Respiratory and Allergic Health Effects of Dampness, Mold, and Dampness-related Agents

A Review of the Epidemiologic Evidence

Mark J. Mendell; Anna G. Mirer; Kerry Cheung; My Tong; Jeroen Douwes


Environ Health Perspect. 2011;119(6):748-756. 

In This Article


Epidemiologic evidence from primary studies and quantitative meta-analyses shows evident indoor dampness or mold to be associated consistently with a wide range of respiratory or allergic health effects, including asthma development and exacerbation, current and ever diagnosis of asthma, dyspnea, wheeze, cough, respiratory infections, bronchitis, allergic rhinitis, eczema, and upper respiratory tract symptoms. In addition to the consistently positive associations across many study designs, populations, ages, and health outcomes, dose–response relations with observed dampness and mold were often reported (e.g., Biagini et al. 2006; Cummings et al. 2008; Park et al. 2004; Pekkanen et al. 2007). Although available epidemiologic evidence does not yet establish that indoor dampness or mold causes human health effects, findings from one strong epidemiologic intervention study (Kercsmar et al. 2006), in conjunction with other available studies, strongly suggest causation of asthma exacerbation in children by dampness or mold. Several studies provide evidence for temporal association of dampness/mold and health effects by demonstrating increased incidence density of new asthma diagnosis among occupants of water-damaged buildings compared with periods before water damage (Cox-Ganser et al. 2005; Laney et al. 2009).

It is well accepted that hypersensitivity pneumonitis (HP), a granulomatous, cell-mediated lung inflammation, is caused by inhalation of antigens from microorganisms or other sources, although causal exposures often cannot be determined (Fink et al. 2005). Current knowledge is based on outbreak investigations and limited epidemiology, mostly in industrial and agricultural settings, but also in office buildings (Cox-Ganser et al. 2005; Kreiss 1989; Park et al. 2004) and, in both adults and children, in homes (Venkatesh and Wild 2005). One specific dampness-related mold exposure (Trichosporon cutaneum) is documented to cause HP in homes (Ando et al. 1995). [For more on HP, see Supplemental Material, Text A4.1 (doi:10.1289/ehp.1002410).]

Few studies included objective, replicable assessments of dampness. Both Karvonen et al. (2009) and Park et al. (2004), using scales combining area of water damage or area of water stains with subjective assessments, found exposure–response relations with multiple health outcomes. Williamson et al. (1997), using a scale based only on moisture meter readings from walls, also found positive adjusted associations, for example, ORs (95% CIs) for asthma and any dampness of 3.03 (1.65–5.57), exceeding ORs for subjective inspector-determined visible mold. Williamson et al. (1997) also found positive correlations between total moisture meter dampness score and both asthma severity (p = 0.0006) and predicted FEV1 (forced expiratory volume in 1 sec) (p = 0.006). One potential advantage of quantitative dampness measurements as indicators of exposure, relative to specific quantitative microbial measurements, is that they can be proxies for various dampness-related causal agents, whether microbial or chemical. Quantifying visible mold may also prove useful; however, Dales et al. (2010) found no significant relationship between measured area of visible mold and respiratory health outcomes.

Although evidence is limited that links any quantitative microbial measurements to specific health effects, in this review we have identified some preliminary associations (Table 4), all for measurements in dust: increased ergosterol with increased current asthma; increased endotoxin with increased wheeze; and for (1→3)-β-D-glucans, medium concentrations with increased wheeze but the highest concentrations with decreased wheeze. We consider these associations to be only suggestive, because of the limited number of studies, the limited factors considered in summarizing them, and the demonstrated complexity of some of these relationships, such as for endotoxin and (1→3)-β-D-glucans, each associated in multiple studies with both adverse and protective associations (Douwes et al. 2004, 2006).

Current findings thus cannot define causal microbiologic exposures or dose–response relations sufficiently to define safe levels of exposure to dampness-related agents. At present, subjectively assessed dampness or mold has the most consistently documented associations with respiratory and allergic disease. Quantifying dampness objectively has shown promise (Karvonen et al. 2009; Park et al. 2004; Williamson et al. 1997), but findings are few. For quantifying microbiologic factors, concentrations of culturable airborne organisms have fared poorly in empirical health research. Some assessments in dust, such as ergosterol as an indicator of total biomass of fungi, are more promising; others, such as endotoxin and glucans, have relationships with health too complex for simple interpretation. Polymerase chain reaction (PCR) assays for specific fungi in dust also have promise, but no studies using PCR met inclusion criteria for this review, and a standard scale now used to group PCR findings across fungi seems premature (e.g., Vesper et al. 2007). [For details, see Supplemental Material, Text A4.2 (doi:10.1289/ehp.1002410).]

Difficulties in finding clear relationships with measured microbiologic exposures may be attributable to measurement errors in exposure assessment, including measurement of noncausal factors; to effects that change with intensity and duration of exposure or age at exposure; or to interaction effects occurring with multiple exposures. Endotoxin, traditionally associated with non-dampness-related exposures such as farm animals and pets and with potential protection against atopy, has now been shown to be associated in water-damaged office buildings with observed dampness, fungal spores, and increased building-related asthmatic symptoms (Park et al. 2006; Rao et al. 2005). Adverse effects from endotoxin may be increased by other dampness-associated agents and vice versa (Park et al. 2006). In addition, moisture in buildings can increase nonbiologic emissions not measured in most dampness research, including formaldehyde [associated with increased asthma (McGwin et al. 2009; Mendell 2007)] from composite wood products (Matthews et al. 1986) and 2-ethyl-1-hexanol from moisture-related degradation of plasticizer in vinyl flooring (Norbäck et al. 2000).

Based on available evidence, dampness and mold may have enormous health and social costs worldwide. A northern European study found an 18% prevalence of indoor dampness (Gunnbjornsdottir et al. 2006). The IOM review (IOM 2004), using European and North American data, estimated that at least 20% of buildings had problems with dampness. Mudarri and Fisk (2007) estimated a 50% prevalence of dampness or fungi in U.S. houses. Fisk et al. (2007) concluded that "building dampness and mold are associated with approximately 30–50% increases in a variety of respiratory and asthma-related health outcomes." Mudarri and Fisk (2007) estimated that 21% of current U.S. asthma cases were potentially attributable to dampness and mold in housing, for an annual national cost of $3.5 billion. Fisk et al. (2010) estimated that residential dampness or mold is associated with 8–20% of U.S. respiratory infections.

With regard to practical implications of these findings, we did not evaluate health benefits of specific strategies for remediation of dampness or mold. However, a recent expert review has concluded that the intervention of "combined elimination of moisture intrusion and leaks and removal of moldy items" had sufficient evidence of effectiveness for reducing respiratory symptoms from asthma and allergies and was ready for widespread implementation (Krieger et al. 2010).


Much of the epidemiology on dampness, mold, and health has used subjective reports for assessing exposure or health and thus has potential for reporting bias. Two reviews have considered whether biased subjective response by building occupants in dampness studies might have positively biased findings. On the basis of comparison of results in six studies from occupant reports versus inspector-reported dampness and clinically determined illness, Fisk et al. (2007) concluded that observed associations of respiratory health effects with dampness-related exposures were unlikely to be explained by overreporting. Bornehag et al. (2001) reported that findings of studies with independent assessment of both dampness and health effects were similar to findings of studies with more subjective information sources. Additionally, avoidance behavior (prior exposure reductions by persons with asthma) may be a source of past exposure misclassification with assessment of only current or recent exposure. However, this is not a concern in prospective or intervention studies, which have generally confirmed dampness/health associations.

Quantitative measures of exposure used in the reviewed studies also have important limitations. Measured airborne concentrations of culturable microorganisms have substantial errors, for example, from short-term estimation of airborne concentrations with large and rapid variations over time; from differential abilities of organisms to grow on specific culture media; and from nondetection by culture assays of most bioactive microbial materials, whether intact spores or fragments. Most important, culture-based or non-culture-based microbial measurements used in many studies may not target actual causal factors. All these reasons may explain the lack of consistent associations between reported microbial measurements and health. And as with glucans or endotoxins, even prior demonstration in many studies that a substance causes inflammation does not implicate it as consistently harmful, because both glucans and endotoxins have also demonstrated health-protective associations (Douwes et al. 2006; Iossifova et al. 2007). However, subjectively assessed dampness or mold has not shown protective associations, even in infants.

Finally, definitions of respiratory health effects are not standardized, potentially causing bias. In population studies, asthma is usually defined by self-reported (or parentally reported) asthma symptoms. Self-reports of doctor-diagnosed asthma are also often used. An alternative approach to questionnaires has been to use more objective measures, either alone or in combination with questionnaires. As with measures of home dampness or fungal exposures, differences in asthma definition are likely to result in differences in estimates of RRs. In addition, as mentioned above, several studies (Nafstad et al. 1998; Oie et al. 1999) focused on infants at an age where the diagnosis of asthma is uncertain. Most of these potential sources of bias are expected to underestimate any true association between indoor dampness and health effects.

The restricted scope of this review led to further limitations. The method of evaluating published evidence was largely nonquantitative. Results of available quantitative meta-analyses, however, are consistent with qualitative summaries. Publication bias in this review is likely to have inflated associations of risk factors with health effects. A formal application of available statistical methods for assessing presence of this bias was not feasible for this broad review. A search for unpublished findings, which may decrease publication bias, was not performed. Conclusions drawn from this review should thus be considered provisional until the production of quantitative summary estimates of RRs based on more thorough consideration of all available findings, with formal evaluation for publication bias.

Evidence for Plausible Biologic Mechanisms of Health Effects from Dampness-related Agents

Toxicologic evidence suggests plausible biologic mechanisms for the respiratory health effects associated epidemiologically with dampness or mold (WHO Europe 2009). In vitro and in vivo studies have demonstrated diverse inflammatory, cytotoxic, and immunosuppressive responses after exposure to the spores, metabolites, and components of specific microbial species found in damp buildings. Repeated immune activation and prolonged inflammation by microbiologic exposures may contribute to inflammation-related diseases such as asthma. The immunosuppressive response demonstrated in animals exposed to fungal spores associated with damp buildings may explain a link to respiratory infections.

The wide variety of health effects associated with dampness and mold cannot be explained by a single mechanism. Epidemiologic evidence suggests involvement of both allergic and nonallergic mechanisms, as both atopic and nonatopic individuals are susceptible to adverse effects of dampness or mold (e.g., Cox-Ganser et al. 2005; Dales et al. 2006; Douwes et al. 2006; Kuyucu et al. 2006). The inflammatory responses demonstrated in many microbiologic exposures include histamine release by non-immunoglobulin E–mediated mechanisms, providing plausible mechanisms for the occurrence of allergy-like symptoms in nonsensitized individuals. Increased human susceptibility to severe asthma exacerbation from fungal exposures has been demonstrated with genetic polymorphisms related to chitinase, suggesting mechanisms involving fungal chitin (Wu et al. 2010).

Some available evidence is consistent with involvement of fungal toxins in some health effects associated with damp environments, although this has been debated extensively in the literature (Bennett and Klich 2003; Jarvis and Miller 2005). Recently, animal models with curdlan (a specific triple-helical form of fungal glucan) and several toxic fungal metabolites have demonstrated inflammatory, nonallergic respiratory health effects consistent with the epidemiology of dampness (Miller et al. 2010; Rand et al. 2010). Observed synergistic interactions in toxicologic studies among microbial agents present in damp buildings, including specific fungi, actinomycetes, and amoebae (Penttinen et al. 2006; Yli-Pirila et al. 2007) suggest that immunotoxic effects of fungal and bacterial strains typically found in damp buildings may be potentiated during joint exposures. Such potentiation could explain difficulties in identifying specific causal exposures for health effects in damp buildings.

Many limitations of culture-based microbial assessments for investigating causes of dampness-related health effects have long been evident. Additional support for the need to investigate non-culture-based microbial assessment methods has been provided by the demonstration (Gorny et al. 2002) that fungi and actinomycetes can emit large numbers of airborne particles smaller than spores and not detectable by culture but with demonstrated immunogenic properties. These findings provide additional plausibility for health effects associated with microbial growth but not measurable with culture assays.

The Hygiene Hypothesis

As summarized in this review, indoor dampness or mold is consistently associated with increased respiratory health risks, and microbial exposures have been suggested (but not proven) to play a causal role. On the other hand, an increasing number of studies suggest that early-life microbiologic exposures to endotoxin or specific fungal agents may protect against atopy and allergic disease. This potentially protective effect is consistent with the "hygiene hypothesis," which postulates that growing up in a more microbiologically hygienic environment may increase the risk of developing respiratory allergies (e.g., Douwes et al. 2004, 2006; Liu and Leung 2006).

However, the evidence for protective effects of microbial exposures has not been consistent, as increased health risks have been associated with some specific measured exposures (e.g., Bolte et al. 2003; Dharmage et al. 2001; Michel et al. 1996). Some of these inconsistencies, found for endotoxin, (1→3)-β-D-glucans, and fungi, may be related to timing or dose of exposure, as has been recently hypothesized (Douwes et al. 2007), but evidence is still weak. For instance, Iossifova et al. (2007, 2009), in prospective data, identified nonmonotonic relationships between (1→3)-β-D-glucans in dust and recurrent wheeze, wheeze with atopy, and an index for future asthma: Risks increased at increasing low concentrations, reached a maximum at 60 µg/g dust, and then decreased at increasing high concentrations. Similar patterns have also been observed with dust mite antigen (Tovey et al. 2008).

At present, modest exposure to some microbial exposures under certain circumstances appears to protect against allergies and allergic asthma but not wheeze; however, as indicated previously, the overall evidence is inconsistent. Damp or moldy buildings seem only to increase, not decrease, the development of respiratory disease, both in allergic and nonallergic subjects including infants.

Suggested Research

A focused research program in this area might include a) studies to identify and improve objective tools and metrics that, in assessing either dampness or specific related factors (microbiologic or nonbiologic), optimally predict disease; b) studies to characterize dose–response relations, to determine safe levels and identify age-or dose-related protective effects; and c) strong studies (intervention or prospective) designed in the aggregate to document causality between dampness or mold and key health effects such as asthma or respiratory infections. Genetic epidemiology may enhance abilities to detect causal exposures and identify mechanisms (Wu et al. 2010). Indoor occupational settings and schools, with multiple advantages for study efficiency and logistics, have been underutilized. Good examples to follow include the strong disease prediction by an objective and easily interpreted tool, the electronic resistance-type moisture meter (Williamson et al. 1997), and the well-designed and extremely effective remediation study by Kercsmar et al. (2006). Although future findings will improve health-protective policies, health-protective actions need not await further etiologic research.


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