STACHYBOTRYS WEB SITE:  Pathology, Symptoms

Like many other molds, stachybotrys can spread both through the generation of spores and the growth of root-like structures called mycelia. Stachybotrys spores grow in clusters at the end of stem-like structures known as hyphae. The spores do not easily disperse into the air if the colonized material is wet, as the spores are held together by a sticky/slimy coating. Distribution through the air is possible when the mold dries out or is disturbed. Because of this danger of the airborne dispersion of spores, all cleaning and removal of stachybotrys mold should be done using appropriate controls.

Stachybotrys 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). 

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.

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)

· 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. 

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).
 

When inhaled or ingested stachybotrys can cause:

· Sore/hoarse throat
· Cold and flu symptoms (headaches, slight fever, and muscle aches) 
· Nose bleeds 
· Tingling or burning of nose, mouth, and perspiration areas (under the arms or 
   between the legs)
· Chronic fatigue
· Dizziness
· Nausea/vomiting
· Memory loss
· Attention deficit/concentration problems
· Personality changes such as irritability or depression 
· Neurological disorders such as tremors 
· Hair loss
· Coughing with blood 
· Bleeding in the lungs (hemosiderosis)
· Damage to internal organs including blood, liver, kidneys, and lungs 

Although not supported by definitive studies at this point, there are some concerns about stachybotrys exposure promoting cancer. The symptoms and health effects related to stachybotrys depend on an individual's pre-existing health situation, length of exposure, and the amount of stachybotrys in the environment. Because of this, different people in the same situation, even family members, may experience different sets and severity of symptoms. 
 

Many physicians believe that the following tests are appropriate in conducting a medical screening for stachybotrys:
· Complete medical exam 
· Chest x-ray · Pulmonary function test
· Complete red and white blood cell count 
· Blood sedimentation rate 
· Stachybotrys specific RAST antibody test
· Immunoglobulin panel 
· Immune competence tests

Doctors should be encouraged to discuss the environmental situation with the industrial hygiene professionals who have conducted sampling in the building in question.tc.
 

1. they are non-porous (they have durable, smooth surfaces)

2. they contain no cellulose or other organic material such as paper,    cardboard, wood, 
    leather, cotton, wool, wall board etc.

3. they could be thoroughly washed in a washing machine.

4. Such items would include glass ware, dishes, silverware, CD ROMS, coins etc.
   There are at least two important considerations when one deals with this mold. 

  (1). How long do the spores remain potentially viable once they are released from the living 
         stachybotrys mold?

The best answer I have received regarding this is: "Stachybotrys spores can suvive for at least a year after release. However, the viability does decline with time. The environment they arein will affect survival and rate of decline." 

Thus, any item you try to salvage can carry some spores that potentially could germinate, under the right conditions, in your new enviornment. 

   (2). How long do the mycotoxins on stachybotrys spores remain potent after the spores are 
         discharged into the air? 

The best answer I have received regarding this is: "The trichothecene toxins are very stable. Again the environment matters, if stored dry, there is little loss of activity for a year." 
Thus, if mycotoxins on the mold cause you symptoms, if you carried some of the dead spores on the material you tried to salvage, that material could continue to make you ill for as long as the mycotoxins remained potent. 

The answers, in quotations, were kindly provided by Mr. Stephen Vesper of the EPA. 
Finally, there is no question that Five percent sodium hypochlorite (bleach) will kill live mold. But, that dosen't solve your problem. You need to denature the mycotoxins on the mold spores that are on your contaminated material. This requires a substance that can denature the mycotoxins, while preserving the material beeing treated. I haven't found the answer to this question with any degree of reasonable certianty. 

I have tried to salvage some clothing, but it has been difficult, risky, time consuming and in many cases failed, causing me a great deal of grief. I managed to salvage some super silk shirts (100% polyester) by repeated washings. In retrospect, it probably wasn't worth the effort. Very porous clothing, such as sweaters, even of the synthetic variety, don't seem to respond to a reasonable number of washings, at least in my experience. Using bleach on these clothing doesn't seem to help insofar as toxicity is concerned. And, forget paper products, such as books, articles, magazines, miscellaneous papers etc. 

My problem now is that I can't go near, much less work with, any paper or books 
contaminated by the mold spores. This includes medical books, charts, magazines 
etc. If I do get exposed become ill again anywhere from a few days to a few 
weeks, depending upon the intensity and length of exposure.

I found that with each exposure I got, my sensitivity would increase; that is, 
it would take increasingly smaller amounts of the mycotoxins on the spores to
make me ill.

Also, I have become sensitized to incredibly small quantities of smoke.  If I
get a few whiffs of smoke from a cigarette, cigar or chimney (smoke from a 
fireplace), I'll get symptoms of fatigue, malaise, flu-like symptoms and eve
more severe burning in the chest with exertion for a few hours to a day or two.

Regarding treatment, the five most effective measures are:

1. avoidance of living mold
2. avoidance of the mold spores
3. avoidance of contaminated items 
4. avoidance of smoke
5. avoidance of fatigue (getting enough sleep)

The next five measures are:

6. inhalation ipatropium bromide (four times daily in a nebulizer)
7. inhalation albuterol sulfate (four times daily in a nebulizer)
8. inhalation fluticasone propionate 500 mcg and samletrol 50 mcg (powder), 2 
puffs daily (Advaid Diskus 500/50)
9. Theophylline 200-300 mg daily in divided doses
10. Being careful to get enough potassium and calcium (combination of diet & 
pills)