Species Richness-Environment Relationships of European Arthropods at Two Spatial Grains: Habitats and Countries

We study how species richness of arthropods relates to theories concerning net primary productivity, ambient energy, water-energy dynamics and spatial environmental heterogeneity. We use two datasets of arthropod richness with similar spatial extents (Scandinavia to Mediterranean), but contrasting spatial grain (local habitat and country). Samples of ground-dwelling spiders, beetles, bugs and ants were collected from 32 paired habitats at 16 locations across Europe. Species richness of these taxonomic groups was also determined for 25 European countries based on the Fauna Europaea database. We tested effects of net primary productivity (NPP), annual mean temperature (T), annual rainfall (R) and potential evapotranspiration of the coldest month (PETmin) on species richness and turnover. Spatial environmental heterogeneity within countries was considered by including the ranges of NPP, T, R and PETmin. At the local habitat grain, relationships between species richness and environmental variables differed strongly between taxa and trophic groups. However, species turnover across locations was strongly correlated with differences in T. At the country grain, species richness was significantly correlated with environmental variables from all four theories. In particular, species richness within countries increased strongly with spatial heterogeneity in T. The importance of spatial heterogeneity in T for both species turnover across locations and for species richness within countries suggests that the temperature niche is an important determinant of arthropod diversity. We suggest that, unless climatic heterogeneity is constant across sampling units, coarse-grained studies should always account for environmental heterogeneity as a predictor of arthropod species richness, just as studies with variable area of sampling units routinely consider area.

Translocation and potential neurological effects of fine and ultrafine particles a critical update

ABSTRACT: Particulate air pollution has been associated with respiratory and cardiovascular disease. Evidence for cardiovascular and neurodegenerative effects of ambient particles was reviewed as part of a workshop. The purpose of this critical update is to summarize the evidence presented for the mechanisms involved in the translocation of particles from the lung to other organs and to highlight the potential of particles to cause neurodegenerative effects.Fine and ultrafine particles, after deposition on the surfactant film at the air-liquid interface, are displaced by surface forces exerted on them by surfactant film and may then interact with primary target cells upon this displacement. Ultrafine and fine particles can then penetrate through the different tissue compartments of the lungs and eventually reach the capillaries and circulating cells or constituents, e.g. erythrocytes. These particles are then translocated by the circulation to other organs including the liver, the spleen, the kidneys, the heart and the brain, where they may be deposited. It remains to be shown by which mechanisms ultrafine particles penetrate through pulmonary tissue and enter capillaries. In addition to translocation of ultrafine particles through the tissue, fine and coarse particles may be phagocytized by macrophages and dendritic cells which may carry the particles to lymph nodes in the lung or to those closely associated with the lungs. There is the potential for neurodegenerative consequence of particle entry to the brain. Histological evidence of neurodegeneration has been reported in both canine and human brains exposed to high ambient PM levels, suggesting the potential for neurotoxic consequences of PM-CNS entry. PM mediated damage may be caused by the oxidative stress pathway. Thus, oxidative stress due to nutrition, age, genetics among others may increase the susceptibility for neurodegenerative diseases. The relationship between PM exposure and CNS degeneration can also be detected under controlled experimental conditions. Transgenic mice (Apo E -/-), known to have high base line levels of oxidative stress, were exposed by inhalation to well characterized, concentrated ambient air pollution. Morphometric analysis of the CNS indicated unequivocally that the brain is a critical target for PM exposure and implicated oxidative stress as a predisposing factor that links PM exposure and susceptibility to neurodegeneration.Together, these data present evidence for potential translocation of ambient particles on organs distant from the lung and the neurodegenerative consequences of exposure to air pollutants.

The role of macrophages in the clearance of inhaled ultrafine titanium dioxide particles

The role of macrophages in the clearance of particles with diameters less than 100 nm (ultrafine or nanoparticles) is not well established, although these particles deposit highly efficiently in peripheral lungs, where particle phagocytosis by macrophages is the primary clearance mechanism. To investigate the uptake of nanoparticles by lung phagocytes, we analyzed the distribution of titanium dioxide particles of 20 nm count median diameter in macrophages obtained by bronchoalveolar lavage at 1 hour and 24 hours after a 1-hour aerosol inhalation. Differential cell counts revealing greater than 96% macrophages and less than 1% neutrophils and lymphocytes excluded inflammatory cell responses. Employing energy-filtering transmission electron microscopy (EFTEM) for elemental microanalysis, we examined 1,594 macrophage profiles in the 1-hour group (n = 6) and 1,609 in the 24-hour group (n = 6). We found 4 particles in 3 macrophage profiles at 1 hour and 47 particles in 27 macrophage profiles at 24 hours. Model-based data analysis revealed an uptake of 0.06 to 0.12% ultrafine titanium-dioxide particles by lung-surface macrophages within 24 hours. Mean (SD) particle diameters were 31 (8) nm at 1 hour and 34 (10) nm at 24 hours. Particles were localized adjacent (within 13-83 nm) to the membrane in vesicles with mean (SD) diameters of 592 (375) nm at 1 hour and 414 (309) nm at 24 hours, containing other material like surfactant. Additional screening of macrophage profiles by conventional TEM revealed no evidence for agglomerated nanoparticles. These results give evidence for a sporadic and rather unspecific uptake of TiO(2)-nanoparticles by lung-surface macrophages within 24 hours after their deposition, and hence for an insufficient role of the key clearance mechanism in peripheral lungs.

Effects of combustion-derived ultrafine particles and manufactured nanoparticles on heart cells in vitro

Evidence from epidemiological studies indicates that acute exposure to airborne pollutants is associated with an increased risk of morbidity and mortality attributed to cardiovascular diseases. The present study investigated the effects of combustion-derived ultrafine particles (diesel exhaust particles) as well as engineered nanoparticles (titanium dioxide and single-walled carbon nanotubes) on impulse conduction characteristics, myofibrillar structure and the formation of reactive oxygen species in patterned growth strands of neonatal rat ventricular cardiomyocytes in vitro. Diesel exhaust particles as well as titanium dioxide nanoparticles showed the most pronounced effects. We observed a dose-dependent change in heart cell function, an increase in reactive oxygen species and, for titanium dioxide, we also found a less organized myofibrillar structure. The mildest effects were observed for single-walled carbon nanotubes, for which no clear dose-dependent alterations of theta and dV/dt(max) could be determined. In addition, there was no increase in oxidative stress and no change in the myofibrillar structure. These results suggest that diesel exhaust as well as titanium dioxide particles and to a lesser extent also single-walled carbon nanotubes can directly induce cardiac cell damage and can affect the function of the cells.

A ~ 32-70 K formation temperature range for the ice grains agglomerated by Comet 67P/Churyumov-Gerasimenko

Grand Canonical Monte Carlo simulations are used to reproduce the N₂/CO ratio ranging between 1.7 x 10⁻³ and 1.6 x 10⁻² observed in situ in the Jupiter-family comet 67 P/Churyumov-Gerasimenko (67 P) by the ROSINA mass spectrometer on board the Rosetta spacecraft. By assuming that this body has been agglomerated from clathrates in the protosolar nebula (PSN), simulations are developed using elaborated interatomic potentials for investigating the temperature dependence of the trapping within a multiple-guest clathrate formed from a gas mixture of CO and N₂ in proportions corresponding to those expected for the PSN. By assuming that 67 P agglomerated from clathrates, our calculations suggest the cometary grains must have been formed at temperatures ranging between ~ 31.8 and 69.9 K in the PSN to match the N₂/CO ratio measured by the ROSINA mass spectrometer. The presence of clathrates in Jupiter-family comets could then explain the potential N₂ depletion (factor of up to ~ 87 compared to the protosolar value) measured in 67 P/Churyumov-Gerasimenko.

Effect of locally increased zinc contents on zinc transport from the flag leaf lamina to the maturing grains of wheat

From previous experiments, it was evident that the accumulation of zinc in maturing wheat grains is highly regulated, but the regulatory mechanisms involved are not yet identified. In this study, we determined the transfer of radiolabelled zinc (fed directly into a leaf flap) from the flag leaf lamina to the grains. We also determined how this zinc transfer was affected by feeding additional unlabeled zinc (1 μmol per plant) either into the flag leaf sheath or the peduncle. Most of the 65Zn was retained in the feeding flap. A high percentage of the zinc exported from the flap accumulated in the grains with little accumulation of radiolabel in the other parts of the shoot. Unlabeled zinc remained mainly in the feeding flap and in the parts reached by the transpiration stream from the feeding position. The transfer of radiolabelled zinc was essentially not influenced by unlabeled zinc fed into another plant part. Our results suggest that the loading of zinc into the phloem and the mass flow in the sieve tubes might regulate zinc redistribution within the wheat shoot.