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Epidemiological studies highlighted the possibility that exposure to cyanotoxins leads to the development of the neurodegenerative disease amyotrophic lateral sclerosis (ALS).We devised a population-based case-control study in two Italian populations. We used residential proximity of the residence to water bodies as a measure of possible exposure to cyanotoxins.Based on 703 newly-diagnosed ALS cases and 2737 controls, we calculated an ALS odds ratio (OR) of 1.41 (95% CI: 0.72-2.74) for current residence in the vicinity of water bodies, and a slightly lower estimate for historical residence (OR: 1.31; 95% CI: 0.57-2.99). Subjects65 years and people living in the Northern Italy province of Modena had higher ORs, especially when historical residence was considered.Overall, despite some risk of bias due to exposure misclassification and unmeasured confounding, our results appear to support the hypothesis that cyanotoxin exposure may increase ALS risk.

The aetiology of amyotrophic lateral sclerosis (ALS), a rare and extremely severe neurodegenerative disease, has been associated with magnetic fields exposure. However, evidence for such a relation in the general population is weak, although the previous null results might also be due to exposure misclassification, or a relationship might exist only for selected subgroups. To test such a hypothesis we carried out a population-based case-control study in two Northern and Southern Italy regions, including 703 ALS cases newly diagnosed from 1998 to 2011 and 2737 controls randomly selected from the residents in the study provinces. Overall, we found that a residence near high-voltage power lines, within the corridors yielding a magnetic fields of ≥0.1 μT, was not associated with an excess disease risk, nor did we identify a dose-response relationship after splitting the exposed corridor according to the 0.1, 0.2 and 0.4 μT cut-points of exposure. These results were confirmed taking into account age at onset, period of diagnosis, sex, geographical area, and length of exposure. Overall, despite the residual possibility of unmeasured confounding or small susceptible subgroups not identified in our study, these results appear to confirm that the exposure to magnetic fields from power lines occurring in the general population is not associated with increased ALS risk.

Background Bronchial thermoplasty (BT) is a non-pharmacological intervention for severe asthma whose mechanism of action is not completely explained by a reduction of airway smooth muscle (ASM). In this study we analyzed the effect of BT on nerve fibers and inflammatory components in the bronchial mucosa at 1 year. Methods Endobronchial biopsies were obtained from 12 subjects (mean age 47 ± 11.3 years, 50% male) with severe asthma. Biopsies were performed at baseline (T0) and after 1 (T1), 2 (T2) and 12 (T12) months post-BT, and studied with immunocytochemistry and microscopy methods. Clinical data including Asthma Quality of Life Questionnaire (AQLQ) and Asthma Control Questionnaire (ACQ) scores, exacerbations, hospitalizations, oral corticosteroids use were also collected at the same time points. Results A statistically significant reduction at T1, T2 and T12 of nerve fibers was observed in the submucosa and in ASM compared to T0. Among inflammatory cells, only CD68 showed significant changes at all time points. Improvement of all clinical outcomes was documented and persisted at the end of follow up. Conclusions A reduction of nerve fibers in epithelium and in ASM occurs earlier and persists at one year after BT. We propose that nerve ablation may contribute to mediate the beneficial effects of BT in severe asthma. Trial registration Registered on April 2, 2013 at ClinicalTrials.gov Identifier: NCT01839591.

Bronchial thermoplasty (BT) is a novel intervention for asthma but the mechanism of action is not yet well understood. The aim of our study is to analyze the impact of BT on the inflammatory state and the nerve C-fibers in the bronchial mucosa. We obtained bronchial biopsies from 12 subjects (age mean 47 year; 6Male and 6 Female) with severe refractory asthma recruited from the Pneumology A.S.M Hospital-IRCCS Reggio Emilia Italyfrom march 2013 to july 2014. The severity of asthma was classified according to the GINA criteria. Biopsies were performed before (T0) ,after 1 (T1) and 2 (T2) months following the BT treatment. A significant reduction at T1 and T2 times of total scored nerve C-fibers was observed in the submucosa (Wilcoxon test p=0.007 and p=0.003, respectively) and in the smooth muscle (p=0.005 and p=0.003, respectively) compared to T0. Nerve C-fibers in the epithelium and bronchial glands was only occasionally observed. Total inflammatory cells CD45+, CD8+ cells and eosinophils were not changed in T1 and T2 compared to T0. The CD4+ cells and macrophages CD68+ was significantly higher in T1 (p=0.018 and p=0.041, respectively) and T2 (p=0.020 and p=0.041, respectively)compared to T0. A transitory increase of neutrophils was observed at T1 (p=0.049) returning at basic values at T2 (p=0.507) compared to T0. In the two months after treatment, the BT causes a significant reduction of nerve C-Fibers, a transitory increase of neutrophils and a more persistent increase of mononuclear cell infiltration of the bronchial mucosa.