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Cooling towers (CTs) are used to dissipate excess heat from water by evaporation, common in large facilities as hospital, companies, and hotels. The main risk attributed to CTs is represented by Legionella, a Gram-negative bacterium associated with a severe form of pneumonia known as Legionnaires' disease (LD). The infection route is by inhalation of aerosols reaching the lower respiratory tract. Despite several events associated with CTs, the knowledge in this field is still limited. The aim of this study was to develop a predictive model of bioaerosol dispersion using PM10 particles as a proxy, to generate risk maps of Legionella spread in the surrounding area in several weather and microbiological conditions. The Legionella contamination in the CT basin was 40938 ± 24523 cfu/L, with four peaks independent of the season, associated with an increase in air minimum temperature values (+1–2 °C) and a high relative humidity (66–100%) preceded by rainfall (0.2–30.6 mm/day). The model revealed that the most extensive bioaerosol spread is predicted in winter and summer, with an increase in Legionella risk at a distance of up to 1.5 km from the CT. This method represents a novel integrated approach for the prevention and management of LD risk in CTs.

Genome-wide association studies have revealed several genes predisposing to autoimmunity, however, concordance rates in monozygotic twins are significantly below 50% for several autoimmune diseases. The limited presence of a strong genetic association only in some patients supports that other non-genetic mechanisms are active in these pathologies. Epigenetic modifications such as DNA methylation, histone modification, and microRNA signaling regulate gene expression and are sensitive to external stimuli and they might be as bridging between genetic and environmental factors. Some evidence has highlighted the involvement of epigenetic alterations in the pathogenesis of various autoimmune diseases giving rise to great expectations among clinicians and researchers. The direct role of these alterations in the initiation/progression of autoimmune diseases is still unclear. The knowledge in depth of these pathogenic and epigenetic mechanisms will increase the possibility of the control and/or prevention of autoimmune diseases through the use of drugs that target epigenetic pathways. Moreover, we could use epigenetic-related biomarkers to follow this complicated framework (for example H3K4me3 and miRNA-155 are among those proposed biomarkers). This article reviews current understanding of the epigenetic involvement in the field of autoimmune diseases especially in systemic lupus erythematosus, rheumatoid arthritis, sclerosis multiple and type 1 diabetes.