Is Indoor Mold Contamination a
Threat to Health?
Ammann, Ph.D., D.A.B.T.
Washington State Department of Health
Fungus Among Us
Membrane and Trigeminal Nerve Irritation
Reactions To Odor
in Sampling Methodology, Toxicology, and Epidemiology of Toxic Mold
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 to grow.
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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
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.
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
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
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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
Membrane and Trigeminal Nerve Irritation Top
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
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 effects.
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.
Reactions to Odor Top
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 symptoms.
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 infections.
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, including humans.
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,
1995). The presence of competitive organisms may play a role,
as some molds grown in monoculture in the laboratory lose their toxic
1995). Until relatively recently, mold poisons were regarded
with concern primarily as contaminants in foods.
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
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
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
- Vascular system (increased vascular
fragility, hemorrhage into body tissues, or from lung, e.g.,
aflatoxin, satratoxin, roridins).
- Digestive system (diarrhea, vomiting,
intestinal hemorrhage, liver effects, i.e., necrosis, fibrosis:
aflatoxin; caustic effects on mucous membranes: T-2 toxin; anorexia:
- 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.
- Reproductive system; infertility,
changes in reproductive cycles, e.g. T-2 toxin, zearalenone.
- Immune system: changes or
suppression: many mycotoxins.
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
can arise from exposure to mycotoxins via inhalation of
mycotoxin-containing mold spores or through skin contact with the
toxigenic molds (Forgacs,
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,
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.
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 (Burge,
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
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).
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 teratogenic (Smith
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 precursor (Gravesen
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).
chartarum (atra) Top
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.
has a well-known history in
, 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).
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; Jarvis,
(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 infections.
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;
et al., 1998;
et al., 1998;
2000; CDC, 1999). The infants in the
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
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
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
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)
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
et al., 1994).
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 toxic exposure.
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.
in Sampling Methodology, Toxicology, and Epidemiology of Toxic Mold
of the difficulties and limitations encountered in establishing links
between toxic mold contaminated buildings and illness are listed here:
- 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)
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 vitro effects.
of multiple exposures to mixtures of mycotoxins in air, plus other
toxic air pollutants present in all air breathed indoors, are not
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
- 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
and Recommendations Top
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.
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 be addressed.
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.
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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