Is Indoor Mold Contamination a
Threat to Health?
Harriet M. Ammann, Ph.D., D.A.B.T.
Washington State Department of Health
The Fungus Among Us
Molds, a subset of the fungi, are ubiquitous on our planet. Fungi are
found in every ecological niche, and are necessary for the recycling
of organic building blocks that allow plants and animals to live.
Included in the group "fungi" are yeasts, molds and mildews, as well
as large mushrooms, puffballs and bracket fungi that grow on dead
trees. Fungi need external organic food sources and water to be able
Molds can grow on cloth, carpets, leather, wood, sheet rock,
insulation (and on human foods) when moist conditions exist (Gravesen
et al., 1999). Because molds grow in
moist or wet indoor environments, it is possible for people to become
exposed to molds and their products, either by direct contact on
surfaces, or through the air, if mold spores, fragments, or mold
products are aerosolized.
Many molds reproduce by making spores, which,
if they land on a moist food source, can germinate and begin producing
a branching network of cells called hyphae. Molds have varying
requirements for moisture, food, temperature and other environmental
conditions for growth. Indoor spaces that are wet, and have organic
materials that mold can use as a food source, can and do support mold
growth. Mold spores or fragments that become airborne can expose
people indoors through inhalation or skin contact.
Molds can have an impact on human health,
depending on the nature of the species involved, the metabolic
products being produced by these species, the amount and duration of
individual’s exposure to mold parts or products, and the specific
susceptibility of those exposed.
Health effects generally fall into four
categories. These four categories are allergy, infection, irritation
(mucous membrane and sensory), and toxicity.
The most common response to mold exposure may be allergy. People who
are atopic, that is, who are genetically capable of producing an
allergic response, may develop symptoms of allergy when their
respiratory system or skin is exposed to mold or mold products to
which they have become sensitized. Sensitization can occur in atopic
individuals with sufficient exposure.
Allergic reactions can range from mild,
transitory responses, to severe, chronic illnesses. The Institute of
Medicine (1993) estimates that one in five Americans suffers from
allergic rhinitis, the single most common chronic disease experienced
by humans. Additionally, about 14 % of the population suffers from
allergy-related sinusitis, while 10 to 12% of Americans have
allergically-related asthma. About 9% experience allergic dermatitis.
A very much smaller number, less than one percent, suffer serious
chronic allergic diseases such as allergic bronchopulmonary
aspergillosis (ABPA) and hypersensitivity pneumonitis (Institute
of Medicine, 1993). Allergic fungal
sinusitis is a not uncommon illness among atopic individuals residing
or working in moldy environments. There is some question whether this
illness is solely allergic or has an infectious component. Molds are
just one of several sources of indoor allergens, including house dust
mites, cockroaches, effluvia from domestic pets (birds, rodents, dogs,
cats) and microorganisms (including molds).
While there are thousands of different molds
that can contaminate indoor air, purified allergens have been
recovered from only a few of them. This means that atopic individuals
may be exposed to molds found indoors and develop sensitization, yet
not be identified as having mold allergy. Allergy tests performed by
physicians involve challenge of an individual’s immune system by
specific mold allergens. Since the reaction is highly specific, it is
possible that even closely related mold species may cause allergy, yet
that allergy may not be detected through challenge with the few
purified mold allergens available for allergy tests. Thus a positive
mold allergy test indicates sensitization to an antigen contained in
the test allergen (and perhaps to other fungal allergens) while a
negative test does not rule out mold allergy for atopic individuals.
Infection from molds that grow in indoor environments is not a common
occurrence, except in certain susceptible populations, such as those
with immune compromise from disease or drug treatment. A number of
Aspergillus species that can grow indoors are known to be
pathogens. Aspergillus fumigatus (A. fumigatus) is a
weak pathogen that is thought to cause infections (called
aspergilloses) only in susceptible individuals. It is known to be a
source of nosocomial infections, especially among immune-compromised
patients. Such infections can affect the skin, the eyes, the lung, or
other organs and systems. A. fumigatus is also fairly commonly
implicated in ABPA and allergic fungal sinusitis. Aspergillus
flavus has also been found as a source of nosocomial infections (Gravesen
et al., 1994).
There are other fungi that cause systemic
infections, such as Coccidioides, Histoplasma, and
Blastomyces. These fungi grow in soil or may be carried by bats
and birds, but do not generally grow in indoor environments. Their
occurrence is linked to exposure to wind-borne or animal-borne
Mucous Membrane and Trigeminal Nerve
A third group of possible health effects from fungal exposure
derives from the volatile compounds (VOC) produced through fungal
primary or secondary metabolism, and released into indoor air. Some of
these volatile compounds are produced continually as the fungus
consumes its energy source during primary metabolic processes.
(Primary metabolic processes are those necessary to sustain an
individual organism’s life, including energy extraction from foods,
and the syntheses of structural and functional molecules such as
proteins, nucleic acids and lipids). Depending on available oxygen,
fungi may engage in aerobic or anaerobic metabolism. They may produce
alcohols or aldehydes and acidic molecules. Such compounds in low but
sufficient aggregate concentration can irritate the mucous membranes
of the eyes and respiratory system.
Just as occurs with human food consumption,
the nature of the food source on which a fungus grows may result in
particularly pungent or unpleasant primary metabolic products. Certain
fungi can release highly toxic gases from the substrate on which they
grow. For instance, one fungus growing on wallpaper released the
highly toxic gas arsine from arsenic containing pigments (Gravesen,
et al., 1994).
Fungi can also produce secondary metabolites
as needed. These are not produced at all times since they require
extra energy from the organism. Such secondary metabolites are the
compounds that are frequently identified with typically "moldy" or
"musty" smells associated with the presence of growing mold. However,
compounds such as pinene and limonene that are used as solvents and
cleaning agents can also have a fungal source. Depending on
concentration, these compounds are considered to have a pleasant or
"clean" odor by some people. Fungal volatile secondary metabolites
also impart flavors and odors to food. Some of these, as in certain
cheeses, are deemed desirable, while others may be associated with
food spoilage. There is little information about the advantage that
the production of volatile secondary metabolites imparts to the fungal
organism. The production of some compounds is closely related to
sporulation of the organism. "Off" tastes may be of selective
advantage to the survival of the fungus, if not to the consumer.
In addition to mucous membrane irritation,
fungal volatile compounds may impact the "common chemical sense" which
senses pungency and responds to it. This sense is primarily associated
with the trigeminal nerve (and to a lesser extent the vagus nerve).
This mixed (sensory and motor) nerve responds to pungency, not odor,
by initiating avoidance reactions, including breath holding,
discomfort, or paresthesias, or odd sensations, such as itching,
burning, and skin crawling. Changes in sensation, swelling of mucous
membranes, constriction of respiratory smooth muscle, or dilation of
surface blood vessels may be part of fight or flight reactions in
response to trigeminal nerve stimulation. Decreased attention,
disorientation, diminished reflex time, dizziness and other effects
can also result from such exposures (Otto
et al., 1989)
It is difficult to determine whether the
level of volatile compounds produced by fungi influence the total
concentration of common VOCs found indoors to any great extent. A
mold-contaminated building may have a significant contribution derived
from its fungal contaminants that is added to those VOCs emitted by
building materials, paints, plastics and cleaners. Miller and
co-workers (1988) measured a total VOC concentration approaching the
levels at which Otto et al., (1989) found trigeminal nerve
At higher exposure levels, VOCs from any
source are mucous membrane irritants, and can have an effect on the
central nervous system, producing such symptoms as headache, attention
deficit, inability to concentrate or dizziness.
Adverse Reactions to Odor
Odors produced by molds may also adversely affect some individuals.
Ability to perceive odors and respond to them is highly variable among
people. Some individuals can detect extremely low concentrations of
volatile compounds, while others require high levels for perception.
An analogy to music may give perspective to odor response. What is
beautiful music to one individual is unbearable noise to another. Some
people derive enjoyment from odors of all kinds. Others may respond
with headache, nasal stuffiness, nausea or even vomiting to certain
odors including various perfumes, cigarette smoke, diesel exhaust or
moldy odors. It is not know whether such responses are learned, or are
time-dependent sensitization of portions of the brain, perhaps
mediated through the olfactory sense (Bell,
et al., 1993a;
Bell et al., 1993b), or whether they
serve a protective function. Asthmatics may respond to odors with
Molds can produce other secondary metabolites such as
antibiotics and mycotoxins. Antibiotics are isolated from mold (and
some bacterial) cultures and some of their bacteriotoxic or
bacteriostatic properties are exploited medicinally to combat
Mycotoxins are also products of secondary
metabolism of molds. They are not essential to maintaining the life of
the mold cell in a primary way (at least in a friendly world), such as
obtaining energy or synthesizing structural components, informational
molecules or enzymes. They are products whose function seems to be to
give molds a competitive advantage over other mold species and
bacteria. Mycotoxins are nearly all cytotoxic, disrupting various
cellular structures such as membranes, and interfering with vital
cellular processes such as protein, RNA and DNA synthesis. Of course
they are also toxic to the cells of higher plants and animals,
Mycotoxins vary in specificity and potency
for their target cells, cell structures or cell processes by species
and strain of the mold that produces them. Higher organisms are not
specifically targeted by mycotoxins, but seem to be caught in the
crossfire of the biochemical warfare among mold species and molds and
bacteria vying for the same ecological niche.
Not all molds produce mycotoxins, but
numerous species do (including some found indoors in contaminated
buildings). Toxigenic molds vary in their mycotoxin production
depending on the substrate on which they grow (Jarvis,
1990). The spores, with which the toxins are
primarily associated, are cast off in blooms that vary with the mold’s
diurnal, seasonal and life cycle stage (Burge,
Yang, 1995). The presence of competitive
organisms may play a role, as some molds grown in monoculture in the
laboratory lose their toxic potency (Jarvis,
1995). Until relatively recently, mold
poisons were regarded with concern primarily as contaminants in foods.
More recently concern has arisen over
exposure to multiple mycotoxins from a mixture of mold spores growing
in wet indoor environments. Health effects from exposures to such
mixtures can differ from those related to single mycotoxins in
controlled laboratory exposures. Indoor exposures to toxigenic molds
resemble field exposures of animals more closely than they do
controlled experimental laboratory exposures. Animals in controlled
laboratory exposures are healthy, of the same age, raised under
optimum conditions, and have only the challenge of known doses of a
single toxic agent via a single exposure route. In contrast, animals
in field exposures are of mixed ages, and states of health, may be
living in less than optimum environmental and nutritional conditions,
and are exposed to a mixture of toxic agents by multiple exposure
routes. Exposures to individual toxins may be much lower than those
required to elicit an adverse reaction in a small controlled exposure
group of ten animals per dose group. The effects from exposure may
therefore not fit neatly into the description given for any single
toxin, or the effects from a particular species, of mold.
Field exposures of animals to molds (in
contrast to controlled laboratory exposures) show effects on the
immune system as the lowest observed adverse effect. Such immune
effects are manifested in animals as increased susceptibility to
infectious diseases (Jakab
et al., 1994). It is
important to note that almost all mycotoxins have an immunosuppressive
effect, although the exact target within the immune system may differ.
Many are also cytotoxic, so that they have route of entry effects that
may be damaging to the gut, the skin or the lung. Such cytotoxicity
may affect the physical defense mechanisms of the respiratory tract,
decreasing the ability of the airways to clear particulate
contaminants (including bacteria or viruses), or damage alveolar
macrophages, thus preventing clearance of contaminants from the deeper
lung. The combined result of these activities is to increase the
susceptibility of the exposed person to infectious disease, and to
reduce his defense against other contaminants. They may also increase
susceptibility to cancer
Because indoor samples are usually comprised
of a mixture of molds and their spores, it has been suggested that a
general test for cytotoxicity be applied to a total indoor sample to
assess the potential for hazard as a rough assessment (Gareis,
The following summary of toxins and their
targets is adapted from Smith and Moss (1985), with a few additions
from the more recent literature. While this compilation of effects
does not describe the effects from multiple exposures, which could
include synergistic effects, it does give a better idea of possible
results of mycotoxin exposure to multiple molds indoors.
(diarrhea, vomiting, intestinal hemorrhage, liver effects, i.e.,
necrosis, fibrosis: aflatoxin; caustic effects on mucous membranes:
T-2 toxin; anorexia: vomitoxin.
- Vascular system (increased vascular
fragility, hemorrhage into body tissues, or from lung, e.g.,
aflatoxin, satratoxin, roridins).
- Respiratory system:
respiratory distress, bleeding from lungs e.g., trichothecenes.
- Nervous system, tremors,
incoordination, depression, headache, e.g., tremorgens,
- Cutaneous system : rash,
burning sensation sloughing of skin, photosensitization, e.g.,
- Urinary system,
nephrotoxicity, e.g. ochratoxin, citrinin.
- Reproductive system;
infertility, changes in reproductive cycles, e.g. T-2 toxin,
- Immune system: changes
or suppression: many mycotoxins.
It should be noted that not all mold genera
have been tested for toxins, nor have all species within a genus
necessarily been tested. Conditions for toxin production varies with
cell and diurnal and seasonal cycles and substrate on which the mold
grows, and those conditions created for laboratory culture may differ
from those the mold encounters in its environment.
Toxicity can arise from exposure to
mycotoxins via inhalation of mycotoxin-containing mold spores or
through skin contact with the toxigenic molds (Forgacs,
Croft et al., 1986;
Kemppainen et al.,
1988 -1989). A number of toxigenic molds
have been found during indoor air quality investigations in different
parts of the world. Among the genera most frequently found in numbers
exceeding levels that they reach outdoors are Aspergillus,
Penicillium, Stachybotrys, and Cladosporium (Burge,
Smith et al., 1992;
Hirsh and Sosman, 1976;
Verhoeff et al., 1992;
Miller et al., 1988;
Gravesen et al.,
1999). Penicillium, Aspergillus and
Stachybotrys toxicity, especially as it relates to indoor
exposures, will be discussed briefly in the paragraphs that follow.
Penicillium species have been shown
to be fairly common indoors, even in clean environments, but certainly
begin to show up in problem buildings in numbers greater than outdoors
Miller et al., 1988;
Flannigan and Miller, 1994). Spores have the
highest concentrations of mycotoxins, although the vegetative portion
of the mold, the mycelium, can also contain the poison. Viability of
spores is not essential to toxicity, so that the spore as a dead
particle can still be a source of toxin.
Important toxins produced by penicillia include nephrotoxic
citrinin, produced by P. citrinum, P. expansum and P.
viridicatum; nephrotoxic ochratoxin, from P. cyclopium and
P. viridicatum, and patulin, cytotoxic and carcinogenic in
rats, from P. expansum (Smith
and Moss, 1985).
Aspergillus species are also
fairly prevalent in problem buildings. This genus contains several
toxigenic species, among which the most important are, A.
parasiticus, A. flavus, and A. fumigatus. Aflatoxins
produced by the first two species are among the most extensively
studied mycotoxins. They are among the most toxic substances known,
being acutely toxic to the liver, brain, kidneys and heart, and with
chronic exposure, potent carcinogens of the liver. They are also
and Moss, 1985;
Burge, 1986). Symptoms of acute
aflatoxicosis are fever, vomiting, coma and convulsions (Smith
and Moss, 1985). A. flavus is found
indoors in tropical and subtropical regions, and occasionally in
specific environments such as flowerpots. A. fumigatus has
been found in many indoor samples. A more common aspergillus species
found in wet buildings is A. versicolor, where it has been
found growing on wallpaper, wooden floors, fibreboard and other
building material. A. versicolor does not produce aflatoxins,
but does produce a less potent toxin, sterigmatocystin, an aflatoxin
et al., 1994). While symptoms of
aflatoxin exposure through ingestion are well described, symptoms of
exposure such as might occur in most moderately contaminated buildings
are not know, but are undoubtedly less severe due to reduced exposure.
However, the potent toxicity of these agents advise that prudent
prevention of exposures are warranted when levels of aspergilli
indoors exceed outdoor levels by any significant amount. A.
fumigatus has been found in many indoor samples. This mold is
more often associated with the infectious disease aspergillosis, but
this species does produce poisons for which only crude toxicity tests
have been done (Betina,
1989). Recent work has found a number of
tremorgenic toxins in the conidia of this species (Land
et al., 1994). A. ochraceus
produces ochratoxins (also produced by some penicillia as mentioned
above). Ochratoxins damage the kidney and are carcinogenic (Smith
and Moss, 1985).
Stachybotrys chartarum (atra)
Stachybotrys chartarum (atra)
has been much discussed in the popular press and has been the subject
of a number of building related illness investigations. It is a mold
that is not readily measured from air samples because its spores, when
wet, are sticky and not easily aerosolized. Because it does not
compete well with other molds or bacteria, it is easily overgrown in a
sample, especially since it does not grow well on standard media (Jarvis,
1990). Its inability to compete may also
result in its being killed off by other organisms in the sample
mixture. Thus, even if it is physically captured, it will not be
viable and will not be identified in culture, even though it is
present in the environment and those who breathe it can have toxic
exposures. This organism has a high moisture requirement, so it grows
vigorously where moisture has accumulated from roof or wall leaks, or
chronically wet areas from plumbing leaks. It is often hidden within
the building envelope. When S. chartarum is found in an air
sample, it should be searched out in walls or other hidden spaces,
where it is likely to be growing in abundance. This mold has a very
low nitrogen requirement, and can grow on wet hay and straw, paper,
wallpaper, ceiling tiles, carpets, insulation material (especially
cellulose-based insulation). It also grows well when wet filter paper
is used as a capturing medium.
S. chartarum has a well-known history in Russia and the
Ukraine, where it has killed thousands of horses, which seem to be
especially susceptible to its toxins. These toxins are macrocyclic
trichothecenes. They cause lesions of the skin and gastrointestinal
tract, and interfere with blood cell formation. (Sorenson,
1993). Persons handling material heavily
contaminated with this mold describe symptoms of cough, rhinitis,
burning sensations of the mouth and nasal passages and cutaneous
irritation at the point of contact, especially in areas of heavy
perspiration, such as the armpits or the scrotum (Andrassy
et al., 1979).
One case study of toxicosis associated with macrocyclic
trichothecenes produced by S. chartarum in an indoor exposure,
has been published (Croft
et al., 1986), and has proven seminal
in further investigations for toxic effects from molds found indoors.
In this exposure of a family in a home with water damage from a leaky
roof, complaints included (variably among family members and a maid)
headaches, sore throats, hair loss, flu symptoms, diarrhea, fatigue,
dermatitis, general malaise, psychological depression. (Croft
et al, 1986;
Johanning, (1996) in an epidemiological and immunological
investigation, reports on the health status of office workers after
exposure to aerosols containing S. chartarum. Intensity and
duration of exposure was related to illness. Statistically significant
differences for more exposed groups were increased lower respiratory
symptoms, dermatological, eye and constitutional symptoms, chronic
fatigue, and allergy history. Duration of employment was associated
with upper respiratory, skin and central nervous system disorders. A
trend for frequent upper respiratory infections, fungal or yeast
infections, and urinary tract infections was also observed. Abnormal
findings for components of the immune system were quantified, and it
was concluded that higher and longer indoor exposure to S.
chartarum results in immune modulation and even slight immune
suppression, a finding that supports the observation of more frequent
Three articles describing different aspects of an investigation of
acute pulmonary hemorrhage in infants, including death of one infant,
have been published recently, as well as a CDC evaluation of the
et al., 1997;
Etzel et al., 1998;
Jarvis et al., 1998;
MMWR, 2000; CDC, 1999). The infants in the
Cleveland outbreak were reported with pulmonary hemosiderosis, a sign
of an uncommon of lung disease that involves pulmonary hemorrhage.
Stachybotrys chartarum was shown to have an association with acute
pulmonary bleeding. Additional studies are needed to confirm
association and establish causality.
Animal experiments in which rats and mice were exposed intranasally
and intratracheally to toxic strains of S. chartarum,
demonstrated acute pulmonary hemorrhage (Nikkulin
et al. 1996). A number of case
studies have been more recently published. One involving an infant
with pulmonary hemorrhage in Kansas, reported significantly elevated
spore counts of Aspergillus/Penicillium in the patient’s
bedroom and in the attic of the home. Stachybotrys spores were
also found in the air of the bedroom, and the source of the spores
tested highly toxigenic (Flappan
et al., 1999). In another case
study in Houston, Stachybotrys was isolated from
bronchopulmonary lavage fluid of a child with pulmonary hemorrhage. (Elidemir
et al., 1999), as well as recovered
from his water damaged-home. The patient recovered upon removal and
stayed well after return to a cleaned home. Another case study
reported pulmonary hemorrhage in an infant during induction of general
anesthesia. The infant was found to have been exposed to S.
chartarum prior to the anesthetic procedure (Tripi
et al., 2000). Still another case
describes pulmonary hemorrhage in an infant whose home contained
toxigenic species of Penicillium and Trichoderma (a mold
producing trichothecene poisons similar to the ones produced by S.
chartarum) as well as tobacco smoke (Novotny
and Dixit, 2000)
Toxicologically, S. chartarum can produce extremely potent
trichothecene poisons, as evidenced by one-time lethal doses in mice
(LD50) as low as 1.0 to 7.0 mg/kg, depending on the toxin
and the exposure route. Depression of immune response, and hemorrhage
in target organs are characteristic for animals exposed experimentally
and in field exposures (Ueno,
Jakab et al., 1994).
While there are insufficient studies to establish cause and effect
relationships between Stachybotrys exposure indoors and
illness, including acute pulmonary bleeding in infants, toxic
endpoints and potency for this mold are well described. What is less
clear, and has been difficult to establish, is whether exposures
indoors are of sufficient magnitude to elicit illness resulting from
Some of these difficulties derive from the nature of the organisms
and the toxic products they produce and varying susceptibilities among
those exposed. Others relate to problems common to retrospective case
control studies. Some of the difficulties in making the connection
between toxic mold exposures and illness are discussed below.
Limitations in Sampling Methodology,
Toxicology, and Epidemiology of Toxic Mold Exposure
Some of the difficulties and limitations encountered in establishing
links between toxic mold contaminated buildings and illness are listed
- Few toxicological experiments involving
mycotoxins have been performed using inhalation, the most probable
route for indoor exposures. Defenses of the respiratory system
differ from those for ingestion (the route for most mycotoxin
experiments). Experimental evidence suggests the respiratory route
to produce more severe responses than the digestive route (Cresia
et al., 1987)
- Effects from low level or chronic low
level exposures, or ingestion exposures to mixtures of mycotoxins,
have generally not been studied, and are unknown. Effects from high
level, acute sub-acute and sub-chronic ingestion exposures to single
mycotoxins have been studied for many of the mycotoxins isolated.
Other mycotoxins have only information on cytotoxicity or in
- Effects of multiple exposures to mixtures
of mycotoxins in air, plus other toxic air pollutants present in all
air breathed indoors, are not known.
- Effects of other biologically active
molecules, having allergic or irritant effects, concomitantly acting
with mycotoxins, are not known.
- Measurement of mold spores and fragments
varies, depending on instrumentation and methodology used.
Comparison of results from different investigators is rarely, if
ever, possible with current state of the art.
- While many mycotoxins can be measured in
environmental samples, it is not yet possible to measure mycotoxins
in human or animal tissues. For this reason exposure measurements
rely on circumstantial evidence such as presence of contamination in
the patient’s environment, detection of spores in air, combined with
symptomology in keeping with known experimental lesions caused by
mycotoxins, to establish an association with illness.
- Response of individuals exposed indoors to
complex aerosols varies depending on their age, gender, state of
health, and genetic make-up, as well as degree of exposure.
- Microbial contamination in buildings can
vary greatly, depending on location of growing organisms, and
exposure pathways. Presence in a building alone does not constitute
- Investigations of patients’ environments
generally occur after patients have become ill, and do not
necessarily reflect the exposure conditions that occurred during
development of the illness. All cases of inhalation exposure to
toxic agents suffer from this deficit. However exposures to
chemicals not generated biologically can sometimes be re-created,
unlike those with active microbial growth. Indoor environments are
dynamic ecosystems that change over time as moisture, temperature,
food sources and the presence of other growing microorganisms
change. Toxin production particularly changes with age of cultures,
stage of sporulation, availability of nutrients, moisture, and the
presence of competing organisms. After-the-fact measurements of
environmental conditions will always reflect only an estimate of
exposure conditions at the time of onset of illness. However,
presence of toxigenic organisms, and their toxic products, are
indicators of putative exposure, which together with knowledge of
lesions and effects produced by toxins found, can establish
Conclusions and Recommendations
Prudent public health practice then indicates removal from exposure
through clean up or remediation, and public education about the
potential for harm. Not all species within these genera are toxigenic,
but it is prudent to assume that when these molds are found in excess
indoors that they are treated as though they are toxin producing. It
is not always cost effective to measure toxicity, so cautious practice
regards the potential for toxicity as serious, aside from other health
effects associated with excessive exposure to molds and their
products. It is unwise to wait to take action until toxicity is
determined after laboratory culture, especially since molds that are
toxic in their normal environment may lose their toxicity in
laboratory monoculture over time (Jarvis,
1995) and therefore may not be identified as
toxic. While testing for toxins is useful for establishing etiology of
disease, and adds to knowledge about mold toxicity in the indoor
environment, prudent public health practice might advise speedy
clean-up, or removal of a heavily exposed populations from exposure as
a first resort.
Health effects from exposures to molds in indoor environments can
result from allergy, infection, mucous membrane and sensory irritation
and toxicity alone, or in combination. Mold growth in buildings (in
contrast to mold contamination from the outside) always occurs because
of unaddressed moisture problems. When excess mold growth occurs,
exposure of individuals, and remediation of the moisture problem must
Harriet M. Ammann is a senior toxicologist for Washington State
Department of Health, Office of Environmental Health Assessments. She
provides support to a variety of environmental health programs
including ambient and indoor air programs. She has participated in
evaluations of schools and public buildings with air quality problems,
and has presented on toxic effects from air contaminants, indoors and
out, effect on sensitive populations, and other health issues
throughout the state. Through her work, she has developed an interest
in the toxicology of mold as an indoor air contaminant, and has
published and presented on mold toxicity relating to human health.
If you have a comment on this paper, please email Harriet Ammann at
firstname.lastname@example.org. We are always
happy to hear your views.
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