Abstract

Water damage in buildings is a universe problem. Long-lasting or cumulative stay in water damaged buildings is a serious health hazard. Exposure to fungal and bacterial toxins, nanoparticles from dampness microbiota as well as decay products from construction materials together with biocides used for cleaning will first cause irritation of the mucosa and later chronic inflammation with stimulation or inhibition of the compartments of the innate and/or adaptive immunity. Mold-related disease has been called Dampness and Mold Hypersensitive Syndrome (DMHS) because hypersensitivity is the cornerstone feature of the disease. The background of hypersensitivity is both immunologic processes and hyperactivation of sensory receptors, neurogenic inflammation and central sensitisation. Immunologic hypersensitivity can occur either through the production of mold specific IgE-class antibodies, which is rare, or through sensitisation and proliferation of T and B specific lymphocyte clones. Immunological switch to Th2/Th17 arm of adaptive immunity often occurs. DMHS is a systemic and multi-organ disease where involvement of mucosa of pulmonary or gastrointestinal tract is central to the pathology. Symptoms include recurrent infections, chronic rhinosinusitis, swelling of the sinuses, irritation of the eyes and skin, voice problems, chronic non-productive cough, neurological symptoms, joint and muscle symptoms, irritable bowel syndrome and cognitive problems. Underdiagnosed or neglected continuous insidious inflammation may lead to Myalgic Encephalitis/Chronic Fatigue Syndrome (ME/CFS) especially when trigged by new infections or even vaccination. Multiple Chemical Sensitivity (MCS) may also develop, however in the later stages of the disease. Chronic cough is sometimes diagnosed as asthma if the criteria for asthma are met. Non-productive cough may also manifest allergic alveolitis, which is often overlooked. Avoidance of new exposure to dampness microbiota is crucial for recovery. We review the underlying toxicological and immunological mechanisms that are central in the pathology of DMHS.

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