Exposure to mold can cause illness in humans, including asthma, allergic rhinitis, allergic bronchopulmonary aspergillosis, sinusitis, and hypersensitivity pneumonitis. This is well documented. Now, researchers are suggesting that many new mold-related illnesses may exist even though more studies need to be conducted.
Molds cause adverse human health effects through 3 defined mechanisms: toxic-irritant effects from mold byproducts, direct infection by the organism, and triggering a harmful immune response. Each of these mechanisms has scientifically documented mold-related human diseases. However, there may be many more mold-related illnesses. Litigation has pushed the possibility into the public sphere with assertions that exposure to indoor mold causes an array of poorly defined illnesses. Scientists are typically quick to point out the lack of evidence supporting these assertions.
Let’s take a further look at what is and what is not supported by scientific evidence.
The relationship between mold and asthma
Some estimates suggest that around 10% of the general population has IgE antibodies to common inhalant molds. Around 50% of those individuals have or will have allergic reactions after exposure to mold (fungal allergens). While exposure to indoor mold happens, exposure to outdoor fungal allergens is more relevant to sensitization and symptoms of disease. Sensitization to fungi, particularly Alternaria alternata, has been linked to the occurrence and severity of asthma. Exposure to atmospheric fungal spores outdoors has been linked to asthma symptoms and medication use in children with asthma.
The links between asthma and exposure to indoor mold is less clearly established. However, a review of the available literature suggests that children living in damp homes with visible mold were more likely to have lower respiratory tract symptoms like coughing and wheezing when compared to children living in drier, mold-free homes.
In addition, recent prospective epidemiologic studies have shown that infants at risk for asthma, defined by maternal history of asthma, who are exposed to high concentrations of indoor fungi (in addition to cockroach allergen and nitrogen dioxide sources) in the first year of life are at risk for persistent wheezing and cough.
Unfortunately, these studies lack do not control for confounding factors like other airborne allergens and irritants, and humidity. Studies that try to link indoor molds with symptomatic allergic rhinitis have methodological problems such as a lack of quantitative mold sampling and including upper respiratory tract infections.
In addition, no studies have established a causative role for airborne molds in atopic dermatitis. Instead, the reports show a relationship between IgE antibodies and an expected concomitant atopic presence.
Therefore, atopic patients with allergic asthma, atopic dermatitis, and allergic rhinitis typically have IgE antibodies due to polysensitization. Allergic responses to mold is a recognized factor in lower respiratory tract disease. However, the research currently does not prove conclusively that indoor mold plays a role in these conditions.
Atopic patients (those with allergic asthma, allergic rhinitis, and atopic dermatitis) commonly have IgE antibodies to molds as part of polysensitization.
Allergic bronchopulmonary aspergillosis and sinusitis
Allergic bronchopulmonary aspergillosis (ABPA) is a well-recognized condition that impacts people with asthma or cystic fibrosis.
A variety of fungi may produce a similar clinical presentation. The difference is that ABPA has an underlying anatomic change in the lung and not a specific exposure to mold, such as A fumigatus, which is found indoors and outdoors. Allergic fungal sinusitis is similar to ABPA because it is a localized hypersensitivity condition that results from fungal growth in an area of abnormal tissue drainage.
In addition to A fumigatus, other fungi can also cause problems. These include Deuteromycetes, Curvalaria, and Bipolaris species. The condition can be differentiated from chronic sinusitis through skin tests, vitro tests, nasal polyposis, and radiographic findings.
Although some researchers suspect that chronic rhinosinusitis may be due to a sensitivity to mold, conclusive evidence is lacking to support this hypothesis.
We can make the following conclusions:
- ABPA and allergic fungal sinusitis are manifestations of significant hypersensitivity to fungi, particularly Aspergillus species.
- Data supporting the role of fungi in CRS are lacking at this time.
Hypersensitivity pneumonitis
HP is a disease that exists in acute, subacute, and chronic forms but with considerable overlap. It is caused by inhaling an allergen in the organic dust of fungal, bacterial, vegetable or avian origins. It typically requires high-dose exposure, prolonged exposure, or both the trigger HP. Some cases of HP may be caused by exposure to inhaled chemicals such as isocyanates.
HP is rare and typically occurs in certain occupations like farming or raising pigeons. It is not a reportable disease, which makes it difficult to determine an accurate rate of prevalence. It is believed to be a delayed hypersensitivity. Allergen-specific precipitins are frequently present in serum and are important in establishing exposure. Precipitins might also play a role in the mechanism of the acute phase of the disease. HP results in acute episodes of noninfectious, immunologically mediated interstitial pneumonitis (ie, alveolitis), which may eventually produce restrictive irreversible lung disease.
A doctor will need a clinical and environmental history, physical exam, chest scans, pulmonary function testing, bronchoalveolar lavage, or open lung biopsy to make a diagnosis of HP. They may test for the presence of precipitins in the Ouchterlony double-diffusion assay.
Exposure to domestic specific indoor fungal spores is an extremely unlikely cause of HP, except in highly unusual circumstances, such as workplace exposure.HP is an uncommon disease that can occur as a result of mold exposure, particularly in occupational settings with high levels of exposure.
Infection
Superficial mold infections ( tinea cruris, onychomycosis, and thrush) are common in healthy individuals and result primarily from local changes in the cutaneous or mucosal barrier, resident microflora, or both.
These infections typically are not due to environmental exposure. In fact, molds of the Malassezia genus exist in most humans and only cause a visible infection during periods of overgrowth. Other molds may cause infection as well including coccidioidomycosis, histoplasmosis, and blastomycosis, which are aggressive pathogens in otherwise healthy persons. Exposure commonly occurs outdoors, and people with immunodeficiency disorders have a higher risk for infection. Typically, host factors, instead of environmental exposure, lead to mold infection.
Common superficial fungal infections are determined by local changes in the skin barrier, resident microflora, or both. A very limited number of aggressive fungal pathogens can be acquired through specific outdoor exposures. And, host factors are the key determinant of opportunistic fungal infection.
Toxic effects of mold exposure
Ingestion of mycotoxins in large doses from spoiled or contaminated foods can cause severe human illness. Toxicity from ingested mycotoxins is mostly a concern in animal husbandry, although human outbreaks do occur occasionally when starvation forces individuals to eat severely contaminated food.
Some mycotoxins, such as ochratoxins and aflatoxins, are commonly found in foodstuffs, including grain products and wines, and peanut products, respectively, such that there are governmental regulations as to the amounts of allowable aflatoxin in foods.
Acute high-intensity work-related exposure to mixed bioaerosols has led to “toxic dust syndrome.” The actual agent the causes this syndrome has not been clearly identified, and symptoms may last only a short time. This type of exposure is very rare outside of workplace settings.
Toxicity due to inhalation
The term mold toxicity refers to the direct injurious effects of mold-produced molecules, mycotoxins, on cellular function. Toxicity does not mean changes in innate immune responses or adaptive immune responses. Mycotoxins are low-molecular-weight chemicals produced by molds. Only certain mold species generate specific mycotoxins under specific circumstances. For a toxic effect to occur in a subject, (1) the toxin must be present, (2) there must be a route of exposure, and (3) the subject must receive a sufficient dose to have a toxic effect. I
In non-work-related settings, most exposure occurs through inhalation. Mycotoxins are not volatile and do not accumulate due to a half-life of hours or days. The level of exposure that leads to toxicity depends on the mycotoxin, although the levels are high enough that it would be unlikely that home or office exposure would result in toxicity.
We can conclude the following:
- The occurrence of mold-related toxicity from exposure to inhaled mycotoxins in non-work-related settings is not supported by the current data, and its occurrence is unlikely.
Irritant effects of mold exposure
OSHA defines an irritant as a material causing “a reversible inflammatory effect on living tissue by chemical action at the site of contact.” Irritant effects are dose-related, and the effects are transient, disappearing when the exposure has decreased or ceased.
Molds create quite a few potentially irritating substances that fall into one of two categories: volatile organic compounds (VOCs) and particulates (eg, spores, hyphae fragments, and their components). The threshold level of irritant response depends on the intrinsic properties of the specific material involved, the level plus length of exposure, and the innate sensitivity of the exposed tissues (eg, the skin versus nasal mucosa).
VOCs made by molds (MVOCs) are responsible for their musty odor. MVOCs include a wide range of alcohols, ketones, aldehydes, esters, carboxylic acids, lactones, terpenes, sulfur and nitrogen compounds, and aliphatic and aromatic hydrocarbons.
Although levels causing irritant effects have been established for many VOCs, MVOC levels measured in damp buildings are typically so low that exposure would not be expected to cause complaints of irritation in human subjects. Most indoor environments have multiple sources of VOCs, so measurement of indoor MVOCs is rare.
Mold particles are not volatile. Some researchers have suggested that these structural mold compounds cause inflammation by being deposited on mucus membranes of their attached glucans and mannans. However, whether such effects occur clinically still lacks conclusive scientific evidence. Thus mold particulates generally found indoors, even in damp buildings, are not likely to be irritating.
We can conclude the following:
- The occurrence of reactions from exposure to fungal irritants in non-work-related settings is theoretically possible, although unlikely to occur in the general population because the level of intensity and length of exposure is not probable.
- These irritant effects would produce transient symptoms-signs related to the mucus membranes of the eyes and upper and lower respiratory tracts but would not be expected to manifest in other organs or in a systemic fashion.
- Further information about thresholds for irritant reactions in at-risk populations is needed to better define the role of molds, mold products, and other potential irritants in such individuals.
Immune dysfunction
Currently, no conclusive evidence exists to show the mold or mycotoxin exposure can trigger immune system disorders. However, it is highly suspected and studies are linked. People who have experienced intense work-related mold exposure do not necessarily always develop opportunistic infections or other issues with immunodeficiency. Some mycotoxins are immunosuppressive and used for this purpose clinically (eg, cyclosporine).
Look for serum tests including C4a, MSH, leptin, ADH, TGF-beta.
We can conclude the following:
- Exposure to mold and its products MAY induce a state of immune dysregulation (eg, immunodeficiency or autoimmunity).
- The practice of performing large numbers of nonspecific immune-based tests as an indication of mold for mold-related illness is not always evidence-based but may be helpful.
Measurement of fungi in your environment
Measurement of fungi in your home involves culture methods, non-culture methods, or both. Air testing is the most relevant measure of exposure and is typically reported as colony-forming units or spores per cubic meter of air. However, this testing provides a snapshot that does not integrate exposure over time and provides data only about the location of sampling. Indoor testing must be compared with outdoor testing and preferably with more than one outdoor sample. Currently, there are no standards as to what constitutes acceptable levels of outdoor or indoor airborne fungal spores.
Even so, the levels of airborne fungal spores found in an indoor setting can be considered in relative and absolute terms. Indoor fungal spores come from outdoor sources present within soil and vegetation. Therefore an increase in indoor-outdoor concentrations of specific fungi indicates the presence of an indoor source.
Total fungi spores that are at a higher level of concentration indoors than outdoors may be evidence of an increased fungal presence indoors. However, in normal indoor environments xerophilic fungi, such as Aspergillus and Penicillium species, might be found indoors at levels above those measured outdoors on a given day. Even when the fungal levels are greater indoors than those outdoors.
Bulk, surface, and within-wall cavity measurements of fungi, although sometimes indicating the presence of fungi, do not provide a measure of exposure. Fungi found in these places require a route of exposure through the air that involves many factors not included in these measurements. This testing does not determine exposure.
Measurement of fungal products in your environment
Another approach to measuring potential fungal exposure is to test for fungal products in the environment.
Structural fungal materials:
Testing for the levels of general mold structural material (like β-glucans in settled dust) has been used to determine levels of potential exposure to molds over time. However, this method does not determine the level of exposure to a specific mold or whether the source is indoor or outdoor.
Mycotoxins:
Specific molds can produce mycotoxins or none at all. Determining the level of mold spores does not determine mycotoxin exposure. Some methods based on mass spectroscopy have been used to identify the presence of mycotoxins. However, the typical levels of mycotoxins are too low to measure using these methods. Thus exposure requires inhalation of mycotoxin-containing spores or fungal fragments in the respirable air. For example, satratoxin H can be found in a sample of the material with heavy Stachybotrys chartarum growth, but Stachybotrys species are not easily aerosolized.
We can conclude the following:
- A sampling of both indoor and outdoor air for mold spores provides a measure of potential exposures and can be useful in certain clinical conditions, but it has many shortcomings. Look for the EMMA test by Real Time Labs to test for endotoxins from gram negative bacteria as well as mycotoxins for mold. The ERMI test by Envirobiometics is also recommended.
- Bulk, surface, and within-wall cavity measurement or molds or mycotoxins, although having potential relevance for other purposes, cannot be used to assess exposure.
- Testing for airborne mycotoxins in nonagricultural environments cannot be used to diagnose mold exposure.