Transcriptomic Profiling of Adult-Onset Asthma Related to Damp and Moldy Buildings and Idiopathic Environmental Intolerance

A subset of adult-onset asthma patients attribute their symptoms to damp and moldy buildings. Symptoms of idiopathic environmental intolerance (IEI) may resemble asthma and these two entities overlap. We aimed to evaluate if a distinct clinical subtype of asthma related to damp and moldy buildings can be identified, to unravel its corresponding pathomechanistic gene signatures, and to investigate potential molecular similarities with IEI. Fifty female adult-onset asthma patients were categorized based on exposure to building dampness and molds during disease initiation. IEI patients (n = 17) and healthy subjects (n = 21) were also included yielding 88 study subjects. IEI was scored with the Quick Environmental Exposure and Sensitivity Inventory (QEESI) questionnaire. Inflammation was evaluated by blood cell type profiling and cytokine measurements. Disease mechanisms were investigated via gene set variation analysis of RNA from nasal biopsies and peripheral blood mononuclear cells. Nasal biopsy gene expression and plasma cytokine profiles suggested airway and systemic inflammation in asthma without exposure to dampness (AND). Similar evidence of inflammation was absent in patients with dampness-and-mold-related asthma (AAD). Gene expression signatures revealed a greater degree of similarity between IEI and dampness-related asthma than between IEI patients and asthma not associated to dampness and mold. Blood cell transcriptome of IEI subjects showed strong suppression of immune cell activation, migration, and movement. QEESI scores correlated to blood cell gene expression of all study subjects. Transcriptomic analysis revealed clear pathomechanisms for AND but not AAD patients. Furthermore, we found a distinct molecular pathological profile in nasal and blood immune cells of IEI subjects, including several differentially expressed genes that were also identified in AAD samples, suggesting IEI-type mechanisms.

Effect of Wi-Fi radiation on Salivary Cortisol levels

Introduction and Aim: Sensitivity to electromagnetic radiation is the emerging health problem of the 21st century. The sensitivity to electromagnetic radiations has become the major issue to be highlighted as environmental intolerance to Wi-Fi. These Wi-Fi radiations are a form of stress and thereby tend to increase salivary cortisol levels. Hence this study was done to analyse the effect of Wi-Fi radiations on salivary cortisol levels. The aim of the present study is to study the effect of Wi-Fi radiation from mobile phone towers on salivary cortisol levels. Materials and Methods: This study incorporated analysis of salivary cortisol levels in 72 healthy volunteers who were divided into two groups, subjects residing within 100 mts of the location of mobile phone towers and subjects who were residing outside 100 mts of the location of mobile phone towers and both groups were age & sex matched. The data was statistically analysed using the ANOVA with the SPSS software15.0 version. Results: The study showed that the salivary cortisol level increased in those subjects staying within 100 meters of the location of mobile phone towers compared to the subjects residing outside 100 mts of the location of mobile phone towers. Conclusion: From this study, it is concluded that Wi-Fi radiation causes invisible damaging effects by increasing the levels of salivary cortisol and vigorous measures to be taken to safeguard ourselves from these radiations.

Idiopathic Environmental Intolerance: A treatment model

Idiopathic environmental intolerance (IEI) refers to a health condition characterized by the presence of multiple symptoms in different organ systems in response to a variety of environmental cues, such as chemical exposures, electromagnetic radiation, infrasound from windmill farms, (parts of) buildings, foods etc. Typically, the symptoms arise in response to triggers and at dosages that do not cause symptoms in the majority of people, and no clear link with any physiological dysfunction can be found. The condition varies in a dimensional way from very mild, for which no medical help is sought, to very disabling compromising normal life. The condition is controversial, but several indications strongly suggest that the symptoms result from nocebo mechanisms. Currently, different psychological treatments are explored, but they are generally not based on a clear understanding of the aetiopathological mechanisms and the treatment effects are not well documented. In the present paper, we describe a treatment protocol based on a comprehensive explanatory model of IEI. The goal is to contribute to standardized, mechanism-based treatments as a basis for more systematic treatment studies.