Search for: [Abstract = "Particulate matter with an aerodynamic diameter of less than 2.5 µm, i.e. PM2.5, are considered to be the most toxic components of air pollution. They contain a fraction of nanoparticles \(NPs\), i.e. particles with a diameter less than 0.1 µm, which can enter the circulation through bronchial epithelium and alveoli. Epidemiological and experimental studies strongly indicate that PM2.5 have harmful effects on human health and are associated with an increased prevalence of respiratory and cardiovascular diseases. Nevertheless, the exact mechanisms of PM2.5 biological actions are still unclear.The aim of the study was to assess the potential toxicity of the real particulate matter and selected nanoparticles on human bronchial epithelium and vascular endothelium. PM2.5 were collected in Krakow during the winter months of 2010 and 2011, near a road with heavy traffic and at a location 1 km away from heavy traffic. Elemental composition and polycyclic aromatic hydrocarbon \(PAHs\) content was assessed in both samples. Cytotoxicity of PM2.5 and their organic extracts was examined by testing the viability and genomic response in three\-dimensional cultures of normal human bronchial epithelium \(EpiAirway\) and human umbilical vein endothelial cells \(HUVEC\). In addition, the bioreactivity of zinc oxide \(ZnO\), silicon oxide \(SiO2\) in crystalline and amorphous forms, carbon black \(CB\) and nickel \(Ni\) NPs, the smallest size fraction of a PM2.5 metric, was estimated. To accomplish this, zeta potential was measured, the degree of plasmid DNA damage was assessed, hemolytic properties were determined, as well as the effect of NPs on vascular endothelial cell motility was examined.Elements associated with individual heating houses \(Al, Fe, Zn, Pb, K, P\) and adaptation of roads for winter use \(Na, Si, Ca, Mg\) were found in PM2.5 near and away from heavily trafficked road, yet in different proportions. Moreover, a presence of benzo\[a\]pyrene in concentration exceeding limit values, and 12 other PAHs, which originated from traffic and households emissions, was confirmed. Differences in chemical composition of PM2.5 samples from both locations significantly affected a degree of cytotoxicity in the three\-dimensional cultures of bronchial epithelium. Histopathological analysis revealed the presence of numerous vacuoles deforming the pseudo\-stratified structure of the tissue and cytolysis at the highest used concentration 180 μg\/cm2. Disturbed integrity of the bronchial epithelium was also confirmed by measuring a trans\-epithelial electrical resistance. Analysis of gene expression associated with oxidative stress showed that the four\-hour incubation of bronchial epithelium with PM2.5 particles from both sites, at a dose 20 μg\/cm2, and the corresponding quantities of organic extracts, induced increased expression of cp1a1 gene, which encoded a cytochrome P450 involved in phase I xenobiotic biotransformation. Interestingly, PM2.5 collected away from the busy road was more bioreactive, as it also up\-regulated 10 genes encoding proteins associated with inflammation and apoptosis\: transcription factor NFκB, interleukins \(IL\-1α, IL\-1β\), protein p21, factor CDK, and 5 heat shock proteins HSP. While the organic fraction of the sample caused increased expression of genes encoding XRCC2 protein, which is involved in the repair of damaged DNA, inducible nitric oxide synthase \(iNOS\) and tumor necrosis factor α \(TNF\-α\). The large difference in bioreactivity of PM2.5 collected at sites remote from each other only 1 km most probably stemmed from the different inorganic compositions, as the analysis of PAHs in both samples did not show significant differences in the content of individual hydrocarbons. Elements absent or present in trace quantities in the air near a busy road in the first collection period were P, Zn and Fe. In particular, transition metals such as Fe and Zn may have contributed to the formation of free radicals and promoted inflammation."]

Number of results: 0