Humidity-dependent surface tension measurements of individual inorganic and organic submicrometre liquid particles.

Surface tension, an important property of liquids, is easily measured for bulk samples. However, for droplets smaller than one micron in size, there are currently no reported measurements. In this study, atomic force microscopy (AFM) and force spectroscopy have been utilized to measure surface tension of individual submicron sized droplets at ambient pressure and controlled relative humidity (RH). Since the surface tension of atmospheric aerosols is a key factor in understanding aerosol climate effects, three atmospherically relevant systems (NaCl, malonic and glutaric acids) were studied. Single particle AFM measurements were successfully implemented in measuring the surface tension of deliquesced particles on the order of 200 to 500 nm in diameter. Deliquesced particles continuously uptake water at high RH, which changes the concentration and surface tension of the droplets. Therefore, surface tension as a function of RH was measured. AFM based surface tension measurements are close to predicted values based on bulk measurements and activities of these three chemical systems. Non-ideal behaviour in concentrated organic acid droplets is thought to be important and the reason for differences observed between bulk solution predictions and AFM data. Consequently, these measurements are crucial in order to improve atmospheric climate models as direct measurements hitherto have been previously inaccessible due to instrument limitations

Effects of copper nanoparticle exposure on host defense in a murine pulmonary infection model

<p>Abstract</p> <p>Background</p> <p>Human exposure to nanoparticles (NPs) and environmental bacteria can occur simultaneously. NPs induce inflammatory responses and oxidative stress but may also have immune-suppressive effects, impairing macrophage function and altering epithelial barrier functions. The purpose of this study was to assess the potential pulmonary effects of inhalation and instillation exposure to copper (Cu) NPs using a model of lung inflammation and host defense.</p> <p>Methods</p> <p>We used <it>Klebsiella pneumoniae </it>(<it>K.p.</it>) in a murine lung infection model to determine if pulmonary bacterial clearance is enhanced or impaired by Cu NP exposure. Two different exposure modes were tested: sub-acute inhalation (4 hr/day, 5 d/week for 2 weeks, 3.5 mg/m³) and intratracheal instillation (24 hr post-exposure, 3, 35, and 100 μg/mouse). Pulmonary responses were evaluated by lung histopathology plus measurement of differential cell counts, total protein, lactate dehydrogenase (LDH) activity, and inflammatory cytokines in bronchoalveolar lavage (BAL) fluid.</p> <p>Results</p> <p>Cu NP exposure induced inflammatory responses with increased recruitment of total cells and neutrophils to the lungs as well as increased total protein and LDH activity in BAL fluid. Both inhalation and instillation exposure to Cu NPs significantly decreased the pulmonary clearance of <it>K.p.</it>-exposed mice measured 24 hr after bacterial infection following Cu NP exposure versus sham-exposed mice also challenged with <it>K.p </it>(1.4 × 10⁵bacteria/mouse).</p> <p>Conclusions</p> <p>Cu NP exposure impaired host defense against bacterial lung infections and induced a dose-dependent decrease in bacterial clearance in which even our lowest dose demonstrated significantly lower clearance than observed in sham-exposed mice. Thus, exposure to Cu NPs may increase the risk of pulmonary infection.</p

Mass Size Distribution and Chemical Composition of the Surface Layer of Summer and Winter Airborne Particles in Zabrze, Poland

Mass size distributions of ambient aerosol were measured in Zabrze, a heavily industrialized city of Poland, during a summer and a winter season. The chemical analyses of the surface layer of PM10, PM2.5 and PM1 in this area were also performed by X-ray photoelectron spectroscopy (XPS). Results suggested that the influence of an atmospheric aerosol on the health condition of Zabrze residents can be distinctly stronger in winter than in summer because of both: higher concentration level of particulate matter (PM) and higher contribution of fine particles in winter season compared to summer. In Zabrze in June (summer) PM10 and PM2.5 reached about 20 and 14 μg/m3, respectively, while in December (winter) 57 and 51 μg/m3, respectively. The XPS analysis showed that elemental carbon is the major surface component of studied airborne particles representing about 78%–80% (atomic mass) of all detected elements

Toxicity assessment of zinc oxide nanoparticles using sub-acute and sub-chronic murine inhalation models

BACKGROUND: Although ZnO nanoparticles (NPs) are used in many commercial products and the potential for human exposure is increasing, few in vivo studies have addressed their possible toxic effects after inhalation. We sought to determine whether ZnO NPs induce pulmonary toxicity in mice following sub-acute or sub-chronic inhalation exposure to realistic exposure doses. METHODS: Mice (C57Bl/6) were exposed to well-characterized ZnO NPs (3.5 mg/m(3), 4 hr/day) for 2 (sub-acute) or 13 (sub-chronic) weeks and necropsied immediately (0 wk) or 3 weeks (3 wks) post exposure. Toxicity was assessed by enumeration of total and differential cells, determination of total protein, lactate dehydrogenase activity and inflammatory cytokines in bronchoalveolar lavage (BAL) fluid as well as measurements of pulmonary mechanics. Generation of reactive oxygen species was assessed in the lungs. Lungs were evaluated for histopathologic changes and Zn content. Zn concentration in blood, liver, kidney, spleen, heart, brain and BAL fluid was measured. RESULTS: An elevated concentration of Zn(2+) was detected in BAL fluid immediately after exposures, but returned to baseline levels 3 wks post exposure. Dissolution studies showed that ZnO NPs readily dissolved in artificial lysosomal fluid (pH 4.5), but formed aggregates and precipitates in artificial interstitial fluid (pH 7.4). Sub-acute exposure to ZnO NPs caused an increase of macrophages in BAL fluid and a moderate increase in IL-12(p40) and MIP-1α, but no other inflammatory or toxic responses were observed. Following both sub-acute and sub-chronic exposures, pulmonary mechanics were no different than sham-exposed animals. CONCLUSIONS: Our ZnO NP inhalation studies showed minimal pulmonary inflammation, cytotoxicity or lung histopathologic changes. An elevated concentration of Zn in the lung and BAL fluid indicates dissolution of ZnO NPs in the respiratory system after inhalation. Exposure concentration, exposure mode and time post exposure played an important role in the toxicity of ZnO NPs. Exposure for 13 wks with a cumulative dose of 10.9 mg/kg yielded increased lung cellularity, but other markers of toxicity did not differ from sham-exposed animals, leading to the conclusion that ZnO NPs have low sub-chronic toxicity by the inhalation route

Effects of Eyjafjallajökull volcanic ash on innate immune system responses and bacterial growth in vitro.

To access publisher's full text version of this article click on the hyperlink at the bottom of the pageOn 20 March 2010, the Icelandic volcano Eyjafjallajökull erupted for the first time in 190 years. Despite many epidemiological reports showing effects of volcanic ash on the respiratory system, there are limited data evaluating cellular mechanisms involved in the response to ash. Epidemiological studies have observed an increase in respiratory infections in subjects and populations exposed to volcanic eruptions.We physicochemically characterized volcanic ash, finding various sizes of particles, as well as the presence of several transition metals, including iron. We examined the effect of Eyjafjallajökull ash on primary rat alveolar epithelial cells and human airway epithelial cells (20-100 µg/cm(2)), primary rat and human alveolar macrophages (5-20 µg/cm(2)), and Pseudomonas aeruginosa (PAO1) growth (3 µg/104 bacteria).Volcanic ash had minimal effect on alveolar and airway epithelial cell integrity. In alveolar macrophages, volcanic ash disrupted pathogen-killing and inflammatory responses. In in vitro bacterial growth models, volcanic ash increased bacterial replication and decreased bacterial killing by antimicrobial peptides.These results provide potential biological plausibility for epidemiological data that show an association between air pollution exposure and the development of respiratory infections. These data suggest that volcanic ash exposure, while not seriously compromising lung cell function, may be able to impair innate immunity responses in exposed individuals.National Institutes of Health (NIH) R01 HL079901 NIH RO1 HL096625 R21HL109589 National Science Foundation NSF-EAR0821615 National Institute of Environmental Health Sciences (NIEHS) through the University of Iowa Environmental Health Sciences Research Center NIEHS/NIH P30 ES005605 National Center for Research Resources, NI