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 microbial)
proteins.
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 environment.
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 generally important.
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 intrusion.
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
Recommendations
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
data.20,21
Infection
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 www.cdc.gov.
Toxicity
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 foods.42,43
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 be
feasible.
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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Recommendations
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
mycotoxins.
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 investigated.
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.
Summary
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 available.81-83
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 vulnerable subpopulations.
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 office
environments.
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____________________
Acknowledgments
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
____________________
References
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