Measurement report : Long-range transport and the fate of dimethyl sulfide oxidation products in the free troposphere derived from observations at the high-altitude research station Chacaltaya (5240 m a.s.l.) in the Bolivian Andes

Dimethyl sulfide (DMS) is the primary natural contributor to the atmospheric sulfur burden. Observations concerning the fate of DMS oxidation products after long-range transport in the remote free troposphere are, however, sparse. Here we present quantitative chemical ionization mass spectrometric measurements of DMS and its oxidation products sulfuric acid (H2SO4), methanesulfonic acid (MSA), dimethylsulfoxide (DMSO), dimethylsulfone (DMSO2), methanesulfinic acid (MSIA), methyl thioformate (MTF), methanesulfenic acid (MSEA, CH3SOH), and a compound of the likely structure CH3S(O)(2)OOH in the gas phase, as well as measurements of the sulfate and methanesulfonate aerosol mass fractions. The measurements were performed at the Global Atmosphere Watch (GAW) station Chacaltaya in the Bolivian Andes located at 5240 m above sea level (a.s.l.). DMS and DMS oxidation products are brought to the Andean high-altitude station by Pacific air masses during the dry season after convective lifting over the remote Pacific ocean to 6000-8000 m a.s.l. and subsequent longrange transport in the free troposphere (FT). Most of the DMS reaching the station is already converted to the rather unreactive sulfur reservoirs DMSO2 in the gas phase and methanesulfonate (MS-) in the particle phase, which carried nearly equal amounts of sulfur to the station. The particulate sulfate at Chacaltaya is however dominated by regional volcanic emissions during the time of the measurement and not significantly affected by the marine air masses. In one of the FT events, even some DMS was observed next to reactive intermediates such as methyl thioformate, dimethylsulfoxide, and methanesulfinic acid. Also for this event, back trajectory calculations show that the air masses came from above the ocean (distance > 330 km) with no local surface contacts. This study demonstrates the potential impact of marine DMS emissions on the availability of sulfur containing vapors in the remote free troposphere far away from the ocean.Peer reviewe

Exposition professionnelle aux hydrocarbures aromatiques polycycliques (HAP) dans la poussière de bois

Introduction.- La bérylliose chronique est une granulomatose pulmonaire pour laquelle le diagnostic est rarement posé en raison d'une méconnaissance du risque d'exposition professionnelle au béryllium.En outre, le tableau clinique, les signes radiologiques et les symptômes ressemblent a` une sarcoïdose. Ainsi, la fréquence de la maladie est probablement sous-estimée malgré l'utilisation de béryllium dans la fabrication de nombreux produits industriels et techniques en Suisse, tels que ressorts, prothèses dentaires, micro-électronique... Comme aide au diagnostic, un test de prolifération lymphocytaire au béryllium (BeLPT) a été développé pour évaluer la réponse immunocellulaire spécifique au béryllium. Mais celui-ci présente des inconvénients : utilisation de produits radioactifs, variabilité interlaboratoire importante, valeur prédictive contesteé. L'utilisation de l'Elispot, évaluant également la réponse lymphocytaire pourrait être une alternative au BeLPT. Objectifs.- Les objectifs de l'étude sont, d'une part, de déceler parmi les cas de sarcoïdose du registre SIOLD (Swiss Group for Interstitial and Orphan Lung Diseases) des cas de bérylliose sous-diagnostiqués et, d'autre part, d'améliorer les tests de de´pistage (questionnaire et test immunologique) de sensibilisation et de diagnostic. Méthode.- Cent soixante autoquestionnaires évaluant l'exposition professionnelle au béryllium ont été adressés à des patients référencés dans le registre SIOLD, souffrant de sarcoïdose. Les patients relatant dans l'autoquestionnaire un contact professionnel avec le béryllium ont bénéficié d'une visite médicale à l'Institut universitaire romand de santé au travail (IST) comportant une anamnèse professionnelle, un questionnaire spécifique à l'exposition au béryllium (questionnaire de Cherry) et une prise de sang. Par la suite, le sang a été analysé par Elispot pour évaluer la possibilité d'une sensibilisation au béryllium. En parallèle, des patients déjà diagnostiqués pour une bérylliose par un BeLPT ont servi de cas contrôle positifs pour la mise en place du test. Résultats.- Cinquante pour cents des autoquestionnaires adressés aux patients du registre SIOLD ont été renvoyés. Parmi ceux-ci, 33 %(26 personnes) rapportaient une exposition professionnelle possible au béryllium et ont été reçus a` l'IST pour compléter l'anamnèse professionnelle et répondre au questionnaire adapté de Cherry. Il ressort de ce questionnaire que 3 personnes ont effectivement travaillé avec du béryllium au cours de leur carrière professionnelle et que 4 ont potentiellement été exposées dans le contexte de leur environnement professionnel. Tous les patients ont été testés par Elispot, mais aucun n'a montré de prolifération évoquant une sensibilisation au béryllium. Des résultats supplémentaires devraient être disponibles dès février. Conclusion.- Au vu de ces résultats où seules 7 personnes sur les 80 ayant répondu au questionnaire (8 %) sont suspectées d'avoir été exposées directement ou indirectement au béryllium au cours de leur activité professionnelle, il est possible que le risque d'exposition au béryllium soit anecdotique, malgré une utilisation importante de ce métal dans certaines régions de Suisse. Une hypothèse envisageable est que la population de l'étude ne soit pas représentative de la population exposée. En outre, le fait que les tests lymphocytaires effectués sur les 7 personnes ayant rapporté une exposition au béryllium soient revenus négatifs peut être expliqué de 2 manières : soit que chez ces personnes, la maladie pulmonaire n'est pas due au béryllium, même si l'anamnèse professionnelle est positive et qu'il s'agit bien d'une sarcoïdose, soit que la prise de corticoïdes modifie la réponse immunitaire, soit que le test n'est pas suffisamment sensible

Toxicity of TiO2 nanoparticles on soil nitrification at environmentally relevant concentrations: Lack of classical dose-response relationships

Titanium-dioxide nanoparticles (TiO2-NPs) are increasingly released in agricultural soils through, e.g. biosolids, irrigation or nanoagrochemicals. Soils are submitted to a wide range of concentrations of TiO2-NPs depending on the type of exposure. However, most studies have assessed the effects of unrealistically high concentrations, and the dose-response relationships are not well characterized for soil microbial communities. Here, using soil microcosms, we assessed the impact of TiO2-NPs at concentrations ranging from 0.05 to 500mg kg(-1)dry-soil, on the activity and abundance of ammonia-oxidizing archaea (AOA) and bacteria (AOB), and nitrite-oxidizing bacteria (Nitrobacter and Nitrospira). In addition, aggregation and oxidative potential of TiO2-NPs were measured in the spiking suspensions, as they can be important drivers of TiO2-NPs toxicity. After 90days of exposure, non-classical dose-response relationships were observed for nitrifier abundance or activity, making threshold concentrations impossible to compute. Indeed, AOA abundance was reduced by 40% by TiO2-NPs whatever the concentration, while Nitrospira was never affected. Moreover, AOB and Nitrobacter abundances were decreased mainly at intermediate concentrations nitrification was reduced by 25% at the lowest (0.05mgkg(-1)) and the highest (100 and 500mgkg(-1)) TiO2-NPs concentrations. Path analyses indicated that TiO2-NPs affected nitrification through an effect on the specific activity of nitrifiers, in addition to indirect effects on nitrifier abundances. Altogether these results point out the need to include very low concentrations of NPs in soil toxicological studies, and the lack of relevance of classical dose-response tests and ecotoxicological dose metrics (EC50, IC50...) for TiO2-NPs impact on soil microorganisms

Sources contribution to the oxidative potential of PM₁₀ at 15 French sites.

International audienc

Oxidative stress-induced inflammation in susceptible airways by anthropogenic aerosol

Ambient air pollution is one of the leading five health risks worldwide. One of the most harmful air pollutants is particulate matter (PM), which has different physical characteristics (particle size and number, surface area and morphology) and a highly complex and variable chemical composition. Our goal was first to comparatively assess the effects of exposure to PM regarding cytotoxicity, release of pro-inflammatory mediators and gene expression in human bronchial epithelia (HBE) reflecting normal and compromised health status. Second, we aimed at evaluating the impact of various PM components from anthropogenic and biogenic sources on the cellular responses. Air-liquid interface (ALI) cultures of fully differentiated HBE derived from normal and cystic fibrosis (CF) donor lungs were exposed at the apical cell surface to water-soluble PM filter extracts for 4 h. The particle dose deposited on cells was 0.9–2.5 and 8.8–25.4 μg per cm2 of cell culture area for low and high PM doses, respectively. Both normal and CF HBE show a clear dose-response relationship with increasing cytotoxicity at higher PM concentrations. The concurrently enhanced release of pro-inflammatory mediators at higher PM exposure levels links cytotoxicity to inflammatory processes. Further, the PM exposure deregulates genes involved in oxidative stress and inflammatory pathways leading to an imbalance of the antioxidant system. Moreover, we identify compromised defense against PM in CF epithelia promoting exacerbation and aggravation of disease. We also demonstrate that the adverse health outcome induced by PM exposure in normal and particularly in susceptible bronchial epithelia is magnified by anthropogenic PM components. Thus, including health-relevant PM components in regulatory guidelines will result in substantial human health benefits and improve protection of the vulnerable population

Exploring the toxicity of the new emerging toxicant 6PPD-Quinone to environmental microorganisms.

International audienceThis study examines the toxicity of the newly discovered molecule 6PPD-Quinone (6PPD-Q) to selected environmental microorganisms. After decades of intense research, this molecule, derived from a very common antioxidant (6PPD) used as a car tyre protector, has recently been identified as the main cause of the death of Coho salmon in the north-western United States, and is suspected to be a common toxicant worldwide through tyre treading. 6PPD-Q is produced by the ozone oxidation of 6PPD during the ageing of tyre particles after deposition on roads. The 6PPD-Q produced in this way at low concentrations can accumulate in surface waters after storm water runoff, resulting in acute mortality of salmon migrating to urban streams. In this context, we assessed the toxicity of a wide range of 6PPD-Q concentrations through its intrinsic oxidative potential, and through the response of single-cell microorganisms commonly found in the environment (3 bacterial species, a yeast, an algal strain and an amoeba) by cell tracking with various modern techniques. To assess the mechanisms involved in 6PPD-Q toxicity, particular attention was paid to model bacteria and their capacity for resistance (role of efflux pumps in the response to the toxicant) and degradation of the molecule, monitored by LC-MS/MS. Overall, our results showed that 6PPD-quinone had no or limited impact on all microorganisms tested, at the realistic concentrations tested. For some bacteria and yeasts, a slight inhibition of growth was observed with some concentrations, while other organisms were not impacted at all or were even stimulated by the presence of 6PPD-quinone, probably used as a carbon source by these organisms. Further investigations are needed to assess the potential chronic effects of 6PPD-Q on microbial communities in natural waters and on their ecosystem services

Exploring the toxicity of the new emerging toxicant 6PPD-Quinone to environmental microorganisms.

International audienceThis study examines the toxicity of the newly discovered molecule 6PPD-Quinone (6PPD-Q) to selected environmental microorganisms. After decades of intense research, this molecule, derived from a very common antioxidant (6PPD) used as a car tyre protector, has recently been identified as the main cause of the death of Coho salmon in the north-western United States, and is suspected to be a common toxicant worldwide through tyre treading. 6PPD-Q is produced by the ozone oxidation of 6PPD during the ageing of tyre particles after deposition on roads. The 6PPD-Q produced in this way at low concentrations can accumulate in surface waters after storm water runoff, resulting in acute mortality of salmon migrating to urban streams. In this context, we assessed the toxicity of a wide range of 6PPD-Q concentrations through its intrinsic oxidative potential, and through the response of single-cell microorganisms commonly found in the environment (3 bacterial species, a yeast, an algal strain and an amoeba) by cell tracking with various modern techniques. To assess the mechanisms involved in 6PPD-Q toxicity, particular attention was paid to model bacteria and their capacity for resistance (role of efflux pumps in the response to the toxicant) and degradation of the molecule, monitored by LC-MS/MS. Overall, our results showed that 6PPD-quinone had no or limited impact on all microorganisms tested, at the realistic concentrations tested. For some bacteria and yeasts, a slight inhibition of growth was observed with some concentrations, while other organisms were not impacted at all or were even stimulated by the presence of 6PPD-quinone, probably used as a carbon source by these organisms. Further investigations are needed to assess the potential chronic effects of 6PPD-Q on microbial communities in natural waters and on their ecosystem services

Seasonal variations of metals and metalloids in atmospheric particulate matter (PM2.5) in the urban megacity Hanoi

International audienceFine particulate matter (PM2.5) in the atmosphere is of particular concern due to its adverse effects on human health and its impact on global warming. southeast Asia is a hot spot for fossil fuel combustion with recurrent release of large plumes spreading over the ocean and neighbouring countries. Due to the complex mixture of PM2.5, the atmospheric sources contribution related to local and regional emissions in Hanoi (northern Vietnam) is still ill-constrained. Here, we present a year-round study (November 2019 to December 2020) with measurements of 18 metals and metalloids (MM) and lead isotopes in the PM2.5 fraction to quantify weather-related atmospheric inputs and to assess risk to human health. Anthropogenic inputs from fossil fuel combustion accounted for about 80% in PM2.5. We found high PM2.5-bound MM concentrations often exceeding national and global standards with a low risk of chronic inhalation and carcinogenicity, mainly attributable to Cr. During winter monsoon (northeastern winds), stable weather conditions led to the enrichment of long-range air mass transport of local particulate emissions. During the summer monsoon (southeastern winds), warm and moist winds reduced coal contribution in PM2.5. Our study highlights the need for a strict implementation of policies to control hazardous MM emissions by reducing fossil fuel combustion. On the one hand, reducing coal-related activities could reduce Cr emissions and therefore improve the risks to human health. On the other hand, public policies should encourage conversion to green transport in order to reduce petrol combustion and thus limit global warming