The issue of mold-related health problems, and in particularly Stachybotrys (“black mold”), is a controversial one. There are known health effects that can result from exposure to certain molds, a form of fungi, such as Aspergillus, which is known to cause occasionally respiratory symptoms. The generalized and often popularized “toxic mold syndrome” and its resultant array of symptomatology caused by exposure to indoor mold, generally Stachybotrys, has not been scientifically proven.
Molds are the most common form of fungi found on earth. Most molds reproduce through the production of spores, which float through the air on a continual basis. Exposure to molds occurs daily just by breathing the air – both indoors and outdoors. Molds can grow on almost every surface and are especially prevalent when excessive moisture accumulates. It is impossible to eliminate molds and mold spores. Moisture control is the most common strategy for reducing, but certainly not eliminating mold growth.
There are three main processes through which human health is affected by molds: (1) allergy; (2) infection; and (3) toxicity. It is estimated that 10 percent of the population has allergic antibodies to fungal (mold) allergens. Only 5 percent of these will show any clinical illness as a result of the allergic antibodies (5 out of 1000 people). Generally outdoor molds are more abundant and more often the cause of allergic response than indoor molds. Allergic responses are most often seen as allergic rhinitis or allergic asthma. Hypersensitivity pneumonitis (HP) has been identified as another potential disease entity due to allergic response to mold, but it is rare and only follows exposure to very high concentrations of fungal material. It responds to steroids and anti-inflammatory treatment, not to antibiotics.
Hypersensitivity and allergic responses to molds may be immunoglobulin E (IgE) or immunoglobulin G (IgG) mediated. Both types are associated with indoor molds. To determine whether or not an individual has an actual allergy to mold, the presence of the specific immunoglobulin antibodies must be demonstrated. Once the specific immunoglobulin had formed, the individual becomes more sensitive to subsequent exposures. This is a testable hypothesis and diagnostic laboratory tests can determine this.
Asthma is the only well-documented form of IgE mediated disease in which airborne fungi are involved. Allergic rhinitis that is caused by fungi is often suspected but is difficult to show with any certainty; it is not well correlated or proven.
Hypersensitivity pneumonitis (HP) is the result of an exaggerated immune response to the inhalation of airborne organic particles, which can be fungal in nature. It is a chronic disease of the peripheral airways and interstitium, which can progress to pulmonary fibrosis. The disease has three stages that often overlap. The first and most acute stage features a mononuclear cell pneumonitis. The subacute stage is characterized by interstitial granulomatous inflammation. The chronic stage has been reached when interstitial fibrosis has developed. HP requires inhalation of large quantities of an organic antigen. HP is diagnosed by abnormal pulmonary function tests (PFT) and abnormal chest x-rays and CT scans, the spiral CT scan being the most sensitive study to detect disease.
Fungal infections caused by mold exposure are usually limited to individuals who are severely immunocompromised such as cancer patients, individuals on immune suppressive regimens such as in rheumatoid arthritis or transplant recipients, and persons with AIDS. Superficial fungal infections on the skin or mucosal surfaces can occur and are not uncommon. Most often skin infections that are attributed to a fungal source occur from outdoor activity exposures.
Some molds produce metabolic by-products known as mycotoxins that can cause toxic reactions in humans. Mycotoxin production will depend on the species of mold, the conditions for growth, and competition with other microorganisms. The presence of a mycotoxin-producing mold does not mean that mycotoxins are present. Toxicity is usually the result of the ingestion of mycotoxins from contaminated foods. For a toxic effect to result the toxin must be present, there must be a route of exposure, and a sufficient “dose” to produce a toxic effect must occur. In non-occupational settings the route of exposure is inhalation; however it is exceedingly rare to inhale sufficient fungal/mold spores and materials to develop HP.
Mycotoxins are not cumulative toxins and have a half-life ranging from hours to days depending on the specific mycotoxin. The levels at which adverse health effects are observed make it highly improbable that home exposure would lead to a toxic adverse health effect.
The American College of Occupational and Environmental Medicine’s evidence-based statement regarding the adverse human health effects associated with molds in the indoor environment in fact does not support at all the contention that mycotoxin-mediated disease (mycotoxicosis) occurs through inhalation in a non-occupational setting. For toxicity to result from mold exposure, the concentration and duration of exposure must be sufficient to deliver a toxic dose.
Most of the effects of mold exposure from an indoor source create irritant effects that are transient and disappear when the exposure has decreased and/or ceased. Irritant effects involve the mucus membranes of the eyes and upper and lower respiratory tracts and are transient.
Many cases of adverse health effects related to indoor mold exposure have been attributed to Stachybotrys Chartarum or Stachybotrys Alternans. These are slow-growing fungi with spores that readily die when released into the atmosphere. Therefore, spores are not often found outdoors and are difficult to isolate even indoors. A documented case of human infection with a Stachybotrys species is reportable.
Testing for causes of health effects thought to have been caused by mold exposure look for abnormalities rather than for a confirmation of an actual exposure. Measurement of IgE antibodies to mold antigens has been validated as a measure of potential allergic reactivity to mold. However, the presence of IgE antibodies to a mold cannot be used to determine the dose or the timing of the exposure. Measurement of other antibodies has not been useful in establishing mold exposure. Measurement of IgG antibodies has demonstrated value only in assessment of individuals with suspected HP but only where a clinical picture suggesting HP is part of the differential diagnosis. In order to have HP however, the individual must also have abnormal pulmonary function tests, abnormal chest x-rays and abnormal CT scans compatible with the diagnosis.
“Toxic mold syndrome” is increasingly being alleged in toxic tort litigation. There are a number of alleged conditions that are attributed to “toxic mold” exposure including brain damage, toxic encephalopathy, cognitive and neural behavior deficits, and logical analysis impairment among others. There is no consistent pattern of symptoms or test results for which a diagnosis of “mold neurotoxicity” can be defined. There is no scientific link with spore levels, fungal levels, specific bacteria or any known pathological entity that would be causing this “mold toxicity”. Such arguments are generally junk science.
The “mold neurotoxicity” argument is not presented in scientific and peer review journals. The studies that purport to show patients with illness from exposure to Stachybotrys do not utilize control groups, standardized test batteries or even alternative explanations of the abnormalities. In fact, some of the only peer review studies done such as that by Hodgson found exposed individuals performed better in case control studies.
References are available upon request.