Is Indoor Mold Contamination a Threat
to Health?
Harriet M. Amman, Ph.D., D.A.B.T.
Senior Toxicologist
Washington State Department of Health
Olympia, Washington
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 to grow.
Molds
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.
Allergy
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
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 contamination
Mucous Membrane and Trigeminal Nerve Irritation
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 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.
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
symptoms.
Toxicity
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,
1990; 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,
1995).
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.
-
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: vomitoxin.
-
Respiratory system:
respiratory distress, bleeding from lungs e.g., trichothecenes.
-
Nervous system,
tremors, incoordination, depression, headache, e.g., tremorgens,
trichothecenes.
-
Cutaneous system :
rash, burning sensation sloughing of skin, photosensitization, e.g.,
trichothecenes.
-
Urinary system,
nephrotoxicity, e.g. ochratoxin, citrinin.
-
Reproductive system;
infertility, changes in reproductive cycles, e.g. T-2 toxin, zearalenone.
-
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,
1972;
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,
1986;
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
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 (Burge,
1986;
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
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 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).
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;
Jarvis, 1995).
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 infections.
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 investigation
( Montaña
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,
1980; 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 toxic exposure.
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 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)
-
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 vitro effects.
-
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.
-
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 association.
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 be addressed.
Author
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
harriet.ammann@doh.wa.gov.
We are always happy to hear your views.
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