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Abstract: The effect of the deposition of Cu and K elements on zirconia was studied in the oxidation of a carbon black (CB), considered as a model of diesel soot. Catalytic tests were carried out using CB–catalyst mixtures prepared under loose and tight contact conditions. The potassium-containing catalysts exhibited high activity in loose contact that differed slightly from that obtained in tight contact. The introduction of both Cu and K on ZrO2 provided synergistic effects in the CB oxidation. It is proposed that these systems can release active oxygen species to oxidize CB even in the absence of gaseous oxygen. Consequently, (CB–catalyst) loose contact mixtures treated at different temperatures under Ar flow were characterized by electron paramagnetic resonance and temperature-programmed reduction measurements. The presence of potassium favours contact between the catalyst and CB and enhances the catalyst''s ability to release active oxygen species. In K/ZrO2, it yields an increase in the amount of Zr3+ ions, which appear to be stabilized mainly in monoclinic ZrO2. In Cu-K/ZrO2 catalysts, the potassium promoter preferentially interacts with the supported copper(II) species and favours their participation following a redox mechanism. [Copyright &y& Elsevier]

Abstract: To identify the nature of active paramagnetic species involved in the carbon black (CB) oxidation, an Electron Paramagnetic Resonance (EPR) study of (CB–ZrO2) and (CB–Cu/ZrO2) loose contact mixtures treated under argon flow has been undertaken. In the presence of pure zirconia catalysts, it was found that ZrO2 interacts with CB and can be reduced into Zr3+ formed in tetragonal phase of this oxide support. In parallel, several EPR signals assigned to carbonaceous radicals were detected: i) carbonaceous radicals on CB surface, ii) radicals located at the CB–ZrO2 interface and iii) oxygen deficit carbonaceous radicals observed at high treatment temperature. The carbonaceous signals disappeared completely after CB oxidation in agreement with a regeneration of the catalyst treated under air. For copper supported on zirconia catalysts, oxygen surrounding isolated Cu(II) species and oxygen from tetragonal ZrO2 lattice are involved in carbon black oxidation. The phenomenon is reversible and this catalyst is also regenerated by air. Carbonaceous radical signals were also observed for (CB–Cu/ZrO2) mixture and their intensity decrease versus temperature appeared in good agreement with the better activity of Cu/ZrO2 compared to pure ZrO2. [Copyright &y& Elsevier]

The aim of this work was to study the relationship between oxidative stress damages and particulate matter (PM) chemical composition, sources, and PM fractions. PM 2.5-0.3 (PM with equivalent aerodynamic diameter between 2.5 and 0.3 μm) were collected at urban, road traffic and industrial sites in the North of France, and were characterized for major and minor chemical species. Four different fractions (whole PM 2.5-0.3 , organic, water-soluble and non-extractable matter) were considered for each of the PM 2.5-0.3 samples from the three sites. After exposure of BEAS-2B cells to the four different fractions, oxidative stress was studied in cells by quantifying reactive oxygen species (ROS) accumulation, oxidative damage to proteins (carbonylated proteins), membrane alteration (8-isoprostane) and DNA damages (8-OHdG). Whole PM 2.5-0.3 was capable of inducing ROS overproduction and caused damage to proteins at higher levels than other fractions. Stronger cell membrane and DNA damages were found associated with PM and organic fractions from the urban site. ROS overproduction was correlated with level of expression of carbonylated proteins, DNA damages and membrane alteration markers. The PM 2.5-0.3 collected under industrial influence appears to be the less linked to cell damages and ROS production in comparison with the other influences., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

The chemical profiles of PM 2.5 emitted from a non-road diesel generator, wood burning and cooking activities including chicken and beef charcoal grilling and general cooking activities were determined. The characterization included the carbonaceous fraction (OC/EC), water-soluble ions, elements, and organic species comprising n-alkanes, polycyclic aromatic hydrocarbons, carboxylic acids, levoglucosan, dioxins, furans, and dioxin-like polychlorinated biphenyls. The main component in the PM 2.5 from the different sources was carbonaceous matter with a mass contribution to PM 2.5 of 49% for cooking activities, 53% for wood burning, 66% for beef grilling, 72% for chicken grilling, and 74% for diesel generator with different OC/EC concentration ratios. The analysis of organic compounds contents using diagnostic ratios and indexes showed differences between the sources and revealed specific source markers. The water-soluble ions had the highest contribution in the cooking activities profile with 17% of PM 2.5 and the least in the chicken grilling profile (1.1%). Additionally, 29 analyzed elements were identified, and their contribution varied with the sources (ranging from 1% to 11% of PM 2.5 ). These findings could be used to differentiate these sources and could assist in the use of source apportionment methods., (Copyright © 2022 Elsevier Inc. All rights reserved.)

The skin is an essential barrier, protecting the body against the environment and its numerous pollutants. Several environmental pollutants are known to affect the skin, inducing premature aging through mechanisms including oxidative stress, inflammation, and impairment of skin functions. Even climate conditions can impact the skin. Therefore, using a Reconstructed Human Epidermis (RHE), we tested the effect of two samples of fine particulate matters (PM 0.3-2.5 - one metals-rich sample and the other organic compounds-rich), two Volatile Organic Compounds mixtures (VOCs - from a solvent-based paint and a water-based paint) and Tobacco Smoke (TS). All pollutants affected cellular functionality, but to a lesser extent for the water-based paint VOC. This effect was enhanced when RHE were preconditioned for 2 h by a semi-dry airflow (45% relative humidity) before pollutants application, compared to preconditioning by a humid airflow (90% relative humidity). In the absence of preconditioning, IL-1α, IL-6, IL-8, and RANTES were almost systematically induced by pollutants. When RHE were preconditioned by a semi-dry or humid airflow before being subjected to pollutants, the increase of IL-1α, IL-8, and RANTES falls into two groups. Similarly to RHE not treated with pollutants, RHE treated with VOCs after preconditioning by a semi-dry airflow showed increased IL-1α, IL-8, and RANTES release. On the contrary, RHE treated with PM or TS after preconditioning by a semi-dry airflow show a lower increase in IL-1α, IL-8, and RANTES compared to preconditioning by a humid airflow. The effect of real environmental relative humidity conditions of the air, combined with acute exposure to various environmental pollutants, seemed to relate mainly to structural changes of the skin, determining the outcome of the inflammatory response depending on the physicochemical characteristics of pollutants., (Copyright © 2020 Elsevier Inc. All rights reserved.)

The aim of this study was to assess the integrity and kidney overall functional capacity of subjects exposed to landfill emissions. Urine and blood levels of Pb and Cd, and several of the newly biomarkers of nephrotoxicity (Kim Injury Molecule 1 (KIM-1), alpha-1 Microglobulin (α1 M), beta-2 Microglobulin (β2 M), Cystatin-C (Cyst C), Clusterin, alpha-glutathione S-transferase (GSTα), pi-glutathione S-transferase (GSTπ), Tissue Inhibitor of Metalloproteinase-1 (TIMP1), Calbindin, Neutrophil Gelatinase-Associated Lipocalin (NGAL), Osteopontin (OPN), (Retinol Binding Protein(RBP), Liver-type Fatty Acid-Binding Protein (FABP-1), Trefoil Factor 3 (TFF3), Collagen VI) were measured in order to assess glomerular and tubule damage in adults living near a landfill. Our results indicate glomerular dysfunction in exposed subjects, and supported evidence of necrosis of proximal and distal tubule epithelial cells as specific biomarkers began to appear in the urine. Positive correlation by Pearson test were obtained between : blood Pb and B-OPN, B-Cyst C, Calbindin, U-KIM-1, TIMP1, U-OPN, and U-Clusterin; and also, between urinary Cd and TIMP1, B-Clusterin, U-OPN, FABP-1, Albumin, and U-Clusterin. The relation between biomarkers of Cd/Pb exposure and early effect biomarkers in this study clearly predicts the future risk of severe kidney injury in subjects living close to the landfill., Competing Interests: The authors report no declarations of interest., (© 2021 Published by Elsevier B.V.)

New toxicological research is still urgently needed to improve the current knowledge about the induction of some underlying mechanisms of toxicity by the different chemical fractions of ambient particulate matter (PM). This in vitro study sought also to better evaluate and compare the respective toxicities of fine particles (PM 2.5-0.3 ) and their inorganic and organic chemical fractions, and the respective toxicities of the organic chemical fractions of PM 2.5-0.3 and quasi-ultrafine particles (PM 0.3 ). Human bronchial epithelial BEAS-2B cells were also exposed for 6-48 h to relatively low doses of PM 2.5-0.3 and their organic extractable (OEM 2.5-0.3 ) and non-extractable (NEM 2.5-0.3 ) fractions, and the organic extractable fraction (OEM 0.3 ) of PM 0.3 . We reported that not only PM 2.5-0.3 , but also, to a lesser extent, its inorganic chemical fraction, NEM 2.5-0.3 , and organic chemical fraction, OEM 2.5-0.3 , were able to significantly induce ROS overproduction and oxidative damage notwithstanding the early activation of NRF2 signaling pathway. Moreover, for any exposure, inflammatory and apoptotic events were noticed. Similar results were observed in BEAS-2B cells exposed to OEM 0.3 , rich of polycyclic aromatic hydrocarbons and their nitrated and oxygenated derivatives. In BEAS-2B cells exposed for 24 and 48 h to OEM 2.5-0.3 and OEM 0.3 , to a higher extent, there was an alteration of the levels of some critical proteins even though crucial for the autophagy rather than a real reduction of autophagy. It is noteworthy that the toxicological effects were equal or mostly higher in BEAS-2B cells exposed for 6 and/or 24 h to PM 2.5-0.3 from those exposed to NEM 2.5-0.3 or OEM 2.5-0.3 , and in BEAS-2B cells exposed for 6 and/or mostly 24 h to OEM 0.3 from those exposed to OEM 2.5-0.3 . Taken together, these results revealed the higher potentials for toxicity, closely linked to their respective physical and chemical characteristics, of PM 2.5-0.3 vs NEM 2.5-0.3 and/or OEM 2.5-0.3 , and OEM 0.3 vs OEM 2.5-0.3 ., Competing Interests: Declaration of interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

To date no study has been able to clearly attribute the observed toxicological effects of atmospheric particles (PM) to a specific class of components. The toxicity of both the organic extractable matter (OEM 2.5-0.3 ) and non-extractable matter (NEM 2.5-0.3 ) of fine particles (PM 2.5-0.3 ) was compared to that of PM 2.5-0.3 in its entirety on normal human epithelial bronchial BEAS-2B cells in culture. The specific effect of the quasi-ultrafine fraction (PM 0.3 ) was assessed, by comparing the responses of cells exposed to the PM 2.5-0.3 and PM 0.3 organic extractable matter, OEM 2.5-0.3 and OEM 0.3 respectively. Chemically, PAH, O-PAH, and N-PAH were respectively 43, 17, and 4 times more concentrated in PM 0.3 than in PM 2.5-0.3 , suggesting thereby a predominant influence of anthropogenic activities and combustion sources. BEAS-2B cells exposed to PM 2.5-0.3 , NEM 2.5-0.3 , EOM 2.5-0.3 and OEM 0.3 lead to different profiles of expression of selected genes and proteins involved in the metabolic activation of PAH, O-PAH, and N-PAH, and in the genotoxicity pathways. Specifically, OEM 0.3 was the most inducer for phase I and phase II enzymes implicated in the metabolic activation of PAH (AHR, AHRR, ARNT, CYP1A1, CYP1B1, EPHX-1, GSTA-4) thereby producing the highest DNA damage, felt by ATR and, thereafter, a cascade of protein phosphorylation (CHK1/CHK2/MDM2) closely related to the cell cycle arrest (P21 and P53 induction). This study underlined the crucial role played by the organic chemicals present in PM 0.3 . These results should be considered in any future study looking for the main chemical determinants responsible for the toxicity of ambient fine PM., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Exposure to fine atmospheric Particulate Matter (PM) is one of the major environmental causes involved in the development of inflammatory lung diseases, such as chronic obstructive pulmonary disease (COPD) or asthma. When PM is penetrating in the pulmonary system, alveolar macrophages represent the first line of defense, in particular by triggering a pro-inflammatory response, and also by their ability to recruit infiltrating macrophages from the bone marrow. The aim of this in vitro study was to evaluate the gene expression and cytokine production involved in the toxicological and inflammatory responses of infiltrating macrophages, as well as the Extracellular Vesicles (EVs) production, after their exposure to PM. The ability of these EVs to convey information related to PM exposure from exposed macrophages to pulmonary epithelial cells was also evaluated. Infiltrating macrophages respond to fine particles exposure in a conventional manner, as their exposure to PM induced the expression of Xenobiotic Metabolizing Enzymes (XMEs) such as CYP1A1 and CYP1B1, the enzymes involved in oxidative stress SOD2, NQO1 and HMOX as well as pro-inflammatory cytokines in a dose-dependent manner. Exposure to PM also induced a greater release of EVs in a dose-dependent manner. In addition, the produced EVs were able to induce a pro-inflammatory phenotype on pulmonary epithelial cells, with the induction of the release of IL6 and TNFα proinflammatory cytokines. These results suggest that infiltrating macrophages participate in the pro-inflammatory response induced by PM exposure and that EVs could be involved in this mechanism., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Eighteen polycyclic aromatic hydrocarbons (PAHs) and fourteen nitrated PAHs (NPAHs) in PM 2.5 samples were collected during the 2016 Chinese New Year's holiday (CNY) at one suburban and three rural sites in Shandong and Henan Provinces. The PAH and NPAH concentrations were highest at the suburban site. The rural PAH concentrations in Qingzhou (QZ), Heze (HZ), and Liaocheng (LC) were higher than those measured at many other urban sites, indicating that PAHs pollution was notably higher in the suburban and rural sites during this festive period. Elevated PAH concentrations were observed during fireworks periods, but fireworks burning was not a significant or direct PAHs or NPAHs source based on molecular profiles and diagnostic ratios. The measured PAHs and NPAHs at the sampling sites mainly originated from coal and biomass burning. The increased concentrations during CNY's Eve may be related to behavioural changes during the period. Secondary formation of NPAHs mainly occurred via OH radical chemistry at all four sites. Fireworks burning did not increase secondary formation of NPAHs. ∑BaP eq concentrations exhibited strong correlations with PAHs concentrations, and the highest and lowest concentrations were observed in QZ and Xiping (XP), respectively. The incremental lifetime cancer risk (ILCR) was calculated to be between 10 -6 and 10 -4 for 1-70 years old persons, with the highest risks observed in the adult (30-70 years) and the toddler (1-6 years) groups., (Copyright © 2019. Published by Elsevier Ltd.)

A particular attention has been devoted to the type of toxicological responses induced by particulate matter (PM), since their knowledge is greatly complicated by the fact that it is a heterogeneous and often poorly described pollutant. However, despite intensive research effort, there is still a lack of knowledge about the specific chemical fraction of PM, which could be mainly responsible of its adverse health effects. We sought also to better investigate the toxicological effects of organic extractable matter (OEM) in normal human bronchial epithelial lung BEAS-2B cells. The wide variety of chemicals, including PAH and other related-chemicals, found in OEM, has been rather associated with early oxidative events, as supported by the early activation of the sensible NRF-2 signaling pathway. For the most harmful conditions, the activation of this signaling pathway could not totally counteract the ROS overproduction, thereby leading to critical oxidative damage to macromolecules (lipid peroxidation, oxidative DNA adducts). While NRF-2 is an anti-inflammatory, OEM exposure did not trigger any significant change in the secretion of inflammatory cytokines (i.e., TNFα, IL-1β, IL-6, IL-8, MCP-1, and IFNγ). According to the high concentrations of PAH and other related organic chemicals found in this OEM, CYP1A1 and 1B1 genes exhibited high transcription levels in BEAS-2B cells, thereby supporting both the activation of the critical AhR signaling pathway and the formation of highly reactive ultimate metabolites. As a consequence, genotoxic events occurred in BEAS-2B cells exposed to this OEM together with cell survival events, with possible harmful cell cycle deregulation. However, more studies are required to implement these observations and to contribute to better decipher the critical role of the organic fraction of air pollution-derived PM 2.5 in the activation of some sensitive signaling pathways closely associated with G1/S and intra-S checkpoint blockage, on the one hand, and cell survival, on the other hand., (Copyright © 2019 Elsevier Inc. All rights reserved.)

In this paper, we propose informed weighted non-negative matrix factorization (NMF) methods using an α β -divergence cost function. The available information comes from the exact knowledge/boundedness of some components of the factorization-which are used to structure the NMF parameterization-together with the row sum-to-one property of one matrix factor. In this contribution, we extend our previous work which partly involved some of these aspects to α β -divergence cost functions. We derive new update rules which are extendthe previous ones and take into account the available information. Experiments conducted for several operating conditions on realistic simulated mixtures of particulate matter sources show the relevance of these approaches. Results from a real dataset campaign are also presented and validated with expert knowledge.

Exposure to atmospheric pollutants has been recognized as a major risk factor of respiratory and cardiovascular diseases. Fine particles (PM 2.5 ) and a coarser fraction (PM >2.5 ) sampled at an urban site in Dakar (HLM), characterized by high road traffic emissions, were compared with particles sampled at a rural area, Toubab Dialaw located about 40 km from Dakar. The physicochemical characteristics of samples revealed that PMs differ for their physical (surface area) and chemical properties (in terms of CHN, metals, ions, paraffins, VOCs and PAHs) that were 65-75% higher in urban samples. Moreover the fine PMs contain higher amounts of anthropogenic related pollutants than the PM >2.5 one. These differences are sustained by the ratios reported for the analysed PAHs which suggest as predominant primary emission sources vehicle exhausts at urban site and biomass combustion at the rural site. The inflammatory response and the oxidative damages were evaluated in BEAS-2B cells by the quantification of 4 selected inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8) and of total carbonylated proteins and the oxidative DNA adduct 8-OHdG after 8 or 24 h exposure. In accordance with the different sources and different physical and chemical properties, the inflammatory response and the oxidative damages were found higher in bronchial cells exposed to urban PMs. These data confirm the importance, also for West African countries, to evaluate the correlation between PM physico-chemical properties and potential biological impacts., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

PM 2.5 have been related to various adverse health effects, mainly due to their ability to penetrate deeply and to convey harmful chemical components, such as metals inside the body. In this work, PM 2.5 were sampled at Saint-Omer, a medium-sized city located in northern France, in March-April 2011 and analyzed for their total carbon, water-soluble ions, major and trace elements. More specifically, the origin of 15 selected elements was examined using different tools including enrichment factors, conditional bivariate probability function (CBPF) representations, diagnostic ratios and receptor modelling. The results indicated that PM 2.5 metal composition is affected by both emissions of a local glassmaking factory and an integrated steelworks located at a distance of 35 km from the sampling site. For the first time, diagnostic ratios were proposed for the glassmaking activity. Therefore, metals in PM 2.5 could be attributed to the following anthropogenic sources: (i) local glassmaking industry for Sn, As, Cu and Cr, (ii) distant integrated steelworks for Ag, Fe, Cd, Mn, Rb and Pb, (iii) heavy fuel oil combustion for Ni, V and Co and (iv) non-exhaust traffic for Zn, Pb, Mn, Sb, and Cu. The impact of such sources on metal concentrations in PM 2.5 was assessed using a constrained receptor model. Despite their low participation to PM 2.5 concentration (2.7%), the latter sources were found as the main contributors (80%) to the overall concentration levels of the 15 selected elements in PM 2.5 ., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Numerous studies have associated air manganese (Mn) exposure with negative health effects, primarily neurotoxic disorders. Despite there is not a specific European regulation, institutions such as the World Health Organization (WHO) have proposed an annual average guideline value of 150 ng/m 3 . Bioaccessibility and toxicity mechanisms of Mn remain unclear, however it is generally agreed that adverse health effects are strongly linked to particle size and morphology, chemical composition and oxidation state. This study aims to deepen the understanding of the physico-chemical characteristics of PM 10 and deposition samples collected in an urban area in the proximities of a ferromanganese alloy plant. Total Mn content was determined by ICP-MS after a microwave-assisted acid digestion. The size, morphology and chemical composition of individual particles were studied by SEM-EDX. XRD was used to identify the major crystalline phases. Most of the particles observed by SEM-EDX contain Mn. 60% of Mn-PM 10 particles were spheres of small size and were attributed to condensation processes at the smelting unit. Mn-bearing particles present in deposition were characterized by irregular shapes and bigger sizes, most of them consisting of SiMn slags and Mn ores and alloys, and attributed to diffuse emissions from raw material and product handling and processing. Due to the differences in the characteristics of Mn-bearing particles found in the different matrices, further studies on the potential toxicity and health effects of these particles should be done, especially in relation with the small and spherical particles present in PM 10 , which are expected to be more problematic., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Particulate Matter (PM) air pollution is one of the major concerns for environment and health. Understanding the heterogeneity and complexity of fine and ultrafine PM is a fundamental issue notably for the assessment of PM toxicological effects. The aim of this study was to evaluate mutagenicity and cytotoxicity of a multi-influenced urban site PM, with or without the ultrafine fraction. For this purpose, PM 2.5-0.3 (PM with aerodynamic diameter ranging from 0.3 to 2.5 μm) and PM 2.5 were collected in Dunkerque, a French coastal industrial city and were extensively characterized for their physico-chemical properties, including inorganic and organic species. In order to identify the possible sources of atmospheric pollution, specific criteria like Carbon Preference Index (CPI) and PAH characteristic ratios were investigated. Mutagenicity assays using Ames test with TA98, TA102 and YG1041 Salmonella strains with or without S9 activation were performed on native PM sample and PM organic extracts and water-soluble fractions. BEAS-2B cell viability and cell proliferation were evaluated measuring lactate dehydrogenase release and mitochondrial dehydrogenase activity after exposure to PM and their extracts. Several contributing sources were identified in PM: soil resuspension, marine emissions including sea-salt or shipping, road traffic and industrial activities, mainly related to steelmaking or petro-chemistry. Mutagenicity of PM was evidenced, especially for PM 2.5 , including ultrafine fraction, in relation to PAHs content and possibly nitro-aromatics compounds. PM induced cytotoxic effects at relatively high doses, while alteration of proliferation with low PM doses could be related to underlying mechanisms such as genotoxicity., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Toluene is one of the most used Volatile Organic Compounds (VOCs) in the industry despite its major health impacts. Catalytic oxidation represents an efficient remediation technique in order to reduce its emission directly at the source, but it can release by-products. To complete the classical performance assessment using dedicated analytical chemistry methods, we propose to perform an untargeted toxicological validation on two efficient catalysts. Using biological system allows integrating synergy and antagonism in toxic effects of emitted VOCs and by-products, often described in case of multi-exposure condition. Catalysts Pd/α-Al 2 O 3 and Pd/γ-Al 2 O 3 developed for the oxidation of toluene were both coupled to a Vitrocell ® Air-Liquid Interface (ALI) system, for exposure of human A549 lung cells during 1h to toluene or to catalysts exhaust before quantification of xenobiotics metabolizing enzymes. This study validated initially the Vitrocell ® as an innovative, direct and dynamic model of ALI exposure in the assessment of the performances of new catalysts, showing the presence of chemically undetected by-products. The comparison of the two catalysts showed then that fewer organic compounds metabolizing genes were induced by Pd/γ-Al 2 O 3 in comparison to Pd/α-Al 2 O 3 , suggesting that Pd/γ-Al 2 O 3 is more efficient for toluene total oxidation from a toxicological point of view., (Copyright © 2016. Published by Elsevier Inc.)

Although its adverse health effects of air pollution particulate matter (PM2.5) are well-documented and often related to oxidative stress and pro-inflammatory response, recent evidence support the role of the remodeling of the airway epithelium involving the regulation of cell death processes. Hence, the overarching goals of the present study were to use an in vitro coculture model, based on human AM and L132 cells to study the possible alteration of TP53-RB gene signaling pathways (i.e. cell cycle phases, gene expression of TP53, BCL2, BAX, P21, CCND1, and RB, and protein concentrations of their active forms), and genetic instability (i.e. LOH and/or MSI) in the PM2.5-0.3-exposed coculture model. PM2.5-0.3 exposure of human AM from the coculture model induced marked cell cycle alterations after 24h, as shown by increased numbers of L132 cells in subG1 and S+G2 cell cycle phases, indicating apoptosis and proliferation. Accordingly, activation of the TP53-RB gene signaling pathways after the coculture model exposure to PM2.5-0.3 was reported in the L132 cells. Exposure of human AM from the coculture model to PM2.5-0.3 resulted in MS alterations in 3p chromosome multiple critical regions in L132 cell population. Hence, in vitro short-term exposure of the coculture model to PM2.5-0.3 induced cell cycle alterations relying on the sequential occurrence of molecular abnormalities from TP53-RB gene signaling pathway activation and genetic instability., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Aided phytostabilisation using trees and fly ashes is a promising technique which has shown its effectiveness in the management of highly metal-contaminated soils. However, this success is generally established based on topsoil physicochemical analysis and short-term experiments. This paper focuses on the long-term effects of the afforestation and two fly ashes (silico-aluminous and sulfo-calcic called FA1 and FA2, respectively) by assessing the integrity of fly ashes 10 years after their incorporation into the soil as well as the vertical distribution of the physicochemical parameters and trace elements (TEs) in the amended soils (F1 and F2) in comparison with a non-amended soil (R). Ten years after the soil treatment, the particle size distribution analysis between fly ashes and their corresponding masses (fly ash + soil particles) showed a loss or an agglomeration of finer particles. This evolution matches with the appearance of gypsum (CaSO4 2H2O) in FA2m instead of anhydrite (CaSO4), which is the major compound of FA2. This finding corresponds well with the dissolution and the lixiviation of Ca, S and P included in FA2 along the F2 soil profile, generating an accumulation of these elements at 30 cm depth. However, no variation of TE contamination was found between 0 and 25 cm depth in F2 soil except for Cd. Conversely, Cd, Pb, Zn and Hg enrichment was observed at 25 cm depth in the F1 soil, whereas no enrichment was observed for As. The fly ashes studied, and notably FA2, were able to reduce Cd, Pb and Zn availability in soil and this capacity persists over the time despite their structural and chemical changes., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

The purpose of the study was to determine Pb and Cd concentrations in humans and to assess the effect of co-exposure to these metals on biomarkers of oxidative stress and nephrotoxicity. Blood and urine levels of Pb and Cd, oxidative stress and urinary renal biomarkers were measured in 77 subjects neighboring a discharge and 52 in the control site. Exposed subjects showed significantly higher levels of lead and cadmium in blood and urine than the controls. Excessive production of reactive oxygen species induced by these metals in exposed subjects conducted to a decrease in antioxidant defense system (GPx, Selenium, GSH) and an increase in lipid peroxidation (MDA). Moreover, changes in markers of nephrotoxicity (high urinary concentrations of total protein, RBP and CC16, as well as GSTα and LDH increased activities) suggested the occurrence of discrete and early signs of impaired renal function for the discharge neighboring population., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

During the last few years, the induction of toxicological mechanisms by atmospheric ultrafine particles (UFP) has become one of the most studied topics in toxicology and a subject of huge debates. Fine particles (FP) and UFP collected at urban and rural sites in Lebanon were studied for their chemical composition and toxicological effects. UFP were found more enriched in trace elements, secondary inorganic ions, total carbon and organic compounds than FP. For toxicological analysis, BEAS-2B cells were exposed for 24, 48 and 72 h to increasing concentrations of FP, water-UFP suspension (UFPw) and UFP organic extract (UFPorg). Our findings showed that UFP caused earlier alterations of mitochondrial metabolism and membrane integrity from the lowest concentrations. Moreover, a significant induction of CYP1A1, CYP1B1 and AhRR genes expression was showed after cells exposure to UFPorg and to a lesser extent to UFPw and FP samples., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

While the evidence for the health adverse effects of air pollution Particulate Matter (PM) has been growing, there is still uncertainty as to which constituents within PM are most harmful. Hence, to contribute to fulfill this gap of knowledge, some physicochemical characteristics and toxicological endpoints (i.e. cytotoxicity, oxidative damage, cytokine secretion) of PM2.5-0.3 samples produced during two different seasons (i.e. spring/summer or autumn/winter) in three different surroundings (i.e. rural, urban, or industrial) were studied, thereby expecting to differentiate their respective adverse effects in human bronchial epithelial cells (BEAS-2B). Physicochemical characteristics were closely related to respective origins and seasons of the six PM2.5-0.3 samples, highlighting the respective contributions of industrial and heavy motor vehicle traffic sources. Space- and season-dependent differences in cytotoxicity of the six PM2.5-0.3 samples could only be supported by considering both the physicochemical properties and the variance in air PM concentrations. Whatever spaces and seasons, dose- and even time-dependent increases in oxidative damage and cytokine secretion were reported in PM2.5-0.3-exposed BEAS-2B cells. However, the relationship between the chemical composition of each of the six PM2.5-0.3 samples and their oxidative or inflammatory potentials seemed to be very complex. These results supported the role of inorganic, ionic and organic components as exogenous source of Reactive Oxygen Species and, thereafter, cytokine secretion. Nevertheless, one of the most striking observation was that some inorganic, ionic and organic chemical components were preferentially associated with early oxidative events whereas others in the later oxidative damage and/or cytokine secretion. Taken together, these results indicated that PM mass concentration alone might not be able to explain the health outcomes, because PM is chemically nonspecific, and supported growing evidence that PM-size, composition and emission source, together with sampling season, interact in a complex manner to produce PM2.5-0.3-induced human adverse health effects., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Assessment of air pollution by particulate matter (PM) is strongly required in Lebanon in the absence of an air quality law including updated air quality standards. Using two different PM2.5-0.3 samples collected at an urban and a rural site, we examined genotoxic/epigenotoxic effects of PM exposure within a human bronchial epithelial cell line (BEAS-2B). Inorganic and organic contents evidence the major contribution of traffic and generating sets in the PM2.5-0.3 composition. Urban PM2.5-0.3 sample increased the phosphorylation of H2AX, the telomerase activity and the miR-21 up-regulation in BEAS-2B cells in a dose-dependent manner. Furthermore, urban PM2.5-0.3 induced a significant increase in CYP1A1, CYP1B1 and AhRR genes expression. The variable concentrations of transition metals and organic compounds detected in the collected PM2.5-0.3 samples might be the active agents leading to a cumulative DNA damage, critical for carcinogenesis., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Traffic-related volatile organic compounds (VOCs) pollution has frequently been demonstrated to be a serious problem in the developing countries. Benzene and 1,3-butadiene (BD) have been classified as a human carcinogen based on evidence for an increased genotoxic and epigenotoxic effects in both occupational exposure assessment and in vivo/in vitro studies. We have undertaken a biomonitoring of 25 traffic policemen and 23 office policemen in Beirut, through personal air monitoring, assessed by diffusive samplers, as well as through the use of biomarkers of exposure to benzene and BD. Personal benzene, toluene, ethylbenzene, and xylene (BTEX) exposure were quantified by GC-MS/MS, urinary trans, trans-muconic acid (t,t-MA) by HPLC/UV, S-phenyl mercapturic acid (S-PMA), monohydroxy-butenyl mercapturic acid (MHBMA) and dihydroxybutyl mercapturic acid (DHBMA) by ultra-performance liquid chromatography-electrospray tandem mass spectrometry (UPLC/ESI(-)-MS/MS) in MRM (Multiple Reaction Monitoring) mode. We found that individual exposure to benzene in the traffic policemen was higher than that measured in traffic policemen in Prague, in Bologna, in Ioannina and in Bangkok. t,t-MA levels could distinguish between office and traffic policemen. However, median MHBMA levels in traffic policemen were slightly elevated, though not significantly higher than in office policemen. Alternatively, DHBMA concentrations could significantly distinguish between office and traffic policemen and showed a better correlation with personal total BTEX exposure. DHMBA, measured in the post-shift urine samples, correlated with both pre-shift MHMBA and pre-shift DHMBA. Moreover, there was not a marked effect of smoking habits on DHBMA. Taken together, these findings suggested that DHBMA is more suitable than MHBMA as biomarker of exposure to BD in humans. Traffic policemen, who are exposed to benzene and BD at the roadside in central Beirut, are potentially at a higher risk for development of diseases such as cancer than office policemen., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

After particulate matter (PM) collection in Cotonou (Benin), a complete physicochemical characterization of PM2.5 and PM>2.5 was led. Then, their adverse health effects were evaluated by using in vitro culture of human lung cells. BEAS-2B (bronchial epithelial cells) were intoxicated during short-term exposure at increasing PM concentrations (1.5-96 μg/cm(2)) to determine global cytotoxicity. Hence, cells were exposed to 3 and 12 μg/cm(2) to investigate the potential biological imbalance generated by PM toxicity. Our findings showed the ability of both PM to induce oxidative stress and to cause inflammatory cytokines/chemokines gene expression and secretion. Furthermore, PM were able to induce gene expression of enzymes involved in the xenobiotic metabolism pathway. Strong correlations between gene expression of metabolizing enzymes, proinflammatory responses and cell cycle alteration were found, as well as between proinflammatory responses and cell viability. Stress oxidant parameters were highly correlated with expression and protein secretion of inflammatory mediators., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

The massive increase in emissions of air pollutants due to economic and industrial growth in developing countries has made air quality a crucial health problem in this continent. Hence, it is somewhat critical to have a better knowledge on the air pollution in Sub-Saharan Africa countries. Three air pollution PM2.5 samples were also collected in two urban sites (i.e., Fann and Faidherbe) in Dakar (Senegal) and in a rural site near Dakar (i.e., Ngaparu). The two urban sites mainly differ in the type of used vehicles: in Fann, most of the traffic is made of buses, which are absent, in Faidherbe. The physicochemical characteristics of the three PM2.5 samples revealed their high heterogeneities and complexities, related to the multiple natural and anthropogenic emission sources. Results from 5-bromodeoxyuridine incorporation into DNA, mitochondrial dehydrogenase activity, and extracellular lactate dehydrogenase activity in PM2.5-exposed BEAS-2B cells suggested the exposure conditions (i.e., 3 and 12 μg PM/cm² during 24, 48, and 72 h) to further consider. The organic fractions (i.e., mainly PAHs) of the PM(2.5) samples were able to induce a time and/or concentration-dependent gene expression of CYP1A1 and CYP1B1, and, to a lesser extent, NQO1. There was a time and/or dose-dependent increase of both the gene expression and/or protein secretion of inflammatory mediators (i.e., TNF-α, IL-1β, IL-6, and/or IL-8) in PM(2.5)-exposed BEAS-2B cells. In agreement with the physicochemical characterization, urban PM(2.5) samples caused greater biological responses in BEAS-2B cells than the rural one. Variable concentrations of transition metals (i.e., Fe, Al, Pb, Mn, Zn) and organic compounds (i.e., PAHs) founded in the three PM2.5 samples might be firmly involved in a time- and/or dose-dependent toxicity, relying on inflammatory processes., (Copyright © 2011 Elsevier Inc. All rights reserved.)

To contribute to complete the knowledge of the underlying mechanisms of action involved in air pollution particulate matter (PM)-induced cytotoxicity, an aerosol was collected in Dunkerque, a French seaside City heavily industrialized. In this work, we focused our attention on its physical and chemical characteristics, its cytotoxicity, and its role in the induction of the volatile organic compound (VOC) and/or polycyclic aromatic hydrocarbon (PAH)-metabolizing enzymes in human lung epithelial cells (A549). Size distribution showed that 92.15% of the collected PM were PM2.5 and the specific surface area was 1 m2/g. Inorganic (i.e. Fe, Al, Ca, Na, K, Mg, Pb, etc.) and organic (i.e. VOC, PAH, etc.) chemicals were found in collected PM, revealing that much of them derived from wind-borne dust from the industrial complex and the heavy motor vehicle traffic. The thermal desorption study indicated that organic chemicals were not only adsorbed onto the surface but also highly incrusted in the structure of PM. The lethal concentrations at 10% and 50% of collected PM were 23.72 microg/mL (or 6.33microg/cm2) and 118.60 microg/mL (or 31.63 microg/cm2), respectively. The VOC and/or PAH-coated onto PM induced significant increases in mRNA expressions of cytochrome P450 (cyp) 1a1, cyp2e1, cyp2f1, nadph quinone oxydo-reductase-1, and glutathione s-transferase-pi 1, versus controls. Hence, we concluded that the metabolic activation of the very low doses of VOC and/or PAH-coated onto the inorganic condensation nuclei from Dunkerque City's PM is one of the underlying mechanisms of action closely involved in its cytotoxicity in human lung epithelial cells.