Environmental concentrations of fibers with fluoro-edenitic composition and population exposure in Biancavilla (Sicily, Italy).

INTRODUCTION: The town of Biancavilla (Sicily) was included in the National Priorities List of Contaminated Sites due to environmental dispersion of amphibole fibers owing to the extraction of materials from a local quarry. The present report summarizes results from several, hitherto unpublished, environmental surveys carried out in the area, as well as from published analyses of the chemistry and composition of fibers. METHODS: Data included here comprises environmental fiber concentrations by scanning electron microscopy with energy dispersive spectroscopy (SEM-EDS) analysis in soil, indoor and outdoor air, personal monitoring, as well as a chemical characterization of the fibers. The full chemical structure and spectroscopic characterization of fibers were obtained through a multi-analytical approach: SEM-EDS, X-ray powder diffraction (XRPD), as well as Mössbauer (MS) and Fourier transform infrared (FT-IR) spectroscopies. RESULTS: Data analyzed provided a spatial and temporal picture of fiber concentrations in Biancavilla, and a qualitative assessment of population exposure. Results suggest that until 2000, the population had been exposed to high levels of amphibole fibers. Mitigation measures adopted since 2001, gradually reduced exposure levels to about 0.1-0.4 ff/l. Previous studies on fibrous amphiboles from Biancavilla reported considerable chemical variability. Differences in composition, especially concerning the presence of Si, Ca, Fe, and Na, were found both within and between samples. Compared to the previously investigated prismatic fluoro-edenite, these fibrous fluorine amphiboles consistently showed higher average values of Si and Fe content, whereas Ca was significantly lower, which we consider a distinctive characteristic of the fluorine fibrous variety. CONCLUSIONS: The population of Biancavilla had been highly exposed to a suite of fibrous amphiboles for over 50 years. Dust mitigation measures have gradually reduced exposure, but continuous environmental follow-up is necessary in order to monitor exposure levels and prevent adverse health effects for future generations.

Weight loss is associated with improved endothelial dysfunction via NOX2-generated oxidative stress down-regulation in patients with the metabolic syndrome.

The aim of this study was to assess whether adherence to a restricted-calorie, Mediterranean-type diet improves endothelial dysfunction and markers of oxidative stress in patients with metabolic syndrome. A moderately low-calorie (600 calories/day negative energy balance), low-fat, high-carbohydrate diet (<30% energy from fat, <10% from saturated fat and 55% from carbohydrate) was prescribed to 53 outpatients with the metabolic syndrome. Participants were divided into two groups according to body weight loss > or < 5% after 6 months. Group A (n = 23) showed a remarkable decrease in body weight (-6.8%), body-mass-index (-4.6%), waist circumference (-4.8%), HOMA-IR (-27.2%), plasma glucose, glycosylated haemoglobin, total and LDL-cholesterol, blood pressure, serum NOX2 (the catalytic core of NADPH oxidase) (-22.2%) and urinary8-isoprostanes (-39.0%) and an increase of serum NOx (Nitrite/Nitrate) (+116.8%) and adiponectine (+125.5%) as compared with those in group B (n = 30). A statistically significant increase in brachial artery flow-mediated dilatation was observed in group A (+24.7%; p < 0.001), while no changes were present in group B. Variations of flow-mediated dilatation were statistically and negatively correlated with changes of serum NOX2 levels (p = 0.04), body-mass-index (p < 0.01), waist circumference (0.01), glycosylated haemoglobin (p < 0.01), LDL-cholesterol (p < 0.01) and triglycerides (p < 0.05) and positively correlated with changes of serum NOx (p < 0.001) and adiponectin (p = 0.01). The results show that moderate weight loss is able to improve endothelial dysfunction in patients with the metabolic syndrome. The coexistent decrease of NOX2 activation suggests a role for oxidative stress in eliciting artery dysfunction.