In indoor environments, mold originates from two sources: mold infiltrating from outdoors (e.g., through open windows), and mold colonization on the interior of the home. Molds can obtain nutrients and moisture sufficient for growth from water-affected building materials such as wallboard and insulation materials, as well as carpets, furniture, and clothing. Using a score system based on material bioavailability, Gravesen evaluated the susceptibility of various building materials to mold attack. They found that the products most vulnerable to mold attack were water damaged, aged organic materials containing cellulose, such as wooden materials, jute, wallpaper, and cardboard.
Different fungal species vary with regard to environmental conditions required for optimal growth, but all are influenced by moisture, temperature, light, and the substrate nutrient concentration and type. One of the most important factors affecting mold growth in homes, however, is moisture level. In general, most molds require fairly wet conditions (near saturation), lasting for many days, to extensively colonize an environment. However, the U.S. Environmental Protection Agency (USEPA) and the Centers for Disease Control and Prevention (CDC) recommend that it should be assumed that buildings or materials soaked for more than 48 hours are contaminated with mold unless proven otherwise by adequate environmental sampling or cleaned according to EPA recommendations. In addition to affecting the extent of mold colonization, moisture availability can also affect the types of fungi present. For example, certain Penicillium species grow in relatively dry environments (e.g., in house dust with a high relative humidity), while others, such as Basidiomycetes and Stachybotrys species, require continuously wet substrates such as soaked wallboard, water reservoirs for humidifiers, or drip pans. Relative humidity also affects spore release for some molds (e.g., Aspergillus and Penicillium), with spore release occurring with lowering humidity after initial growth at high humidity levels. One reviewer concluded that “the worst-case scenario for the development of an indoor mold problem involves a series of water intrusion events that allow large quantities of biomass and mycotoxins to form, then a period of drying that promotes the dispersion of spores and colony fragments, followed by their deposition throughout the building”.
As moisture availability changes, it has been observed that the species composition (i.e., the rank order of dominant species) will also often change. Some of the most abundant fungi genera found in homes without severe water damage include: Alternaria, Cladosporium, Penicillium, yeasts, and Aspergillus . Most of these molds do not typically produce mycotoxins, but may be important as sources of mold allergens. In contrast, under certain very damp conditions (i.e., in the presence of water-soaked cellulosic materials), toxin producing Stachybotrys chartarum may be prominent. In general, whether or not a potentially toxigenic fungus produces toxins is dependent on environmental conditions and nutrient source.
Housing features that can increase moisture levels and growth of mold include poor ventilation, excess production or condensation of water in the house. Basements are likely to have higher mold concentrations than other indoor areas, especially in the winter. In fifteen homes investigated in Ontario, overall fungal levels (as assessed by counting spores in environmental samples) were highest in living rooms, followed by family rooms, kitchens, bathrooms, and bedrooms. It was observed that fungal levels increased with the presence of damp conditions and carpets, and decreased where forced-air heating systems, dehumidifiers, air filters, and air conditioners were present. It has also been found that fungal levels, as assessed by measurement of extracellular polysaccharide (EPS) fungal cell wall components from Aspergillus and Penicillium species (EPS-Asp/Pen), were highest in living room floor dust. In addition, EPS-Asp/Pen levels were 2 to 3 times higher on carpeted floors than on smooth floors, and this was confirmed by another study that adjusted for repeated measures. However, fungal spores in indoor air could not be consistently predicted by housing characteristics. In one study leakage, or water damage, as reported by household questionnaires, were not significantly related to the presence of culturable fungi measured in indoor air. Of note, geographic differences in home furnishings and climate should be considered when evaluating home characteristics and concentrations of fungi in air or dust samples.
Several studies have characterized mold in homes without significant moisture problems or visual mold growth. One such HUD-funded study that was conducted in 50 post-1945 detached single family homes in metropolitan Atlanta, Georgia. Indoor and outdoor air and interior settled dust samples were collected in summer and winter and culturable fungi were counted and identified. Although higher airborne mold concentrations were found in the indoor and outdoor samples collected in the summer, the indoor samples collected did not differ by rankings of mold type prevalence or abundance with outdoor samples. Water indicator fungi (Chaetomium, Ulocladium, and Stachybotrys) were identified in only 3% of the settled dust samples plated out on two different types of media. The researchers also reported that “leaf surface fungi” (e.g., Cladosporium, Alternaria, Epicoccum, and Curvularia) represented > 20% of the total colonies in at least 85% of the settled dust samples (thus, replicate dust samples with < 20% of colonies from leaf surface fungi may be indicative of a mold/moisture problem).
The Institute of Medicine of the U.S. National Academy of Sciences recently published a comprehensive review of the scientific literature regarding the relationship between damp or moldy indoor environments and the manifestation of adverse health effects, particularly respiratory and allergic symptoms. Table 1 summarizes the Institute’s findings regarding the strength of the association between health outcomes and (a) exposure to damp indoor environments or (b) the presence of mold or other agents in damp indoor environments. (It was necessary to present findings regarding associations with the presence of mold or other agents separately from those regarding exposure to damp indoor environments in general, because much of the reviewed literature did not collect objective measurements of biogenic agents in damp indoor environments.)
The Institute did not find sufficient evidence of a causal relationship with any health outcomes. However, the Institute found sufficient evidence of an association between both categories of exposure and symptoms of the upper respiratory tract (nasal and throat), asthma symptoms in sensitized asthmatic persons, wheeze, and cough. They also found sufficient evidence of an association between mold or bacteria in damp indoor environments and hypersensitivity pneumonitis in susceptible persons (i.e., persons with a family history sensitivity). In addition, the Institute found limited or suggestive evidence of an association between both categories of exposure and lower respiratory illness in otherwise healthy children. They also found suggestive evidence of an association between exposure to damp indoor environments (but not the presence of mold) and dyspnea (shortness of breath) and asthma development. Finally, the Institute concluded that evidence was inadequate or insufficient to determine an association with many other health effects, including but not limited to airflow obstruction (in otherwise healthy persons), mucous membrane irritation syndrome, and chronic obstructive pulmonary disease. “Inadequate or insufficient evidence” does not rule out the possibility of an association; it generally means that published studies did not have the quality, consistency or statistical power to permit a conclusion about an association. The Institute of Medicine also stated that “these conclusions are not applicable to immunocompromised persons, who are at increased risk for fungal colonization or opportunistic infections.”
Mold exposure in homes occurs primarily via inhalation of airborne spores and fungal fragments; some airborne fragments have very small particle size and may be far more numerous than airborne spores. Molds are also present in household dust and on surfaces, with exposure occurring when particles are disturbed and become airborne or, less commonly in residential situations, through dermal contact or ingestion. Release of mold spores or fragments into indoor air from mold colonies is usually dependent on some sort of mechanical disturbance, although for some types of molds slight air movement may be sufficient (e.g., air movement by a fan), or spores may become airborne through natural spore discharge mechanisms. Most molds release spores ranging in size from 2 to 10 micrometers (although some genera, such as Alternaria, have conidia (a type of spore) ranging from 20-60 micrometers), but some may be released as chains or clumps of spores.
Allergens. Many molds produce numerous protein or glycoprotein allergens capable of causing allergic reactions in people. These allergens have been measured in spores, as well as other fungal fragments; however, most allergen seems to be located in germinating spores, in the hyphal tips, and in mycelia. Some of the major fungal allergens identified and isolated to date include those from Aspergillus fumigatus, Aspergillus oryzae, Alternaria alternata, Cladosporium herbarum, Penicillium citrinum, Penicillium chrysogenum, Trichophyton tonsurans, Malassezia furfur, and Psilocybe cubensis . An estimated 6-10% of the general population and 15-50% of those who are genetically susceptible (atopic) are sensitized to mold allergens. Research clearly indicates that exposure to mold plays a role in the exacerbation of asthma symptoms in sensitized individuals, although the association between mold exposure and asthma development remains undetermined. The clearest association between mold exposure and asthma is for sensitization to Alternaria , although this may be because the allergens of this genus (Alt a 1 and Alt a 2) are well characterized relative to other mold species.
Summary of Institute of Medicine Findings Regarding the Association Between Health Outcomes and Exposure to Damp Indoor Environments or the Presence of Mold or Other Agents in Damp Indoor Environments
Sufficient Evidence of a Causal Relationship
(no outcomes met this definition)
Sufficient Evidence of an Association
Upper respiratory (nasal and throat) tract symptoms Wheeze Asthma symptoms in sensitized asthmatic persons Cough Hypersensitivity pneumonitis in susceptible persons
Limited or Suggestive Evidence of an Association
Lower respiratory illness in otherwise-healthy children Asthma development Dyspnea (shortness of breath)
Inadequate or Insufficient Evidence to Determine Whether an Association Exists
Airflow obstruction (in otherwise-healthy persons) Skin symptoms Mucous membrane irritation syndrome Gastrointestinal tract problems Chronic obstructive pulmonary disease Fatigue Inhalation fevers (non-occupational exposures) Neuropsychiatric symptoms Lower respiratory illness in otherwise-healthy adults Cancer Rheumatologic and other immune diseases Reproductive effects Acute idiopathic pulmonary hemorrhage in infants
Results of skin-prick testing of 1,286 children with asthma in the National Cooperative Inner City Asthma Study’s (NCICAS) showed that the most common positive allergen sensitivity in these children was to Alternaria (38%), followed by cockroach (36%) and the Dermatophagoides pteronyssinus house dust mite (31%).
While detecting allergic sensitization to molds is difficult in infants, some data suggest that infants at risk for developing allergic disease experience respiratory symptoms which may or may not be allergic in nature. In a study, a positive exposure-response was found between levels of mold (measured by a portable air sampler) in the home and wheeze/persistent cough in the first year of life among children whose mothers had asthma, and between mold levels and persistent cough among children of mothers without asthma. Gent assessed the potential for increased incidence of respiratory symptoms after household exposure to particular fungal genera, namely Cladosporium (in 62% of homes) and Penicillium (in 41% of homes) in a population of infants 1-12 months of age at high risk for developing asthma. To the extent that the measured mold sampled represented longer-term exposure concentrations, the study results suggested that the infants studied who were exposed to high levels of Penicillium had higher rates of wheeze and persistent cough. The authors also suggested that because there are considerable seasonal variations in some molds, including Cladosporium, intermittent exposures may contribute only sporadically to respiratory symptoms. Other molds, such as Penicillium, seem to be present at more consistent levels year round. Previous studies note that relationships between exposure to mold and respiratory symptoms of children are complicated and may depend on a variety of potentially confounding factors, such as the season in which mold samples were collected and the presence of other moisture dependant biological hazards such as endotoxins.
Toxics and Irritants. Many molds are also known to produce mycotoxins, which are toxic metabolites that can be a health hazard to birds and mammals upon natural exposure, i.e., ingestion, dermal contact, or inhalation. While common outdoor molds present in ambient air, such as Cladosporium cladosporioides and Alternaria alternata, do not usually produce toxins, many other different mold species do. Genera producing fungi associated with wet buildings, such as Aspergillus versicolor, Fusarium verticillioides, Penicillium aurantiogriseum, and Stachybotrys chartarum, can produce potent toxins, measurable in mold mycelia, spores, and the matrix in which the mold is growing. A single mold species may produce several different toxins, and a given mycotoxin may be produced by more than one species of fungi. Furthermore, toxin-producing fungi do not necessarily produce mycotoxins under all growth conditions, with production being dependent on the substrate it is metabolizing, temperature, water content and humidity. Some toxin-producing molds have a higher water requirement than common household molds and tend to thrive only under conditions of chronic and severe water damage. For example, Stachybotrys typically only grows under continuously wet conditions. However, recent literature indicates that temperature is a stronger rate limiting factor in mycotoxin production than water. An overview of some common molds, mycotoxins, and associated health effects is presented in the American Conference of Government of Industrial Hygienists’ publication Bioaerosols: Assessment and Control and the American Industrial Hygiene Association’s Field Guide for the Determination of Biological Contaminants in Environmental Samples .
Although epidemiological studies that specifically examine exposure to mycotoxins in indoor residential environments are relatively limited, there is substantial evidence of a relationship between mycotoxin exposure (via ingestion and inhalation) and adverse health effects in occupational (agricultural and food processing) settings and animal studies. The most frequently studied mycotoxins are produced by species of Aspergillus (e.g., aflatoxins), Fusarium, Penicillium, Stachybotrys, and Myrothecium (e.g., satratoxins, trichothecenes). Known health effects depend on the kind of mycotoxin and the nature of the exposure, but include mucous membrane irritation, skin rashes, dizziness, nausea, and immunosuppression. Although evidence is very limited in residential environments, aflatoxins (produced by Aspergillus flavus and parasiticus) have also been linked to liver cancer in food processing settings. Toxins from Stachybotrys chartarum have been most commonly associated with lung inflammation and hemorrhage in animal studies and non-specific symptoms (headaches, sore throats, flu symptoms, diarrhea, fatigue, and dermatitis) in case studies.
In indoor environments, associations have also been reported for pulmonary hemorrhage deaths in infants and the presence of Stachybotrys atra . Although this specific association has not been conclusive, some research supports the potential for general mycotoxin exposure in the indoor environment to result in adverse effects on respiratory health. It has also been suggested that very young children may be especially vulnerable to certain mycotoxins. For example, it has been suggested that exposure to the trichothecene mycotoxins, which are known to be potent protein synthesis inhibitors, may result in pulmonary capillary fragility in the rapidly growing lungs of infants.
The American College of Occupational and Environmental Medicine concluded that “delivery by the inhalation route of a toxic dose of mycotoxins in the indoor environment is highly unlikely at best, even for the hypothetically most vulnerable subpopulations”. Other reviewers of the literature have come to the same general conclusion.
Other compounds produced by fungi, including (1→3) ß-D-glucans and volatile organic compounds (often referred to as microbial volatile organic compounds or MVOCs), are also suspected to play a role in certain adverse reactions described as “sick building” or “building related symptoms”. Glucans are a major component of the cell walls of most molds, and have been observed to have irritant effects similar to (but less potent than) those of bacterial endotoxins. MVOCs, which are produced by molds as byproducts of growth or degradation of substrates and often have strong or unpleasant odors, may also be responsible for some non-specific building related symptoms such as headaches, nasal irritation, dizziness, fatigue, and nausea. Research on the role of MVOCs in specific disease is still in the early phase. MVOCs should not be used as predictors for mold damage in indoor environments, because the concentrations produced are generally too low to be detected in indoor air.