that reduce
exposure to aeroallergens and to remediate sources of indoor mold amplification.
Sensitized individuals may need to keep windows closed, remove pets, use dust
mite covers, use high-quality vacuum cleaners, or filter outdoor air intakes to
minimize exposures to inhalant allergens. Humidification over 40% encourages
fungal and dust mite growth, so should be avoided. Where there is indoor
amplification of fungi, removal of the fungal source is a key measure to be
undertaken so as to decrease potential for indoor mold allergen exposure.
ABPA and AFS are uncommon disorders while exposure is ubiquitous to the fungal
organisms involved. There is no evidence to link specific exposures to fungi in
home, school, or office settings to the establishment of fungal colonization
that leads to ABPA or AFS.
Once a diagnosis of HP is entertained in an appropriate clinical setting and
with appropriate laboratory support, it is important to consider potential
sources of inhaled antigen. If evaluation of the occupational environment fails
to disclose the source of antigens, exposures in the home, school, or office
should be investigated. Once identified, the source of the mold or other inhaled
foreign antigens should be remediated.
Appropriate measures should be taken in industrial workplaces to prevent mold
growth, eg, in machining fluids and where stored organic materials are handled
such as in agricultural and grain processing facilities. Engineering controls
and personal protective equipment should be used to reduce aerosol generation
and minimize worker exposures to aerosols.
Although it is not relevant to indoor mold exposure, it should be mentioned that
there is a belief among some health practitioners and members of the public
regarding a vague relationship between mold colonization, molds in foods, and a
“generalized mold hypersensitivity state.” The condition was originally proposed
as the “Chronic Candida Syndrome” or “Candida Hypersensitivity Syndrome,” but
now has been generalized to other fungi. Adherents may claim that individuals
are “colonized” with the mold(s) to which they are sensitized and that they
react to these endogenous molds as well as to exposures in foods and other
materials that contain mold products. The proposed hypersensitivity is
determined by the presence of any of a host of non-specific symptoms plus an
elevated (or even normal) level of IgG to any of a host of molds. The claim of
mold colonization is generally not supported with any evidence, eg, cultures or
biopsies, to demonstrate the actual presence of fungi in or on the subject.
Instead, proponents often claim colonization or infection based on the presence
of a wide variety of nonspecific symptoms and antibodies detected in serologic
tests that represent no more than past exposure to normal environmental fungi.
The existence of this disorder is not supported by reliable scientific
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An overview of fungi as human pathogens follows. Exposure to molds indoors is
generally not a specific risk factor in the etiology of mycoses except under
specific circumstances as discussed below for individual types of infection.
1. Serious fungal infections: A very limited number of
pathogenic fungi such as Blastomyces, Coccidioides, Cryptococcus, and
Histoplasma infect normal subjects and may cause a fatal illness. However,
fungal infections in which there is deep tissue invasion are primarily
restricted to severely immunocompromised subjects, eg, patients with
lymphoproliferative disorders including acute leukemia, cancer patients
receiving intense chemotherapy, or persons undergoing bone marrow or solid
transplantation who get potent immunosuppressive drugs.22 Uncontrolled diabetics
and persons with advanced AIDS are also at increased risk. Concern is greatest
when patients are necessarily in the hospital during their most severe
immunocompromise, at which time intense measures are taken to avoid fungal,
bacterial, and viral infection.23 Outside the hospital, fungi, including
Aspergillus, are so ubiquitous that few recommendations can be made beyond
avoidance of known sources of indoor and outdoor amplification, including indoor
plants and flowers because vegetation is a natural fungal growth medium.24,25
Candida albicans is a ubiquitous commensal organism on humans that becomes an
important pathogen for immunocompromised subjects. However, it and other
environmental fungi discussed above that are pathogens in normals as well (eg,
Cryptococcus associated with bird droppings, Histoplasma associated with bat
droppings, Coccidioides endemic in the soil in the southwest US) are not
normally found growing in the office or residential environment, although they
can gain entry from outdoors. Extensive guidelines for specific
immunocompromised states can be found at the Centers for Disease Control and
Prevention (CDC) web site at
2. Superficial fungal infections: In contrast to serious
internal infections with fungi, superficial fungal infections on the skin or
mucosal surfaces are extremely common in normal subjects. These superficial
infections include infection of the feet (tinea pedis), nails (tinea
onychomycosis), groin (tinea cruris), dry body skin (tinea corporis), and
infection of the oral or vaginal mucosa. Some of the common organisms
involved, eg, Trychophyton rubrum, can be found growing as an indoor mold.
Others, such as Microsprum canis and T. mentagrophytes can be found on
indoor pets (eg, dogs, cats, rabbits, and guinea pigs). As a common
commensal on human mucosal surfaces, C. albicans can be cultured from more
than half of the population that has no evidence of active infection. C.
albicans infections are particularly common when the normally resident
microbial flora at a mucosal site are removed by antibiotic use. Local
factors such as moisture in shoes or boots and in body creases and loss of
epithelial integrity are important in development of superficial fungal
Pityriasis (Tinea) versicolor is a chronic asymptomatic infection of the
most superficial layers of the skin due to Pityriasis ovale (also known as
P. orbiculare and Malassesia furfur) manifest by patches of skin with
variable pigmentation. This is not a contagious condition and thus is
unrelated to exposures, but represents the overgrowth of normal cutaneous
fungal flora under favorable conditions.
Only individuals with the most severe forms of immunocompromise need be
concerned about the potential for opportunistic fungal infections. These
individuals should be advised to avoid recognizable fungal reservoirs
including, but not limited, to indoor environments where there is
uncontrolled mold growth. Outdoor areas contaminated by specific materials
such as pigeon droppings should be avoided as well as nearby indoor
locations where those sources may contaminate the intake air.
Individuals with M. canis and T. mentagrophytes infections should have their
pets checked by a veterinarian. No other recommendations are warranted
relative to home, school, or office exposures in patients with superficial
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Mycotoxins are “secondary metabolites” of fungi, which is to say mycotoxins
are not required for the growth and survival of the fungal species
(“toxigenic species”) that are capable of producing them. The amount (if
any) and type of mycotoxin produced is dependent on a complex and poorly
understood interaction of factors that probably include nutrition, growth
substrate, moisture, temperature, maturity of the fungal colony, and
competition from other microorganisms.26-30 Additionally, even under the
same conditions of growth, the profile and quantity of mycotoxins produced
by toxigenic species can vary widely from one isolate to another.31-34 Thus,
it does not necessarily follow from the mere presence of a toxigenic species
that mycotoxins are also present.35-38
When produced, mycotoxins are found in all parts of the fungal colony,
including the hyphae, mycelia, spores, and the substrate on which the colony
grows. Mycotoxins are relatively large molecules that are not significantly
volatile;39,40 they do not evaporate or “off-gas” into the environment, nor
do they migrate through walls or floors independent of a particle. Thus, an
inhalation exposure to mycotoxins requires generation of an aerosol of
substrate, fungal fragments, or spores. Spores and fungal fragments do not
pass through the skin, but may cause irritation if there is contact with
large amounts of fungi or contaminated substrate material.41 In contrast,
microbial volatile organic compounds (MVOCs) are low molecular weight
alcohols, aldehydes, and ketones.42 Having very low odor thresholds, MVOCs
are responsible for the musty, disagreeable odor associated with mold and
mildew and they may be responsible for the objectionable taste of spoiled
Most descriptions of human and veterinary poisonings from molds involve
eating moldy foods.41,43-46 Acute human intoxications have also been
attributed to inhalation exposures of agricultural workers to silage or
spoiled grain products that contained high concentrations of fungi,
bacteria, and organic debris with associated endotoxins, glucans, and
mycotoxins.47,48 Related conditions including “pulmonary mycotoxicosis,”
“grain fever,” and others are referred to more broadly as “organic dust
toxic syndrome” (ODTS).49 Exposures associated with ODTS have been described
as a “fog” of particulates50 or an initial “thick airborne dust” that
“worsened until it was no longer possible to see across the room.”51 Total
microorganism counts have ranged from 105-109 per cubic meter of air52 or
even 109-1010 spores per cubic meter,53,54 extreme conditions not ordinarily
encountered in the indoor home, school, or office environment.
“Sick building syndrome,” or “non-specific building-related illness,”
represents a poorly defined set of symptoms (often sensory) that are
attributed to occupancy in a building. Investigation generally finds no
specific cause for the complaints, but they may be attributed to fungal
growth if it is found. The potential role of building-associated exposure to
molds and associated mycotoxins has been investigated, particularly in
instances when Stachybotrys chartarum (aka Stachybotrys atra) was
identified.55-58 Often referred to in the lay press by the evocative, but
meaningless terms, “toxic mold” or “fatal fungus,” S. chartarum elicits
great concern when found in homes, schools, or offices, although it is by no
means the only mold found indoors that is capable of producing
mycotoxins.35,36,59,60 Recent critical reviews of the literature35,61-67
concluded that indoor airborne levels of microorganisms are only weakly
correlated with human disease or building-related symptoms and that a causal
relationship has not been established between these complaints and indoor
exposures to S. chartarum.
A 1993-1994 series of cases of pulmonary hemorrhage among infants in
Cleveland, Ohio, led to an investigation by the CDC and others. No causal
factors were suggested initially,68 but eventually these same investigators
proposed that the cause had been exposures in the home to S. chartarum and
suggested that very young infants might be unusually vulnerable.69-71
However, subsequent detailed re-evaluations of the original data by CDC and
a panel of experts led to the conclusion that these cases, now called "acute
idiopathic pulmonary hemorrhage in infants,”72 had not been causally linked
to S. chartarum exposure.73
If mycotoxins are to have human health effects, there must be an actual
presence of mycotoxins, a pathway of exposure from source to susceptible
person, and absorption of a toxic dose over a sufficiently short period of
time. As previously noted, the presence of mycotoxins cannot be presumed
from the mere presence of a toxigenic species. The pathway of exposure in
home, school, and office settings may be either dermal (eg, direct contact
with colonized building materials) or inhalation of aerosolized spores,
mycelial fragments, or contaminated substrates. Because mycotoxins are not
volatile, the airborne pathway requires active generation of that aerosol.
For toxicity to result, the concentration and duration of exposure must be
sufficient to deliver a toxic dose. What constitutes a toxic dose for humans
is not known at the present time, but some estimates can be made that
suggest under what circumstances an intoxication by the airborne route might
Experimental data on the in vivo toxicity of mycotoxins are scant.
Frequently cited are the inhalation LC50 values determined for mice, rats,
and guinea pigs exposed for 10 minutes to T-2 toxin, a trichothecene
mycotoxin produced by Fusarium spp.74,75 Rats were most sensitive in these
studies, but there was no mortality in rats exposed to 1.0 mg T-2 toxin/m3.
No data were found on T-2 concentrations in Fusarium spores, but another
trichothecene, satratoxin H, has been reported at a concentration of 1.0 x
10-4 ng/spore in a “highly toxic” S. chartarum strain s. 72.31 To provide
perspective relative to T-2 toxin, 1.0 mg satratoxin H/m3 air would require
1010 (ten billion) of these s. 72 S. chartarum spores/m3.
In single-dose in vivo studies, S. chartarum spores have been administered
intranasally to mice31 or intratracheally to rats.76,77 High doses (30 x 106
spores/kg and higher) produced pulmonary inflammation and hemorrhage in both
species. A range of doses were administered in the rat studies and multiple,
sensitive indices of effect were monitored, demonstrating a graded dose
response with 3 x 106 spores/kg being a clear no-effect dose. Airborne S.
chartarum spore concentrations that would deliver a comparable dose of
spores can be estimated by assuming that all inhaled spores are retained and
using standard default values for human subpopulations of particular
interest78 – very small infants,† school-age children,†† and adults.††† The
no-effect dose in rats (3 x 106 spores/kg) corresponds to continuous 24-hour
exposure to 2.1 x 106 spores/m3 for infants, 6.6 x 106 spores/m3 for a
school-age child, or 15.3 x 106 spores/m3 for an adult.
That calculation clearly overestimates risk because it ignores the impact of
dose rate by implicitly assuming that the acute toxic effects are the same
whether a dose is delivered as a bolus intratracheal instillation or
gradually over 24 hours of inhalation exposure. In fact, a cumulative dose
delivered over a period of hours, days, or weeks is expected to be less
acutely toxic than a bolus dose, which would overwhelm detoxification
systems and lung clearance mechanisms. If the no-effect 3 x 106 spores/kg
intratracheal bolus dose in rats is regarded as a 1-minute administration (3
x 106 spores/kg/min), achieving the same dose rate in humans (using the same
default assumptions as previously) would require airborne concentrations of
3.0 x 109 spores/m3 for an infant, 9.5 x 109 spores/m3 for a child, or 22.0
x 109 spores/m3 for an adult.
In a repeat-dose study, mice were given intranasal treatments twice weekly
for three weeks with “highly toxic” s. 72 S. chartarum spores at doses of
4.6 x 106 or 4.6 x 104 spores/kg (cumulative doses over three weeks of 2.8 x
107 or 2.8 x 105 spores/kg).79 The higher dose caused severe inflammation
with hemorrhage, while less severe inflammation, but no hemorrhage was seen
at the lower dose of s. 72 spores. Using the same assumptions as previously
(and again ignoring dose-rate implications), airborne S. chartarum spore
concentrations that would deliver the non-hemorrhagic cumulative three-week
dose of 2.8 x 105 spores/kg can be estimated as 9.4 x 103 spores/m3 for
infants, 29.3 x 103 spores/m3 for a school-age child, and 68.0 x 103
spores/m3 for adults (assuming exposure for 24 hours per day, 7 days per
week, and 100% retention of spores).
The preceding calculations suggest lower bound estimates of airborne S.
chartarum spore concentrations corresponding to essentially no-effect acute
and subchronic exposures. Those concentrations are not infeasible, but they
are improbable and inconsistent with reported spore concentrations. For
example, in data from 9,619 indoor air samples from 1,717 buildings, when S.
chartarum was detected in indoor air (6% of the buildings surveyed) the
median airborne concentration was 12 CFU/m3 (95% CI 12 to 118 CFU/m3).80
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The presence of toxigenic molds within a home, school, or office environment
should not by itself be regarded as demonstrating that mycotoxins were
present or that occupants of that environment absorbed a toxic dose of
Indoor air samples with contemporaneous outdoor air samples can assist in
evaluating whether or not there is mold growth indoors; air samples may also
assist in evaluating the extent of potential indoor exposure. Bulk, wipe,
and wall cavity samples may indicate the presence of mold, but do not
contribute to characterization of exposures for building occupants.
After the source of moisture that supports mold growth has been eliminated,
active mold growth can be eliminated. Colonized porous materials, eg,
clothing or upholstery, can be cleaned using appropriate routine methods, eg,
washing or dry cleaning clothing, and need not be discarded unless cleaning
fails to restore an acceptable appearance.
When patients associate health complaints with mold exposure, treating
physicians should evaluate all possible diagnoses, including those unrelated
to mold exposure, ie, consider a complete appropriate differential diagnosis
for the patient’s complaints. To the extent that signs and symptoms are
consistent with immune-mediated disease, immune mechanisms should be
The possibility of a mycotoxicosis as an explanation for specific signs and
symptoms in a residential or general office setting should be entertained
only after accepted processes that are recognized to occur have been
appropriately excluded and when mold exposure is known to be uncommonly
high. If a diagnosis of mycotoxicosis is entertained, specific signs and
symptoms ascribed to mycotoxins should be consistent with the potential
mycotoxins present and their known biological effects at the potential
exposure levels involved.
Molds are common and important allergens. About 5% of individuals are
predicted to have some allergic airway symptoms from molds over their
lifetime. However, it should be remembered that molds are not dominant
allergens and that the outdoor molds, rather than indoor ones, are the most
important. For almost all allergic individuals, the reactions will be
limited to rhinitis or asthma; sinusitis may occur secondarily due to
obstruction. Rarely do sensitized individuals develop uncommon conditions
such as ABPA or AFS. To reduce the risk of developing or exacerbating
allergies, mold should not be allowed to grow unchecked indoors. When mold
colonization is discovered in the home, school, or office, it should be
remediated after the source of the moisture that supports its growth is
identified and eliminated. Authoritative guidelines for mold remediation are
Fungi are rarely significant pathogens for humans. Superficial fungal
infections of the skin and nails are relatively common in normal
individuals, but those infections are readily treated and generally resolve
without complication. Fungal infections of deeper tissues are rare and in
general are limited to persons with severely impaired immune systems. The
leading pathogenic fungi for persons with nonimpaired immune function,
Blastomyces, Coccidioides, Cryptococcus, and Histoplasma, may find their way
indoors with outdoor air, but normally do not grow or propagate indoors. Due
to the ubiquity of fungi in the environment, it is not possible to prevent
immune-compromised individuals from being exposed to molds and fungi outside
the confines of hospital isolation units.
Some molds that propagate indoors may, under some conditions, produce
mycotoxins that can adversely affect living cells and organisms by a variety
of mechanisms. Adverse effects of molds and mycotoxins have been recognized
for centuries following ingestion of contaminated foods. Occupational
diseases are also recognized in association with inhalation exposure to
fungi, bacteria, and other organic matter, usually in industrial or
agricultural settings. Molds growing indoors are believed by some to cause
building-related symptoms. Despite a voluminous literature on the subject,
the causal association remains weak and unproven, particularly with respect
to causation by mycotoxins. One mold in particular, Stachybotrys chartarum,
is blamed for a diverse array of maladies when it is found indoors. Despite
its well-known ability to produce mycotoxins under appropriate growth
conditions, years of intensive study have failed to establish exposure to S.
chartarum in home, school, or office environments as a cause of adverse
human health effects. Levels of exposure in the indoor environment,
dose-response data in animals, and dose-rate considerations suggest that
delivery by the inhalation route of a toxic dose of mycotoxins in the indoor
environment is highly unlikely at best, even for the hypothetically most
Mold spores are present in all indoor environments and cannot be eliminated
from them. Normal building materials and furnishings provide ample nutrition
for many species of molds, but they can grow and amplify indoors only when
there is an adequate supply of moisture. Where mold grows indoors there is
an inappropriate source of water that must be corrected before remediation
of the mold colonization can succeed. Mold growth in the home, school, or
office environment should not be tolerated because mold physically destroys
the building materials on which it grows, mold growth is unsightly and may
produce offensive odors, and mold is likely to sensitize and produce
allergic responses in allergic individuals. Except for persons with severely
impaired immune systems, indoor mold is not a source of fungal infections.
Current scientific evidence does not support the proposition that human
health has been adversely affected by inhaled mycotoxins in home, school, or
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This ACOEM statement was prepared by Bryan D. Hardin, PhD, Bruce J. Kelman,
PhD, DABT, and Andrew Saxon, MD, under the auspices of the ACOEM Council on
Scientific Affairs. It was peer-reviewed by the Council and its committees,
and was approved by the ACOEM Board of Directors on October 27, 2002. Dr.
Hardin is the former Deputy Director of NIOSH, Assistant Surgeon General
(Retired), and Senior Consultant to Global Tox, Inc, where Dr. Kelman is a
Principal. Dr. Saxon is Professor of Medicine at the School of Medicine,
University of California at Los Angeles.
† 5th percentile body weight for 1-month-old male infants, 3.16 kg;
respiratory rate for infants under 1 year of age, 4.5 m3/day78
†† 50th percentile body weight for 6-year-old boys, 22 kg; respiratory rate
for children age 6-9, 10.0 m3/day78
††† 50th percentile body weight for men aged 25-34 years, 77.5 kg;
respiratory rate for men age 19-65, 15.2 m3/day78
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Middleton E, Jr et al, eds. Allergy: Principles and Practice. St. Louis:
Mosby Co.; 1998:367-403.
2. Horner WE, et al. Fungal allergens. Clin Microbiol Rev. 1995;8:161-79.
3. Billings CG, Howard P. Damp housing and asthma. Monaldi Arch Chest Dis.
4. Burr ML. Health effects of indoor molds. Rev Environ Health.
5. Macher J. Health effects of bioaerosols. In: Macher J, ed. Bioaerosols:
assessment and control. Cincinnati, OH: American Conference of Governmental
Industrial Hygienists, 1999:3-1 to -12.
6. Purokivi MK, et al. Changes in pro-inflammatory cytokines in association
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