6 research outputs found

    Controlled exposure to diesel exhaust and traffic noise - Effects on oxidative stress and activation in mononuclear blood cells

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    Particulate air pollution increases risk of cancer and cardiopulmonary disease, partly through oxidative stress. Traffic-related noise increases risk of cardiovascular disease and may cause oxidative stress. In this controlled random sequence study, 18 healthy subjects were exposed for 3h to diesel exhaust (DE) at 276μg/m(3) from a passenger car or filtered air, with co-exposure to traffic noise at 48 or 75dB(A). Gene expression markers of inflammation, (interleukin-8 and tumor necrosis factor), oxidative stress (heme oxygenase (decycling-1)) and DNA repair (8-oxoguanine DNA glycosylase (OGG1)) were unaltered in peripheral blood mononuclear cells (PBMCs). No significant differences in DNA damage levels, measured by the comet assay, were observed after DE exposure, whereas exposure to high noise levels was associated with significantly increased levels of hOGG1-sensitive sites in PBMCs. Urinary levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine were unaltered. In auxiliary ex vivo experiments whole blood was incubated with particles from the exposure chamber for 3h without effects on DNA damage in PBMCs or intracellular reactive oxygen species production and expression of CD11b and CD62L adhesion molecules in leukocyte subtypes

    External trade monthly statistics 1/1988/Commerce exterieur statistiques mensuelles 1988.1

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    In urban environments, airborne particles are continuously emitted, followed by atmospheric aging. Also, particles emitted elsewhere, transported by winds, contribute to the urban aerosol. We studied the effective density (mass-mobility relationship) and mixing state with respect to the density of particles in central Copenhagen, in wintertime. The results are related to particle origin, morphology, and aging. Using a differential mobility analyzer-aerosol particle mass analyzer (DMA-APM), we determined that particles in the diameter range of 50–400 nm were of two groups: porous soot aggregates and more dense particles. Both groups were present at each size in varying proportions. Two types of temporal variability in the relative number fraction of the two groups were found: soot correlated with intense traffic in a diel pattern and dense particles increased during episodes with long-range transport from polluted continental areas. The effective density of each group was relatively stable over time, especially of the soot aggregates, which had effective densities similar to those observed in laboratory studies of fresh diesel exhaust emissions. When heated to 300 °C, the soot aggregate volatile mass fraction was ∼10%. For the dense particles, the volatile mass fraction varied from ∼80% to nearly 100%

    Role of oxidative damage in toxicity of particulates

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