Is Indoor Mold Contamination a Threat to Health?

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Is Indoor Mold Contamination a Threat to Health?

Harriet M. Ammann, 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.

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 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;

et al., 1992; Hirsh and Sosman, 1976; Verhoeff et al., 1992; 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; et al., 1988; Flannigan

and , 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 ( 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 ( and Moss, 1985; Burge, 1986).

Symptoms of acute aflatoxicosis are fever, vomiting, coma and convulsions

( 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 ( 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 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 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@.... We are always happy to hear your views.

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