Proton-induced fragmentation of carbon at energies below 100 MeV

Radiation effects caused by single cosmic ray particles have been studied for many years in radiobiological experiments for different biological objects and biological end-points. Additionally, single event effects in microelectronic devices have gained large interest. There are two fundamental mechanisms by which a single particle can cause radiation effects. On the one hand, a cosmic ray ion with high linear energy transfer can deposit a high dose along its path. On the other hand, in a nuclear collision, a high dose can be deposited by short range particles emitted from the target nucleus. In low earth orbits a large contribution to target fragmentation events originates from trapped protons which are encountered in the South Atlantic Anomaly. These protons have energies up to a few hundred MeV. We study the fragmentation of C, O and Si nuclei - the target nuclei of biological material and microelectronic devices - in nuclear collisions. Our aim is to measure production cross sections, energy spectra, emission directions and charge correlations of the emitted fragments. The present knowledge concerning these data is rather poor. M. Alurralde et al. have calculated cross sections and average energies of fragments produced from Si using the cascade-evaporation model. D.M. Ngo et al. have used the semiempirical cross section formula of Silberberg and Tsao to calculate fragment yields and the statistical model of Goldhaber to describe the reaction kinematics. Cross sections used in these models have uncertainties within a factor of two. Our data will help to test and improve existing models especially for energies below 300 MeV/nucleon. Charge correlations of fragments emitted in the same interaction are of particular importance, since high doses can be deposited if more than one heavy fragment with a short range is produced

The SCOUT-O3 Darwin Aircraft Campaign: rationale and mateorology

An aircraft measurement campaign involving the Russian high-altitude aircraft M55 Geophysica and the German DLR Falcon was conducted in Darwin, Australia in November and December 2005 as part of the European integrated project SCOUT-O3. The overall objectives of the campaign were to study the transport of trace gases through the tropical tropopause layer (TTL), mechanisms of dehydration close to the tropopause, and the role of deep convection in these processes. In this paper a detailed roadmap of the campaign is presented, including rationales for each flight, and an analysis of the local and large-scale meteorological context in which they were embedded. The campaign took place during the pre-monsoon season which is characterized by a pronounced diurnal evolution of deep convection including a mesoscale system over the Tiwi Islands north of Darwin known as �\x83¢Â�Â�HectorâÂ�Â�. This allowed studying in detail the role of deep convection in structuring the tropical tropopause region, in situ sampling convective overshoots above storm anvils, and probing the structure of anvils and cirrus clouds by Lidar and a suite of in situ instruments onboard the two aircraft. The large-scale flow during the first half of the campaign was such that local flights, away from convection, sampled air masses downstream of the âÂ�Â�cold trapâÂ�Â� region over Indonesia. Abundant cirrus clouds enabled the study of active dehydration, in particular during two TTL survey flights. The campaign period also encompassed a Rossby wave breaking event transporting stratospheric air to the tropical middle troposphere and an equatorial Kelvin wave modulating tropopause temperatures and hence the conditions for dehydration

Exposure and harm to combustion-derived wood particles

The human respiratory system is the gateway of entry for inhaled detritus from anthropogenic (e.g. combustion-derived (CD) particulate matter (PM; e.g. diesel exhaust and wood-burning PM). Adult humans inhale 20m3 of air and suspended debris (gases and particles) into the airways daily. Inhalation exposure to CDPM (Figure 1) is known to increase the risk of morbidity and mortality of lung and heart diseases in all exposed individuals. The physicochemical properties of size, surface area and presence of transition metals have been implicated as drivers of the oxidative capacity of CDPM. However, the precise role of reactive organic compounds (ROC) in ambient aerosols, present either in the gas or particle phase has not been fully-investigated for their relevance in the induction of the observed adverse health effects. When addressing the toxicity of inhalation hazards such as wood smoke CDPM, a model that resembles the human lung responding to toxic challenges is required. In our in vitro exposure studies, we utilised normal human bronchial epithelial (NHBE) cells grown at the air-liquid interface (ALI) using filter-well technology (Prytherch et al 2011), to create an in vivo-like 3-dimensional lung model. This model is a fully-differentiated, pseudo-stratified, muco-ciliary epithelium containing basal, serous, Clara, goblet and ciliated cells. NHBE cells were exposed to wood smoke derived from Spruce, Beech and Birch at a dose of 152µg/cm2: carbon black (CB; negative control; Monarch 120, Cabot UK; DQ12 quartz (positive control). Following exposure (24 hours), tissue integrity (i.e. transepithelial electrical resistance (TEER) was measured to reveal minor disruption to bronchial tissue integrity (Figure 2). However, changes in cellular energy levels (i.e. ATP) between the types of wood smokes (Figure 3), could infer the smoke acted as an irritant to the lung environment. Wood smoke exposure can depress the immune system and damage the layer of cells in the lungs that protect and cleanse the airways. Further work on the biological and histological impacts of wood smoke will allow us to reveal mechanisms behind the changes observed, as well identifying biomarkers of cell damage by specific CDPM ROCs. For vulnerable populations, such as people with asthma, chronic respiratory disease and those with cardiovascular disease, wood smoke is particularly harmful, even at short exposures it can prove dangerous. Wood smoke interferes with normal lung development in infants and children. It also increases children’s risk of lower respiratory infections such as bronchitis and pneumonia. Prytherch, Z., Job, C., Marshall, H., Oreffo, V., Foster, M. and BéruBé, K.A. (2011) Macro. Bios. 11, 1467–77. This work was supported by HICE (www.hice-vi.eu)

Exposure and harm to combustion-derived particles: Searching for biomarkers

The physicochemical properties of size, surface area and presence of transition metals have been implicated as drivers of the oxidative capacity of CDPM. However, the precise role of reactive organic compounds (ROC) in ambient aerosols, present either in the gas phase or the particle phase or in both phases, have not been fully-investigated for their relevance in the induction of the observed adverse health effects. Oxidation of fatty acids linked to the cell membrane phospholipids leads to many metabolites that have been used as markers of the process. Such metabolites have long been considered to be involved in two possibly inter-related processes: cell/tissue damage and signalling. As one approach to resolve the role played by ROCs, their effects on fatty acid and lipid metabolism in human lung tissues will be studied in detail by using the standard biochemical techniques and lipidomics

Influence of wood species on toxicity of log-wood stove combustion aerosols: A parallel animal and air-liquid interface cell exposure study on spruce and pine smoke

Background Wood combustion emissions have been studied previously either by in vitro or in vivo models using collected particles, yet most studies have neglected gaseous compounds. Furthermore, a more accurate and holistic view of the toxicity of aerosols can be gained with parallel in vitro and in vivo studies using direct exposure methods. Moreover, modern exposure techniques such as air-liquid interface (ALI) exposures enable better assessment of the toxicity of the applied aerosols than, for example, the previous state-of-the-art submerged cell exposure techniques. Methods We used three different ALI exposure systems in parallel to study the toxicological effects of spruce and pine combustion emissions in human alveolar epithelial (A549) and murine macrophage (RAW264.7) cell lines. A whole-body mouse inhalation system was also used to expose C57BL/6 J mice to aerosol emissions. Moreover, gaseous and particulate fractions were studied separately in one of the cell exposure systems. After exposure, the cells and animals were measured for various parameters of cytotoxicity, inflammation, genotoxicity, transcriptome and proteome. Results We found that diluted (1:15) exposure pine combustion emissions (PM1 mass 7.7 ± 6.5 mg m− 3, 41 mg MJ$^{Zahl}$) contained, on average, more PM and polycyclic aromatic hydrocarbons (PAHs) than spruce (PM1 mass 4.3 ± 5.1 mg m− 3, 26 mg MJ− 1) emissions, which instead showed a higher concentration of inorganic metals in the emission aerosol. Both A549 cells and mice exposed to these emissions showed low levels of inflammation but significantly increased genotoxicity. Gaseous emission compounds produced similar genotoxicity and a higher inflammatory response than the corresponding complete combustion emission in A549 cells. Systems biology approaches supported the findings, but we detected differing responses between in vivo and in vitro experiments. Conclusions Comprehensive in vitro and in vivo exposure studies with emission characterization and systems biology approaches revealed further information on the effects of combustion aerosol toxicity than could be achieved with either method alone. Interestingly, in vitro and in vivo exposures showed the opposite order of the highest DNA damage. In vitro measurements also indicated that the gaseous fraction of emission aerosols may be more important in causing adverse toxicological effects. Combustion aerosols of different wood species result in mild but aerosol specific in vitro and in vivo effects

Particulate matter from both heavy fuel oil and diesel fuel shipping emissions show strong biological effects on human lung cells at realistic and comparable in vitro exposure conditions

Background: Ship engine emissions are important with regard to lung and cardiovascular diseases especially in coastal regions worldwide. Known cellular responses to combustion particles include oxidative stress and inflammatory signalling. Objectives: To provide a molecular link between the chemical and physical characteristics of ship emission particles and the cellular responses they elicit and to identify potentially harmful fractions in shipping emission aerosols. Methods: Through an air-liquid interface exposure system, we exposed human lung cells under realistic in vitro conditions to exhaust fumes from a ship engine running on either common heavy fuel oil (HFO) or cleaner-burning diesel fuel (DF). Advanced chemical analyses of the exhaust aerosols were combined with transcriptional, proteomic and metabolomic profiling including isotope labelling methods to characterise the lung cell responses. Results: The HFO emissions contained high concentrations of toxic compounds such as metals and polycyclic aromatic hydrocarbon, and were higher in particle mass. These compounds were lower in DF emissions, which in turn had higher concentrations of elemental carbon (“soot”). Common cellular reactions included cellular stress responses and endocytosis. Reactions to HFO emissions were dominated by oxidative stress and inflammatory responses, whereas DF emissions induced generally a broader biological response than HFO emissions and affected essential cellular pathways such as energy metabolism, protein synthesis, and chromatin modification. Conclusions: Despite a lower content of known toxic compounds, combustion particles from the clean shipping fuel DF influenced several essential pathways of lung cell metabolism more strongly than particles from the unrefined fuel HFO. This might be attributable to a higher soot content in DF. Thus the role of diesel soot, which is a known carcinogen in acute air pollution-induced health effects should be further investigated. For the use of HFO and DF we recommend a reduction of carbonaceous soot in the ship emissions by implementation of filtration devices

An introduction to the SCOUT-AMMA stratospheric aircraft, balloons and sondes campaign in West Africa, August 2006: rationale and roadmap

A multi-platform field measurement campaign involving aircraft and balloons took place over West Africa between 26 July and 25 August 2006, in the frame of the concomitant AMMA Special Observing Period and SCOUT-O3 African tropical activities. Specifically aiming at sampling the upper troposphere and lower stratosphere, the high-altitude research aircraft M55 Geophysica was deployed in Ouagadougou (12.3° N, 1.7° W), Burkina Faso, in conjunction with the German D-20 Falcon, while a series of stratospheric balloon and sonde flights were conducted from Niamey (13.5° N, 2.0° E), Niger. The stratospheric aircraft and balloon flights intended to gather experimental evidence for a better understanding of large scale transport, assessing the effect of lightning on NOx production, and studying the impact of intense mesoscale convective systems on water, aerosol, dust and chemical species in the upper troposphere and lower stratosphere. The M55 Geophysica carried out five local and four transfer flights between southern Europe and the Sahel and back, while eight stratospheric balloons and twenty-nine sondes were flown from Niamey. These experiments allowed a characterization of the tropopause and lower stratosphere of the region. We provide here an overview of the campaign activities together with a description of the general meteorological situation during the flights and a summary of the observations accomplished