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Greater Cairo (Egypt) is a megalopolis where the studies of the air pollution events are of extremely high relevance, for the geographical-climatological aspects, the anthropogenic emissions and the health impact. While preliminary studies on the particulate matter (PM) chemical composition in Greater Cairo have been performed, no data are yet available on the PM’s toxicity. In this work, the in vitro toxicity of the fine PM (PM2.5) sampled in an urban area of Greater Cairo during 2017–2018 was studied. The PM2.5 samples collected during spring, summer, autumn and winter were preliminary characterized to determine the concentrations of ionic species, elements and organic PM (Polycyclic Aromatic Hydrocarbons, PAHs). After particle extraction from filters, the cytotoxic and pro-inflammatory effects were evaluated in human lung A549 cells. The results showed that particles collected during the colder seasons mainly induced the xenobiotic metabolizing system and the consequent antioxidant and pro-inflammatory cytokine release responses. Biological events positively correlated to PAHs and metals representative of a combustion-derived pollution. PM2.5 from the warmer seasons displayed a direct effect on cell cycle progression, suggesting possible genotoxic effects. In conclusion, a correlation between the biological effects and PM2.5 physico-chemical properties in the area of study might be useful for planning future strategies aiming to improve air quality and lower health hazards

The biological effects induced in human alveolar cells by biomass combustion-derived particles (PM10), collected from the emission of heating systems operating with different fuels, have been analysed. Particles emitted from pellet, charcoal and wood combustion, were chemically characterized and used for the exposure of monocultures of human A549 alveolar cell line. Cell viability, pro-inflammatory cytokine expressions, oxidative stress and DNA damage were analysed. Pellet-derived particles seem to have higher toxic properties in comparison with charcoal and wood ones, suggesting a correlation between their chemical properties and toxicological profile. These data demonstrate that biomass combustion-derived particles may activate different toxicological pathways, suggesting that the type of fuel and its quality may have an important role in the strategies to prevent respiratory diseases.

Purpose: The aim of this study is to compare the Wechsler Intelligence Scale for Children® – fourth edition IV (WISC IV) intellectual profile of two groups of children with specific learning disorder, a group of bilingual children and a group of monolingual Italian children, in order to identify possible significant differences between them. Patients and methods: A group of 48 bilingual children and a group of 48 Italian monolingual children were included in this study. A preliminary comparison showed the homogeneity of the two groups regarding learning disorder typology and sociodemographic characteristics (age at WISC IV assessment, sex and years of education in Italy) with the exception of socioeconomic status. Socioeconomic status was then used as a covariate in the analysis. Results: Even if the two groups were comparable in specific learning disorder severity and, in particular, in the text comprehension performance, our findings showed that the WISC IV performances of the bilingual group were significantly worse than the Italian group in Full Scale Intelligence Quotient (P=0.03), in General Ability Index (P=0.03), in Working Memory Index (P=0.009) and in some subtests and clusters requiring advanced linguistic abilities. Conclusion: These results support the hypothesis of a weakness in metalinguistic abilities in bilingual children with specific learning disorders than monolinguals. If confirmed, this result must be considered in the rehabilitation treatment.

The mechanisms leading to cardiovascular effects induced by DEP are still under investigation. The release of mediators from exposed lung cells can contribute to endothelial activation and in vitro cell systems were here used to investigate the effects of three different particles: two standard reference DEP (1650b, 2975) and DEP sampled from a Euro4 vehicle run over a chassis dyno. BEAS cells were exposed to 5ug/cm2 DEP for 20 h and oxidative stress (HMOX1) and the release of cellular mediators (IL6, IL6R, VEGF) were investigated. BEAS supernatants were used for 24 h as conditioned media for the treatment of HPMECST1.6R lung microvascular endothelial cells. Endothelial activation markers ICAM1 and VCAM1 were finally analyzed. Moreover a 3Din vitro alveolar-blood barrier (ABB) was used: epithelial cells were treated with DEP and the release of inflammatory mediators from the endothelial compartment was investigated. In the conditioned media model DEP Euro4, which has the major amount of PAHs, was able to induce oxidative stress, IL6 and IL6R release in BEAS cells and consequent endothelial dysfunction, as evidenced by the increased expression of ICAM1and VCAM1 in HPMECST1.6R. These results were confirmed by the experiments on the ABB. SMR1650b and 2975 did not induce significant biological effects in both in vitro models. These outcomes evidence that vascular effects induced by DEP may derive from the inflammatory response of the lung epithelial cells and are modulated by particles’ physicochemical properties, with PAHs-enriched particles being more reactive. Acknowledgment: Cariplo Foundation (2013-1038); MAECI (ID PGR00786)

Biomass combustion contributes to air pollution and is correlated to adverse health effects. This study aims to investigate the possible diverse cytoxicological properties of particles collected during the combustion of different biomass sources. The particles (PM10) derived from the combustion of pellet, charcoal and wood were collected and characterized for PAH and metal content. Human alveolar A549 cells were exposed for 24 h to 5ug/cm2 PM. Cell viability (Alamar Blue assay and Hoechst/PI staining), inflammatory response (IL-6 and IL-8), antioxidant activity (HO-1 expression), xenobiotic metabolism activation (CYP1A1/1B1) and DNA damage (yH2AX, phospho-ATM/ATR) were evaluated. The results revealed different biological responses after exposure to the different PMs, suggesting a possible correlation between the particles’ chemical properties and their toxicological profile. Pellet-derived PM affected cell viability, inducing necrosis, while charcoal and wood PMs mainly induced apoptosis. Only pellet-derived PM activated inflammatory pathways, through IL-6 and IL-8 synthesis. All the particles caused a significant increase of HO-1, confirming oxidative stress-related responses, and the activation of the cytochrome P450 enzymes. Finally, particles caused an increase in the level of DNA strand breaks. These data demonstrate that combustion particles deriving from different biomasses may activate different toxicological pathways, pointing out the importance of the biomass type and quality in the strategies to prevent respiratory diseases

Background and Aims Diesel and Biomass combustion-derived particles (CDPs) largely contribute to air pollution and likely to the adverse health effects observable in the exposed populations. Anyway our knowledge on the different biological responses deriving from the particles emitted from different sources is still poor, as well as the comprehension of the modes of action of such particles with variable physico-chemical properties. This study aims at comparatively investigate the cytoxic and genotoxic properties of particles collected during the combustion of different diesel and biomass sources. Methods Diesel Exhaust ultrafine Particles (DEP) were from two standard references (DEP 1650b and 2975) and directly sampled from a Euro4 vehicle run over a chassis dyno. Biomass-derived combustion particles were collected from the emission of heating systems operating with pellet, charcoal and wood. CDPs were morphologically and chemically characterized. Monocultures of human lung cells and a 3D in vitro model of the alveolar blood barrier (ABB) were used to study the CDP-induced biological effects. Cell viability, inflammatory response, antioxidant and xenobiotic metabolism activity, DNA damage were investigated. Key results of the study DEP exposure of lung cells did not cause significant cell death, but especially DEP Euro4, collected during a standard urban cycle driving, did induce oxidative stress and release of inflammatory cytokines, that were also able to activate endothelial cells. Pellet-derived particles decreased cell viability, inducing necrosis, while charcoal and wood CDPs mainly induced apoptosis. The strongest cytotoxic action was achieved after exposure to CDPs from not-certified pellet in respect to certified pellet and other biomass-derived CDPs. Significant increase of HO-1, the activation of the cytochrome P450 enzymes and DNA strand breaks were observed for all biomass-derived CDPs, confirming the oxidative-mediated genotoxicity as a shared mechani

Diesel exhaust particles (DEP) and their ultrafine fraction (UFP) are known to induce cardiovascular effects in exposed subjects. The mechanisms leading to these outcomes are still under investigation, but the activation of respiratory endothelium is likely to be involved. Particles translocation through the air-blood barrier and the release of mediators from the exposed epithelium have been suggested to participate in the process. Here we used a conditioned media in vitro model to investigate the role of epithelial-released mediators in the endothelial cells activation.Diesel UFP were sampled from a Euro 4 vehicle run over a chassis dyno and lung epithelial BEAS-2B cells were exposed for 20 h (dose 5 Î1⁄4g/cm2). The exposure media were collected and used for endothelial HPMEC-ST1.6R cells treatment for 24 h. The processes related to oxidative stress and inflammation were investigated in the epithelial cells, accordingly to the present knowledge on DEP toxicity. The release of IL-6 and VEGF was significantly augmented in diesel exposed cells. In endothelial cells, VCAM-1 and ICAM-1 adhesion molecules levels were increased after exposure to the conditioned media. By interfering with IL-6 binding to its endothelial receptor, we demonstrate the role of this interleukin in inducing the endothelial response