Stachybotrys is a greenish black mold that grows on material with a high cellulose content or such as hay, straw, wicker, and wood chips, as well as building materials such as ceiling tile, drywall, paper vapor barriers, wallpaper, insulation backing, cardboard boxes, paper files, fiberboard, the paper covering of gypsum wallboard, particleboard, jute, dust, and wood when these items become water damaged. This mold requires very wet or high humid conditions for days or weeks in order to grow. Excessive indoor humidity resulting in water vapor condensation on walls, plumbing leaks, spills from showering or bathing, water leaking through foundations or roofs may lead to growth of many types of mold, including stachybotrys.

Individuals with chronic exposure to toxins produced by this fungus reported cold and flu symptoms, memory loss, muscle aches, sore throats, diarrhea, headaches, fatigue, dermatitis, intermittent local hair loss, cancer and generalized malaise. The toxins produced by this fungus will suppress and could destroy the immune system affecting the lymphoid tissue and the bone marrow. Animals injected with the toxin from this fungus exhibited the following symptoms: necrosis and hemorrhage within the brain, thymus, spleen, intestine, lung, heart, lymph node, liver, and kidney. Affects by absorption of the toxin in the human lung are known as pneumomycosis. The toxins may also suppress the immune system. In the January 17 issue of the MMWR, stachybotrys was implicated in a cluster of fatal pulmonary hemorrhage/hemosiderosis among infants.

In the past several years, case-control studies of occupational exposure to stachybotrys in water-damaged building environments have generated much controversy. In one of these investigations, significant differences in self-reported symptoms (Chronic fatigue, dermatologic, constitutional, and lower respiratory tract) between cases (n=51) and controls (n=21) were attributed to exposure to stachybotrys and other "atypical fungi." The study design did not include an evaluation for water damage or the presence of these fungi in the work or living environments of control subjects.

Speculation that exposure to stachybotrys produced immune dysfunction in cases was based on observations that cases had a lower proportion of mature T-lymphocyte (CD3) cells than controls (74% vs 76%, respectively), a finding that was statistically significant. The clinical significance of this finding remains difficult to interpret, and could have been affected by laboratory as well as individual daily variation. More important, this observation was the only one of over 20 hematologic and immunologic comparisons made between cases and controls that was found to be statistically significant, an observation that could be explained by chance.

In another case-control study, which concluded that exposure to stachybotrys and other toxigenic fungi was responsible for various pulmonary diseases (including asthma, interstitial lung disease, and "emphysematous-like" disease) among office workers in a water-damaged building, no reliable biomarkers of exposure to stachybotrys or radiographic findings correlating with the self-reported pulmonary symptoms were present.

Toxin ProductionToxicologically, stachybotrys 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).

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.

Stachybotrys is a member of the Deuteromycetes, order Moniliales, family Dematiaceae, and is common on plant debris and in soil. Mycotoxins and another biologically active toxins produced by stachybotrys are the reason why this fungus is of such great concern to human health. Stachybotrys chartarum is one of many molds that are capable of producing one or more mycotoxins (chemicals produced by molds that may be able to cause symptoms or illness and death in people). Mycotoxin poisoning by this fungus is referred to as stachybotryotoxicosis.

Stachybotrys chartarum produces the following types of macrocyclic tricothecenes: verrucarin J, roridin E, satratoxin F, G & H, sporidesmin G, trichoverrols; cyclosporins, stachybotryolactone, trichoverrols, and trichoverrins. Macrocyclic trichothecenes are highly toxic compounds. The severity of mycotoxicosis was related to the duration of consumption of toxic grain. Such severe trichothecene mycotoxicoses, the consequence of continuous ingestion of toxins, have not been recorded since earlier outbreaks. In several cases, trichothecene mycotoxicosis was caused by a single ingestion of bread containing toxic flour or rice. In experimental animals, trichothecenes are 40 times more toxic when inhaled than when given orally.

The satratoxins are generally produced in greater amounts than the other trichothecenes, but all compounds are produced in low quantities. They occur in all parts of the fungus. One isolate was reported to contain about 15 ppm trichothecene in the conidia. The difficulty in obtaining, identifying and purifying these toxins has slowed extensive studies on their biological activity.

In addition, the fungus produces 9-phenylspirodrimanes (spirolactones and spirolactams) and cyclosporin which are potent immunosuppressive agents. Jarvis et al. (1995) suggested that the combination of trichothecenes and these immunosuppressive agents may be responsible for the observed high toxicity of this fungus.

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 (Monta?a 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 Aspergillius and 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 stachybotrys 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 Thrichoderma (a mold producing trichothecene poisons similar to the ones produced by S. chartarum) as well as tobacco smoke (Novotny and Dixit, 2000).

Finding stachybotrys within a building does not necessarily mean that occupants have been exposed either to allergens (pieces of the fungus or spores that can cause allergic symptoms in people prone to allergies) or toxins produced by this fungus. Laboratory studies indicate that molds such as stachybotrys that have the ability to produce toxins do not always do so. Whether a mold produces a toxin while growing in a building may depend on what the mold is growing on, conditions such as temperature, food, pH, humidity or other unknown factors. When mycotoxins are present, they occur on spores and the small mold fragments that may be released into the air.

Much of what is currently known about exposure to mycotoxins has emerged from veterinary science. The toxic effects from mycotoxins produced by stachybotrys chartarum were first reported in the 1920s in Russia, when researchers reported severe morbidity and mortality in cattle and horses that ingested hay contaminated with this mold. Clinical observations included severe skin and mucous membrane inflammation, bleeding disorders, diarrhea, and upper and lower respiratory tract disorders.

Of particular concern is the threat that humans will inhale and ingest these toxic spores. One vague example are Yellow Rain attacks in Southeast Asia during the 1970s that were associated with the use of aerosolized trichothecenes. The toxins are often present on the fungal spores. Recent experimental animal studies have reported severe intra-alveolar, bronchiolar, and interstitial inflammation in mice that were exposed via an intranasal route with trichothecenes.

In contrast to toxicity from direct inhalation of stachybotrys spores, simulated environmental conditions with extensive surface growth of toxigenic stachybotrys and high air flow have not produced significant pulmonary toxicity in exposed mice. This observation may be related to the physical properties of stachybotrys; it produces spores in a slimy mass that are unlikely to become airborne without dry conditions. In addition, the production of mycotoxin by stachybotrys is dependent upon the environmental conditions of its growth. On some building materials and growth substrates, stachybotrys has not demonstrated biologic toxicity or mycotoxin production.

In laboratory animals, acute exposure to large amounts of trichothecene toxins resulting in a rapid release of stored white blood cells into circulation, while repeated or chronic exposure destroys granulocytic precursor cells in bone marrow leading to white cell depletion. Among the reported cellular effects are: mitogen B/T lymphocyte blastogenesis suppression, decrease of IgM, IgG, IgA; impaired macrophage activity and migration-chemotaxis; broad immunosuppressive effects on the cellular and humoral-mediated immune response leading to secondary infections; immunomodulation leading to spontaneous antibody increase and immunosuppressive effects in human peripheral blood lymphocytes.