Re: Re: doctors/toxicologist Harriet Amman

[Guest guest]

This is another really excellent piece! Thanks.

tigerpaw2c <tigerpaw2c@...> wrote: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

http://www.doh.wa.gov/ehp/oehas/mold.html

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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.

References

Andrassy, K, I.; Horvath, T.; Lakos, and Z. Toke. 1979. Mass

incidence of mycotoxicoses in Hajdu-Bihar county. Mykosen 23: 198-

133.

Bell, I.R.; Schwartz, G.E.; sen, J.M.; et al., 1993a. Self-

reported illness from chemical odors in young adults without

clinical symptoms or occupational exposures. Arch. Environ. Health

48:6-13.

Bell, I.R.; Schwartz, G.E.; sen, J.M.; et al., 1993b. Possible

time-dependent sensitization to xenobiotics: self-reported illness

from chemical odors, foods and opiate drugs in an older population.

Arch. Environ. Health 48:315-327.

Betina, V. 1989. Mycotoxins: Chemical, Biological, and Environmental

Aspects. Bioactive Molecules Volume 9. Elsevier, NY.

Burge, H.A. 1986. Toxigenic potential of indoor microbial aerosols.

Fifth Symposium on the Application of Short-Term Bioassays in the

Analysis of Complex Environmental Mixtures. Sheraton University

Center, Durham, NC .

Cresia, D.A.; Thurman, J.D.; , L.J., III; Nealley, M.L.; York,

C.G.; Wannemacher, R.W., Jr.; Bunner, D.L. 1987. Acute inhalation

toxicity of T- mycotoxin in mice. Fund. Applied Toxicol. 8 (2) 230-

235.

Croft, W.A; Jarvis, B.B.; Yatawara, C.S. 1986. Airborne outbreak of

trichothecene toxicosis. Atmos. Environ. 20(3): 549-552.

Elidemir, O.; Colasurdo, G.N.; Rossmann, S.N.; Fan, L.L. 1999.

Isolation of Stachybotrys from the lung of a child with pulmonary

hemosiderosis. Pediatrics 104(4pt 1): 964-6.

Etzel, R.A.; Montaña, E., Sorenson, W.G., Kullman, G.J.; Allan,

T.M.; Dearborn, D.G. 1998. Acute pulmonary hemorrhage in infants

associated with exposure to Stachybotrys atra and other fungi. Arch.

Pediatr. Adolesc. Med. 152:757-761.

Flannigan, B.; McCabe, E.M.; McGarry, F. 1991. Allergenic and

toxigenic microorganisms in houses. J. Applied Bacteriology

Symposium Supplement 70: 61S-73S.

Flannigan, B.; , J.D. 1994. Health implications of fungi in

indoor environments- an overview. Health Implications of Fungi in

Indoor Environments. Air Quality Monographs Vol. 2. R.A. Samson, B.

Flannigan, M.E. Flannigan, A.P. Verhoeff, O.C.G. Adan, Hoekstra,

E.S., editors. Elsevier, NY 3-28.

Flappan, S.M.; Portnoy, J.; , P. , C. 1999. Infant

pulmonary hemorrhage in a suburban home with water damage and mold

(Stachybotrys atra). EHP 107(11): 927-30.

Forgacs, J. 1972. Stachybotryotoxicosis. in Kadis, S.; Agl, S.J.;

eds. Microbial Toxins vol. III, Academic Press, Inc. NY. pp. 95-128.

Gareis, M. 1995. Cytotoxicity testing of samples originating from

problem buildings. Proceedings of the International Conference:

Fungi and Bacteria in Indoor Environments: Health Effects, Detection

and Remediation. Eckart Johanning and Chin S. Yang, editors.

Saratoga Springs, NY, October 6-7, 1994.139-144.

Gravesen, S. Frisvad, J.C, Samson, R.A.. 1994. Descriptions of some

common fungi. in Microfungi. Munksgaard Copenhagen. 141.

Gravesen, S.; Nielsen, P. A.; Iversen, R.; Nielsen, K.F. 1999.

Microfungal contamination of damp buildings – examples of

constructions and risk materials. EHP 1999 Jun; 107 Suppl. 3:505-

508.

Hintikka, E.-L. 1978. Human stachybotrystoxicosis. in Wyllie, T.D.;

Morehouse, L.G., eds. Mycotoxic Fungi, Mycotoxins, Mycotoxicoses; An

Encyclopedic Handbook. Vol. 3., Marcel Dekker, Inc. NY. pp. 87-89.

Hoekstra, ES; Samson, RA; Verhoeff, AP. 1994. Health Implications of

Fungi in Indoor Environments. Air Quality Monographs Vol. 2. R.A.

Samson; B. Flannigan; M.E. Flannigan; A.P. Verhoeff; O.C.G. Adan;

E.S. Hoekstra, editors. Elsevier, NY. 169-177.

Institute of Medicine. 1993. Indoor Allergens. Assessing and

Controlling Adverse Health Effects. Pope, A.M., , R.,

Burge, H.A., editors. Committee on Health effects and Indoor

Allergens, Division of Health Promotion and Disease Prevention,

Institute of Medicine. National Academy Press. Washington, D.C.

Jakab, G.J.; Hmieleski, R.R.; Hemenway, D.R.; Groopman, J.D. 1994.

Respiratory aflatoxicosis: suppression of pulmonary and systemic

host defenses in rats and mice. Toxicol. Applied Pharm. 125: 198-

205.

Jarvis, B.B. 1990. Mycotoxins and indoor air quality. in Biological

Contaminants in Indoor Environments ASTM Symposium, Boulder, CO,

July 16-19, 1989. Morey, P.R.; Feeley, J.C.; Otten, J.A. eds. pp.

201-214.

Jarvis, BB. 1995. Mycotoxins in the air: keep your buildings dry or

the bogeyman will get you. 35-44. Proceedings of the International

Conference: Fungi and Bacteria in Indoor Environments. Health

Effects, Detection and Remediation. Eckardt Johanning and Chin S.

Yang, editors. Saratoga Springs, NY. October 6-7, 1994.

Jarvis, B.B.; Sorenson,W.G. ;Hintikka, e-L.; et al., 1998. Study of

toxin production by isolates of Stachybotrys chartarum and

Memnoniella echinata isolated during a study of pulmonary

hemosiderosis in infants. Appl. Environ. Microbiol. 64(10): 3620-

3625.

Johanning, E.; Biagini, R.; Hull, D.L.; Morey, P.; Jarvis, B.;

Landbergis, P. 1996. Health and immunology study following exposure

to toxigenic fungi (Stachybotrys chartarum) in a water-damaged

office environment. Int. Arch. Environ. Health. 68: 207-218.

Kemppainen, B.W.; Riley, R.T.; Pace, J.G. 1988-1989. Skin Absorption

as a route of exposure for aflatoxin and trichothecenes. J Toxicol -

Toxin Reviews 7(2): 95-120.

Land, C.J.; Rask-Anderssen, A.; Werner, S.; Bardage, S. 1994.

Tremorgenic mycotoxins in conidia of Aspergillus fumigatus.

Mason, C.D.; Rand, T.G.; Oulton, M.; Mac, J.M.; , J.E.

1998. Effects of Stachybotrys chartarum (atra) conidia and isolated

toxin on lung surfactant production and homeostasis. Nat. Toxins. 6

(1): 22-33.

, J.D.; LaFlamme, A.M.; Sobol, Y.; LaFontaine, P.; Greenhalgh,

R. 1988. Fungi and fungal products in some Canadian homes.

International Biodeterioration 24: 103-120.

Montaña, E.; Etzel, R.A.; Allan, T.; Horgan, T.E.; Dearborn, D.G.

1997. Environmental risk factors associated with pediatric

idiopathic pulmonary hemorrhage and hemosiderosis in a clinical

community. Pediatrics 99 (1): 1-8.

Morbidity and Mortality Weekly Report (MMWR). 2000. Update:

pulmonary hemorrhage/hemosiderosis among infants – Cleveland, Ohio,

1993-1996.

Nikulin, M.; Reijula, K.; Jarvis, B.B.; Hintikka, E-L. 1996.

Experimental lung mycotoxicosis in mice induced by Stachybotrys

atra. Int. J. Exp. Path. 77: 213-218.

Northrup, S.C.; Kilburn. 1978. The role of mycotoxins in pulmonary

disease. in Mycotoxic Fungi, Mycotoxins, Mycotoxicoses, An

Encyclopedic Handbook, vol. 3 Wylie, T.; Morehouse, L. NY Marcel

Dekker.

Novotny, W.E.; Dixit, A. 2000. Pulmonary hemorrhage in an infant

following 2 weeks of fungal exposure. Arch. Pediatr. Adolesc. Med.

154(3): 271-5

Otto, D.; Mølhave, L.; Rose, G. et al.1989. Neurobehavioral and

sensory effects of controlled exposure to a complex mixture of

volatile organic compounds. Neurotoxicology and Teratology 12:649-

652.

Pestka, J.J.; Bondy, G.S. 1990. Alteration of immune function

following dietary mycotoxin exposure. Can. J. Physiol. Pharmacol.

68:1009-1016.

Pier, A.C.; McLoughlin, M.E. 1985. Mycotoxic suppression of

immunity. in Trichothecenes and Other Mycotoxins. Proceedings of the

International Mycotoxin Symposium. Sidney, Australia, 1984.

Lacey, ed. Wiley & Sons. NY. pp. 507-519.

Sabbioni, G.; Wild, C.P., 1991. Identification of an aflatoxin G1 -

serum albumin adduct and its relevance to the measurement of human

exposure to aflatoxins. Carcinogenesis 12: 97-103.

, J.E.; Moss, M.O. 1985. Mycotoxins Formation, Analysis, and

Significance Wiley and Sons. NY.

, J.E.; , J.G.; , C.W.; et al., 1992. Cytotoxic

fungal spores in the atmosphere of the damp domestic environment.

FEMS Microbiology Letters. 100: 337-344.

Sorenson, W.G. 1995. Aerosolized mycotoxins; implications for

occupational settings. Proceedings of the International Conference:

Fungi and Bacteria in Indoor Environments. Health Effects, Detection

and Remediation . Eckardt Johanning and Chin S. Yang, editors.

Saratoga Springs, NY. October 6-7, 1994. pp. 57-67.

Sorenson, W.G.; Frazer, D.G.; Jarvis, B.B.; Simpson, J.; ,

V.A. 1987. Trichothecene mycotoxins in aerosolized conidia of

Stachybotrys atra. Applied and Environmental Microbiology 53(6):

1370-1375.

Sorenson, W.G.; Gerberick, G.F.; , D.M.; Castranova, V. 1986.

Toxicity of mycotoxins for the rat pulmonary macrophage in vitro.

Environmental Health Perspectives 66: 45-53.

Sorenson, W.G.; Simpson, J. 1986. Toxicity of penicillic acid for

rat alveolar macrophages in vitro. Environ. Res. 4(2): 505-513.

Sorenson, W.G. 1993. Mycotoxins Toxic Metabolites of Fungi Fungal

Infections and Immune Response, Juneann W. , editor. Plenum

Press, NY. 469-491.

Tobin, R.S.; Baranowski, E.; Gilman, A.P.; Kuiper-Goodman, T.;

, J.D.; Giddings, M. 1987. Significance of fungi in indoor

air: report of a working group. Canadian Journal of Public Health

78: (suppl.), S1-S32.

Tripi, P.A.; Modlin, S.; Sorensen, W.G.; Dearborn, D.G. 2000. Acute

pulmonary haemorrhage in an infant during induction of general

anesthesia. Pediatr. Anesth. 10 (1): 92-4.

Verhoeff, A.P.; van Strien, R.T.; Van Wijjnen et al. 1995. Damp

housing and childhood respiratory symptoms. The role of

sensitization to dust mites and mold. Am. J. of Epidemiology. 141

(20: 103-110.

Ueno, Y. 1980. Trichothecene mycotoxins--mycology, chemistry, and

toxicology. Adv. Nutr. Sci. 3:301-353.

Yang, C.S. 1995. Understanding the biology of fungi indoors.

Proceedings from the International Conference: Fungi and Bacteria in

Indoor Environments: Health Effects, Detection and Remediation.

Saratoga Springs, N.Y. October 6-7, 1994. E. Johanning and C.S.Yang,

editors. Pp. 131-137.

> Harriet Amman is 'not even a dr.'.

> But she can do more to save your life than a thousand dr.s

> Only if you listen and act on her advice.

> For example " Avoid Ozone Machines " .

> I see that the Ionic Breeze has stepped up advertisements and

> aggressively claims that their ozone treatment turns pollution

> into " pure oxygen " .

> Caveat Emptor.

> -

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