Mold exposure and respiratory health in damp indoor environments
ABSTRACT Almost all modern buildings experience at least minor, and sometimes serious, water damage during their life span. Excess moisture in buildings becomes a critical factor for mold (fungal) proliferation in nutrient-rich environments. As a result, building occupants may be exposed to increased levels of microbial agents such as fungal spores, cell fragments, cell wall components, or toxins. Such exposures may result in various diseases and symptoms, both respiratory and non-respiratory. Respiratory health complaints are common in damp buildings and have been more thoroughly studied than non-respiratory complaints. Respiratory diseases and symptoms which may be produced by exposure to indoor fungi include asthma development, exacerbation of asthma, hypersensitivity pneumonitis, cough, wheeze, dyspnea (shortness of breath), nasal and throat symptoms, and respiratory infections. In addition to these illnesses, rhinosinusitis and sarcoidosis in water-damaged building occupants are also drawing more scientific attention. In this article, we explore the evidence for adverse effects of fungal exposure on respiratory health in damp indoor environments and potential disease mechanisms related to the exposure.
Full-textDOI: · Available from: Ju-Hyeong Park, Sep 28, 2015
- SourceAvailable from: Thomas Brüning
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- "Concentration of moulds, such as Aspergillus versicolor, Penicillium chrysogenum and Cladosporium sphaerospermum, and microbial components such as LPS and β-(1,3)-glucan were elevated in rooms with moisture damage [2,3]. The continued exposure to these bioaerosols may increase the risk of developing asthma, bronchitis, rhinosinusitis or hypersensitivity pneumonitis . "
ABSTRACT: In rooms with moisture damage, the indoor air can be enriched with microorganisms causing a variety of symptoms. Due to the highly diverse composition of bioaerosols and the multiple effects on humans, an assessment of the health risk is not sufficiently possible. The aim of this study was to characterize the features of innate immunity using blood from subjects exposed to moisture damage compared to control subjects living in houses without visible moisture damage. We investigated the expression of TLR-2, TLR-4 and dectin-1 on the surface of monocytes from both fresh blood and after in vitro stimulation with the model substances E. coli endotoxin, zymosan A, Pam3Cys and Aspergillus versicolor in 25 exposed subjects and 25 control subjects. In vitro stimulation of whole blood with the same components was performed for 20 h and the release of inflammatory mediators IL-8 and IL-1β were quantified. In addition to an enhanced number of blood leucocytes, the expression of the receptors TLR-2, TLR-4 and dectin-1 on blood monocytes was significantly enhanced in exposed subjects. In contrast, no different alteration in expression was detected between exposed and control group after in vitro stimulation with the model substances. The release of IL-8 and IL-1β after stimulation of whole blood with A. versicolor was increased in subjects exposed to moisture damage. Furthermore, in the exposed subjects the IL-1β release was significantly enhanced after in vitro stimulation with E. coli endotoxin (1000 pg/mL). In conclusion, features of the innate immune system (receptor expression and mediator release of monocytes) are altered in subjects exposed to moisture damage which may be a potential explanation for the increased incidence of respiratory health diseases observed in these populations.PLoS ONE 12/2013; 8(12):e82734. DOI:10.1371/journal.pone.0082734 · 3.23 Impact Factor
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ABSTRACT: A family of five and pet dog who rented a water-damaged home and developed multiple health problems. The home was analyzed for species of mold and bacteria. The diagnostics included MRI for chronic sinusitis with ENT and sinus surgery, and neurological testing for neurocognitive deficits. Bulk samples from the home, tissue from the sinuses, urine, nasal secretions, placenta, umbilical cord, and breast milk were tested for the presence of trichothecenes, aflatoxins, and Ochratoxin A. The family had the following diagnosed conditions: chronic sinusitis, neurological deficits, coughing with wheeze, nose bleeds, and fatigue among other symptoms. An infant was born with a total body flare, developed multiple Cafe-au-Lait pigmented skin spots and diagnoses with NF1 at age 2. The mycotoxins were detected in bulk samples, urine and nasal secretions, breast milk, placenta, and umbilical cord. Pseudomonas aueroginosa, Acinetobacter, Penicillium, and Aspergillus fumigatus were cultured from nasal secretions (father and daughter). RT-PCR revealed A. fumigatus DNA in sinus tissues of the daughter. The dog had 72 skin lesions (sebaceous glands and lipomas) from which trichothecenes and ochratoxin A. were detected. The health of the family is discussed in relation to the most recent published literature regarding microbial contamination and toxic by-products present in water-damaged buildings.Journal of Environmental and Public Health 01/2012; 2012(7):312836. DOI:10.1155/2012/312836
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ABSTRACT: Both genetic and environmental factors are thought to play a role in the etiology of sarcoidosis. An association of the condition with exposure to environmental microbes has been recognized for many years, and has become stronger in the last 10-15 years with the advent of newer investigative techniques. A body of literature now is accumulating suggesting that silica may be yet another trigger in genetically predisposed persons. Impressive support for an etiologic role of mycobacteria derives from earlier studies by several investigators in Japan and in Europe and more recently from the US in Baltimore and Nashville. Other investigators have produced evidence that propionibacteria and fungi can also act as environmental triggers in sarcoidosis patients. We propose that, in an animal model that has been previously sensitized to microbial antigens, the introduction of silica through the gastrointestinal route, or intravenously, may have a granuloma-worsening effect, if the strain of animals is already predisposed to develop granulomatous disease. Here the silica may add a "second hit" to the "first hit" given by the exposure to microbial antigens.Medical Hypotheses 01/2012; 78(1):36-8. DOI:10.1016/j.mehy.2011.09.036 · 1.07 Impact Factor