Search

Coloured pyrotechnic smokes are frequently used in the military field and occasionally by civilians, but their health hazards have been little studied. The main concern could rise from inhalation of smoke particles. Our previous study showed that acute exposure to particles from a red signalling smoke (RSS) induced an antioxidant and inflammatory responses in small airway epithelial cells. The aim of this study was to further explore the toxicity of RSS particles at a more proximal level of the respiratory tract, using normal human bronchial epithelial cells grown at the Air-Liquid Interface. Acute exposure (24 h) induced an oxidative stress that persisted 24 h post-exposure, associated with particle internalization and epithelium morphological changes (cuboidal appearance and loss of cilia). Repeated exposures (4×16h) to RSS particles did not trigger oxidative stress but cell morphological changes occurred. Overall, this study provides a better overview of the toxic effects of coloured smoke particles., 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 © 2023 Elsevier B.V. All rights reserved.)

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.)

Pyrotechnic smokes are widely used in civilian and military applications. The major issue arise from the release of particles after smoke combustion but the health risks related to their exposure are poorly documented whereas toxicity of airborne particles on the respiratory target are very well known. Therefore, this study aimed to explore the in vitro toxicity of the particle fraction of different pyrotechnic smokes. Particles from a red signalling smoke (RSS), an hexachloroethane-based obscuring smoke (HC-OS) and an anti-intrusion smoke (AIS) were collected from the cloud. RSS particles displayed the highest organic fraction (quinones and polycyclic aromatic hydrocarbons) of the three samples characterized. AIS particles contained K and cholesterol derivatives. HC-OS particles were mainly metallic with very high concentrations of Al, Fe and Ca. Intrinsic oxidative potential of smoke particles was measured with two assays. Depletions of DTT by RSS particles was greater than depletion obtained with AIS and HC-OS particles but depletion of acid ascorbic (AA) was only observed with HC-OS particles. In vitro toxicity was assessed by exposing human small airway epithelial cells (SAEC) to various concentrations of particles. After 24 h of exposure, cell viability was not affected but significant modifications of mRNA expression of antioxidant (SOD-1 and -2, catalase, HO-1, NQO-1) and inflammatory markers (IL-6, IL-8, TNF-α) were observed and were dependent on smoke type. Particles rich in metal, such as HC-OS, induced a greatest depletion of AA and a greatest inflammatory response, whereas particles rich in organic compounds, such as RSS, induced a greatest DTT depletion and a greatest antioxidant response. In conclusion, the three smoke particles have an intrinsic oxidative potential and triggered a cell adaptive response. Our study improved the knowledge of particle toxicity of pyrotechnic smokes and scientific approach developed here could be used to study other type of particles., (Copyright © 2022 The Authors. Published by 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.)

Biodiesel is considered as a valuable and less toxic alternative to diesel. However, cellular and molecular effects of repeated exposure to biodiesel emissions from a recent engine equipped with a diesel particle filter (DPF) remain to be characterized. To gain insights about this point, the lung transcriptional signatures were analyzed for rats (n = 6 per group) exposed to filtered air, 30% rapeseed biodiesel (B30) blend or reference diesel (RF0), upstream and downstream a DPF, for 3 weeks (3 h/day, 5 days/week). Genomic analysis revealed a modest regulation of gene expression level (lower than a 2-fold) by both fuels and a higher number of genes regulated downstream the DPF than upstream, in response to either RF0 or to B30 exhaust emissions. The presence of DPF was found to notably impact the lung gene signature of rats exposed to B30. The number of genes regulated in common by both fuels was low, which is likely due to differences in concentrations of regulated pollutants in exhausts, notably for compound organic volatiles, polycyclic aromatic hydrocarbons, NO or NOx. Nevertheless, we have identified some pathways that were activated for both exhaust emissions, such as integrin-, IGF-1- and Rac-signaling pathways, likely reflecting the effects of gas phase products. By contrast, some canonical pathways relative to "oxidative phosphorylation" and "mitochondrial dysfunction" appear as specific to B30 exhaust emission; the repression of transcripts of mitochondrial respiratory chain in lung of rats exposed to B30 downstream of DPF supports the perturbation of mitochondria function. This study done with a recent diesel engine (compliant with the European IV emission standard) and commercially-available fuels reveals that the diesel blend composition and the presence of an after treatment system may modify lung gene signature of rats repeatedly exposed to exhaust emissions, however in a rather modest manner., Competing Interests: Declaration of competing interest The authors have no conflict to interest to declare., (Copyright © 2020. Published by Elsevier Ltd.)

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.)

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.)

Diesel exhaust (DE) contributes to air pollution, an important risk factor for cardiovascular diseases. However, the mechanisms by which DE exposure induces cardiovascular dysfunction remain unknown and there is still debate on the contribution of the primary particulate matter (PM) fraction compared to the gaseous phase. Although the mitochondria play a key role in the events leading to cardiovascular diseases, their role in DE-induced cardiovascular effects has not been investigated. The aim of this study was to highlight cardiac and mitochondrial events that could be disrupted following acute and/or repeated DE exposures and the contribution of gaseous pollutants to these effects. To address this question, Wistar rats were exposed to DE generated under strictly controlled and characterized conditions and extracted upstream or downstream of the diesel particulate filter (DPF). Evaluation of the cardiac function after acute DE exposure showed a disturbance in echocardiographic parameters, which persisted and worsened after repeated exposures. The presence of the DPF did not modify the cardiovascular dysfunction revealing an important implication of the gas phase in this response. Surprisingly, redox parameters were not altered by DE exposures while an alteration in mitochondrial oxidative capacity was observed. Exploration of the mitochondrial function demonstrated a more specific alteration in complex I of the respiratory chain after repeated exposures, which was further confirmed by transcriptional analysis of left ventricular (LV) tissue. In conclusion, this work provides new insights into cardiovascular effects induced by DE, demonstrating a cardiac mitochondrial impairment associated with the gaseous phase. These effects suggest deleterious consequences in terms of cardiac function for vulnerable populations with underlying energy deficit such as patients with heart failure or the elderly., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

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.)

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.)

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.)

A room-temperature continuous-wave (CW) quantum cascade laser (QCL)-based methane (CH4) sensor operating in the mid-infrared near 8 μm was developed for continuous measurement of CH4 concentrations in ambient air. The well-isolated absorption line (7F2,4 ← 8F1,2) of the ν4 fundamental band of CH4 located at 1255.0004 cm(-1) was used for optical measurement of CH4 concentration by direct absorption in a White-type multipass cell with an effective path-length of 175 m. A 1σ (SNR = 1) detection limit of 33.3 ppb in 218 s was achieved with a measurement precision of 1.13%. The developed sensor was deployed in a campaign of measurements of time series CH4 concentration on a site near a suburban traffic road in Dunkirk (France) from 9th to 22nd January 2013. An episode of high CH4 concentration of up to ~3 ppm has been observed and analyzed with the help of meteorological parameters combined with back trajectory calculation using the Hybrid Single Particle Lagrangian Integrated Trajectory (HYSPLIT) model of NOAA.

Concentrations of 11 elements (As, Cd, Cr, Cu, Fe, Mn, Ni, Pb, Se,V and Zn) were quantified in liver and muscle from two commercially important fish species from the Senegalese coast. The fish, a small pelagic species (the round sardinella) and a benthic species (the Senegalese sole) were collected from five sites during the dry and wet seasons in 2013. For both species, elements were more concentrated in liver than in muscle. There was no clear seasonal pattern in concentration of elements, however inter-site differences were observed. We found significant differences in element concentrations between the two studied species, likely associated with their behavior, feeding and habitat use. The concentrations of Cd, Fe, and Pb were significantly higher in sardinella whereas concentration of As, Cu, Cr, Mn and Se were highest in sole. The concentration of cadmium was particularly high in the liver of sardinella (from 0.9 to 56 mg kg(-1), with a mean ± sd of 17.2 ± 11.5 mg kg(-1)) and may be related to anthropogenic pressure such as the phosphate industry but also to the upwelling current which brings dissolved elements to the surface that are taken up by plankton. The results showed that concentrations of Cd and Pb were below the limit values established by the European Community and pose no threat to public health., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

The main objective of this work was to determine the impact of pesticide use practices on vegetables contamination in the Niayes zone of Dakar. A preliminary survey involving 200 farmers, showed the application of pesticides belonging to different groups on vegetable crops. Use practices in terms of application intervals and methods, measuring tools and dosage were not in compliance with good agricultural practices. In view of survey results, investigations on vegetable contamination were conducted. Therefore, 175 vegetable samples including cabbage (31 samples), lettuce (88 samples), tomato (57 samples) collected from four sites of the Niayes zone during four campaigns, were analyzed for residues of 21 pesticides, eighteen of which (18) were cited to be used by farmers. The results indicated that 65% of tomato samples, 71% of lettuce and 93% of cabbage contained one or more detectable residues. Among the monitored pesticides dicofol, chlorpyrifos, DDTs, dimethoate, and λ-cyhalothrin were the most predominant, found in at least 35% of samples for each vegetable. The frequencies of pesticide detection were, generally in agreement with the citation frequencies. The results provided important information on vegetable contamination status and pointed an urgent need to control pesticide use., (Copyright © 2015. Published by Elsevier Ltd.)

Trace metals have the potential to associate with sediments that have been recognised as significant source of contamination for the benthic environment. The current study aims assessing the trace metals contamination level in sediments from Dakar coast and Saint Louis estuary, and to examine their bioavailability to predict potential toxicity of sediments. Surface sediment samples were collected between June 2012 and January 2013 in three sampling periods from eight stations. Trace metals were analysed using inductively coupled plasma-optical emission spectrometer. Geoaccumulation indexes (Igeo) showed strong pollution by Cd, Cr, Cu and Pb confirmed by enrichment factor (EF) suggesting that these metals derived from anthropogenic sources. Toxicity indexes exceeded one in several sites suggesting the potential effects on sediment-dwelling organisms, which may constitute a risk to populations' health. However, seasonal variability of metal bioavailability was noted, revealing the best period to monitor metal contamination. From an ecotoxicological point of view, concentrations of Cd, Cr, Cu and Pb were above the effects range low threshold limit of the sediment quality guidelines for adverse biological effects. In addition, with Pb concentrations above the effect range medium values in some sites, biological effects may occur., (Copyright © 2014 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.)

A new chelating matrix, SiNP, has been prepared by immobilizing 1.5-dimethyl-1H-pyrazole-3-carbaldehyde on silica gel modified with 3-aminopropyl-trimethoxysilane. This new chelating material was well characterized by elemental analysis, FT-IR spectroscopy, cross polarization magic angle spinning solid state 13C-NMR, nitrogen adsorption-desorption isotherm, BET surface area, BJH pore size, and scanning electron microscopy (SEM). The new product exhibits good chemical and thermal stability as determined by thermogravimetry curves (TGA). The new prepared material was used as an adsorbent for the solid-phase extraction (SPE) of Pb(II), Cd(II), Cu(II) and Zn(II) from aqueous solutions using a batch method, prior to their determination by flame atomic adsorption spectrometry. The adsorption capacity was investigated using kinetics and pH effects. Common coexisting ions did not interfere with separation and determination.

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.)

This paper presents the synthesis, the structural determination and the sensing capabilities toward Volatile Organic Compounds (VOCs) of a new class of fluorescent indolizine-cyclodextrin sensors. Two different pathways, both involving bipyridinium ylides and 6-amino-b-cyclodextrin, have been used to carry out the synthesis of these sensors. The macrocycle structures were dominantly established by ¹H-NMR spectra and systematically studied by molecular modelling (MM3, AM1, AM1-COSMO methods). The sensing capabilities of the sensors were evaluated by emission of fluorescence, during the inclusion of the guest (adamantanol or aromatic derivatives) into the cyclodextrin (CD) host cavity. The host/guest complex formation was investigated by formation constant determinations, using experimental methods, coupled with theoretical calculations of formation energies using a specific docking procedure. Both experimental and theoretical results suggest that some compounds would make very attractive sensors for VOC detection. Some compounds could also be taken into consideration as biological markers.

Volatile Organic Compounds (VOCs) in the air provoke health and environmental concerns. This paper focuses on the absorption method to treat industrial polluted air loaded with VOCs. The key variable of this treatment being the choice of a suitable liquid absorbent, the aim of this research work is to investigate the effectiveness and the regeneration of a new potential family of absorbent: cyclodextrins (CDs). All CDs derivatives tested are able to decrease the Henry's law constant of toluene: a reduction of volatility up to 95% may be obtained, depending on CD nature and concentration. Moreover, absorption experiments show that beta-CD, which presents the highest absorption ability, is 250 time more efficient than water. The absorption efficiency is not totally correlated with static experiments, suggesting that, in addition to Henry's law constants and inclusion compounds stability, toluene diffusion into such solutions has to be taken into account. It is also to be noted that salt and pH variations seem to have little influence on the absorption capacity of CDs, which may be of great interest for industrial applications. Finally, since production of solid compounds was not observed during these experiments and since temperature decreases the capture ability in a drastic way, regeneration of the washing solution can be achieved by heating the solution in combination with air stripping.

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.

In order to study the enzymatic mechanisms involved in the successive steps of BaP degradation by a Deuteromycete fungus Fusarium solani, we developed an indirect approach by using inhibitors of enzymes. We used either specific inhibitors of peroxidases (i.e. salicylhydroxamic acid) and of cytochrome P-450 (i.e. piperonyl butoxyde) or inhibitors of both enzymes (i.e. potassium cyanide). Surprisingly, no expected decrease of BaP degradation was observed with most inhibitors tested. On the contrary, more BaP was degraded. Only butylated hydroxytoluene, which acts as a free radical scavenger, inhibited BaP degradation. The inhibition of these enzymes, which use H(2)O(2) as a cosubstrate, might have resulted in an increase of hydrogen peroxide availability in the fungal cultures. This enhancement could induce formation of reactive oxygen species (ROS) which might be the agents that initiate benzo[a]pyrene oxidation. This study proposed a hypothetic alternative metabolic pathway involved in PAH metabolism by Fusarium solani.

Measurements of benzene concentration based on high-resolution laser absorption spectroscopy by use of the R(6) transition in the nu(4) fundamental vibrational band near 14.8 mum (676.6 cm(-1)) are reported. These measurements were performed with a tunable continuous-wave, mid-infrared spectroscopic light source that employs difference-frequency mixing of two Ti:sapphire lasers in a GaSe nonlinear optical crystal. A minimum benzene concentration detection of ~11.5 parts in 10(6) was realized at a reduced pressure of 40 mbars.