共查询到20条相似文献,搜索用时 46 毫秒
1.
Background
Particulate air pollution is reported to cause adverse health effects in susceptible individuals. Since most of these particles are derived form combustion processes, the primary composition product is carbon with a very small diameter (ultrafine, less than 100 nm in diameter). Besides the induction of reactive oxygen species and inflammation, ultrafine particles (UFP) can cause intracellular calcium transients and suppression of defense mechanisms of alveolar macrophages, such as impaired migration or phagocytosis. 相似文献2.
Kiran Ramgolam Olivier Favez Hélène Cachier Annie Gaudichet Francelyne Marano Laurent Martinon Armelle Baeza-Squiban 《Particle and fibre toxicology》2009,6(1):10-12
Background
The contribution of air particles in human cardio-respiratory diseases has been enlightened by several epidemiological studies. However the respective involvement of coarse, fine and ultrafine particles in health effects is still unclear. The aim of the present study is to determine which size fraction from a chemically characterized background aerosol has the most important short term biological effect and to decipher the determinants of such a behaviour. 相似文献3.
Background
Exposure to air pollution particles has been acknowledged to be associated with excess generation of oxidative damage to DNA in experimental model systems and humans. The use of standard reference material (SRM), such as SRM1650 and SRM2975, is advantageous because experiments can be reproduced independently, but exposure to such samples may not mimic the effects observed after exposure to authentic air pollution particles. This study was designed to compare the DNA oxidizing effects of authentic street particles with SRM1650 and SRM2975. The authentic street particles were collected at a traffic intensive road in Copenhagen, Denmark. 相似文献4.
Elvira V Bräuner Peter Møller Lars Barregard Lars O Dragsted Marianne Glasius Peter Wåhlin Peter Vinzents Ole Raaschou-Nielsen Steffen Loft 《Particle and fibre toxicology》2008,5(1):13
Background
Particulate air pollution is associated with increased risk of cardiovascular events although the involved mechanisms are poorly understood. The objective of the present study was to investigate the effects of controlled exposure to ambient air fine and ultrafine particles on microvascular function and biomarkers related to inflammation, haemostasis and lipid and protein oxidation. 相似文献5.
Regina Rückerl Richard P Phipps Alexandra Schneider Mark Frampton Josef Cyrys Günther Oberdörster H Erich Wichmann Annette Peters 《Particle and fibre toxicology》2007,4(1):1-14
Background
Epidemiological studies on health effects of air pollution have consistently shown adverse cardiovascular effects. Toxicological studies have provided evidence for thrombogenic effects of particles. 相似文献6.
Evelyn J Freney Mathew R Heal Robert J Donovan Nicholas L Mills Kenneth Donaldson David E Newby Paul HB Fokkens Flemming R Cassee 《Particle and fibre toxicology》2006,3(1):8-11
Background
An Aerosol Time-of-Flight Mass Spectrometer (ATOFMS) was used to investigate the size and chemical composition of fine concentrated ambient particles (CAPs) in the size range 0.2–2.6 μm produced by a Versatile Aerosol Concentration Enrichment System (VACES) contained within the Mobile Ambient Particle Concentrator Exposure Laboratory (MAPCEL). The data were collected during a study of human exposure to CAPs, in Edinburgh (UK), in February-March 2004. The air flow prior to, and post, concentration in the VACES was sampled in turn into the ATOFMS, which provides simultaneous size and positive and negative mass spectral data on individual fine particles. 相似文献7.
Ilona Jaspers Patricia A Sheridan Wenli Zhang Luisa E Brighton Kelly D Chason Xiaoyang Hua Stephen L Tilley 《Particle and fibre toxicology》2009,6(1):22-11
Background
Viral infections and exposure to oxidant air pollutants are two of the most important inducers of asthma exacerbation. Our previous studies have demonstrated that exposure to diesel exhaust increases the susceptibility to influenza virus infections both in epithelial cells in vitro and in mice in vivo. Therefore, we examined whether in the setting of allergic asthma, exposure to oxidant air pollutants enhances the susceptibility to respiratory virus infections, which in turn leads to increased virus-induced exacerbation of asthma. Ovalbumin-sensitized (OVA) male C57BL/6 mice were instilled with diesel exhaust particles (DEP) or saline and 24 hours later infected with influenza A/PR/8. Animals were sacrificed 24 hours post-infection and analyzed for markers of lung injury, allergic inflammation, and pro-inflammatory cytokine production. 相似文献8.
John M Veranth Erin G Kaser Martha M Veranth Michael Koch Garold S Yost 《Particle and fibre toxicology》2007,4(1):2-18
Background
The induction of cytokines by airway cells in vitro has been widely used to assess the effects of ambient and occupational particles. This study measured cytotoxicity and the release of the proinflammatory cytokines IL-6 and IL-8 by human bronchial epithelial cells treated with manufactured nano- and micron-sized particles of Al2O3, CeO2, Fe2O3, NiO, SiO2, and TiO2, with soil-derived particles from fugitive dust sources, and with the positive controls LPS, TNF-α, and VOSO4. 相似文献9.
Y. H. Taufiq-Yap C. K. Goh G. J. Hutchings N. Dummer J. K. Bartley 《Catalysis Letters》2011,141(3):400-407
Abstract
VOHPO4·0.5H2O synthesized via the alcohol reduction of VOPO4·2H2O was mechanochemical treated for 30 min in three different media, i.e. cyclohexane, ethanol and air. XRD results revealed that their structure became less crystalline compared to the unmilled material. SEM showed that the particles for the milled materials become smaller and unique features were observed in the different type of media used. The reactivity of the oxygen species linked to V5+ and V4+ were also affected by the milling process. The selectivity to maleic anhydride from n-butane oxidation were observed to increase in line with the increase in the oxygen species associated with V5+ and the presence of isolated V5+ phase. A correlation was observed between the crystallite size of the pyrophosphate phase at (020) plane with the maleic anhydride selectivity. 相似文献10.
Christian Mühlfeld Marianne Geiser Nadine Kapp Peter Gehr Barbara Rothen-Rutishauser 《Particle and fibre toxicology》2007,4(1):7-8
Background
Translocation of nanoparticles (NP) from the pulmonary airways into other pulmonary compartments or the systemic circulation is controversially discussed in the literature. In a previous study it was shown that titanium dioxide (TiO2) NP were "distributed in four lung compartments (air-filled spaces, epithelium/endothelium, connective tissue, capillary lumen) in correlation with compartment size". It was concluded that particles can move freely between these tissue compartments. To analyze whether the distribution of TiO2 NP in the lungs is really random or shows a preferential targeting we applied a newly developed method for comparing NP distributions. 相似文献11.
Background
Translocation of ultrafine particles (UFP) into the blood that returns from the lungs to the heart has been forwarded as a mechanism for particle-induced cardiovascular effects. The objective of this study was to evaluate the role of the endothelial barrier in the translocation of inhaled UFP from the lung into circulation. 相似文献12.
Jakob L?ndahl Erik Swietlicki Jenny Rissler Agneta Bengtsson Christoffer Boman Anders Blomberg Thomas Sandstr?m 《Particle and fibre toxicology》2012,9(1):1-8
Background
Air pollution, mainly from combustion, is one of the leading global health risk factors. A susceptible group is the more than 200 million people worldwide suffering from chronic obstructive pulmonary disease (COPD). There are few data on lung deposition of airborne particles in patients with COPD and none for combustion particles.Objectives
To determine respiratory tract deposition of diesel combustion particles in patients with COPD during spontaneous breathing.Methods
Ten COPD patients and seven healthy subjects inhaled diesel exhaust particles generated during idling and transient driving in an exposure chamber. The respiratory tract deposition of the particles was measured in the size range 10?C500?nm during spontaneous breathing.Results
The deposited dose rate increased with increasing severity of the disease. However, the deposition probability of the ultrafine combustion particles (< 100?nm) was decreased in COPD patients. The deposition probability was associated with both breathing parameters and lung function, but could be predicted only based on lung function.Conclusions
The higher deposited dose rate of inhaled air pollution particles in COPD patients may be one of the factors contributing to their increased vulnerability. The strong correlations between lung function and particle deposition, especially in the size range of 20?C30?nm, suggest that altered particle deposition could be used as an indicator respiratory disease. 相似文献13.
Hae Yun Nam Eun-Kyung Ahn Hyung Jung Kim Young Lim Chun Beoun Lee Kyo Young Lee Val Vallyathan 《Particle and fibre toxicology》2006,3(1):9-9
Background
Human β-defensin (hBD)-2, antimicrobial peptide primarily induced in epithelial cells, is a key factor in the innate immune response of the respiratory tract. Several studies showed increased defensin levels in both inflammatory lung diseases, such as cystic fibrosis, diffuse panbronchiolitis, idiopathic pulmonary fibrosis and acute respiratory distress syndrome, and infectious diseases. Recently, epidemiologic studies have demonstrated acute and serious adverse effects of particulate air pollution on respiratory health, especially in people with pre-existing inflammatory lung disease. To elucidate the effect of diesel exhaust particles (DEP) on pulmonary innate immune response, we investigated the hBD-2 and interleukin-8 (IL-8) expression to DEP exposure in interleukin-1 beta (IL-1β)-stimulated A549 cells. 相似文献14.
Lise K Vesterdal Janne K Folkmann Nicklas R Jacobsen Majid Sheykhzade Håkan Wallin Steffen Loft Peter Møller 《Particle and fibre toxicology》2009,6(1):1-13
Background
Growing evidence indicates that ambient air pollution is associated with exacerbation of chronic diseases like chronic pulmonary disease. A prospective panel study was conducted to investigate short-term changes of blood markers of inflammation and coagulation in response to daily changes in air pollution in Erfurt, Germany. 12 clinical visits were scheduled and blood parameters were measured in 38 male patients with chronic pulmonary disease during winter 2001/2002. Additive mixed models with random patient intercept were applied, adjusting for trend, weekday, and meteorological parameters. Hourly data on ultrafine particles (UFP, 0.01-0.1 μm), accumulation mode particles (ACP, 0.1-1.0 μm), PM10 (particulate matter <10 μm in diameter), elemental (EC) and organic carbon (OC), gaseous pollutants (nitrogen monoxide [NO], nitrogen dioxide [NO2], carbon monoxide [CO], and sulphur dioxide [SO2]) were collected at a central monitoring site and meteorological data were received from an official network. For each person and visit the individual 24-hour average of pollutants immediately preceding the blood withdrawal (lag 0) up to day 5 (lag1-4) and 5-day running means were calculated.Results
Increased levels of fibrinogen were observed for an increase in one interquartile range of UFP, PM10, EC, OC, CO, and NO revealing the strongest effect for lag 3. E-selectin increased in association with ACP and PM10 with a delay of one day. The ACP effect was also seen with the 5-day-mean. The pattern found for D-dimer was inconsistent. Prothrombin fragment 1+2 decreased with lag 4 consistently for all particulate pollutants. Von Willebrand factor antigen (vWF) showed a consistent decrease in association with almost all air pollutants with all lags except for lag 0. No associations were found for C-reactive protein, soluble intercellular adhesion molecule 1, serum amyloid A and factor VII.Conclusion
These results suggest that elevated concentrations of air pollution are associated with changes in some blood markers of inflammation and coagulation in patients with chronic pulmonary disease. The clinical implications of these findings need further investigation. 相似文献15.
Background
The burning of biomass in the developing world for heating and cooking results in high indoor particle concentrations. Long-term exposure to airborne particulate matter (PM) has been associated with increased rates of acute respiratory infections, chronic obstructive lung disease and cancer. In this study we determined the oxidative activity of combustion particles derived from the biomass fuel dung cake by examining their capacity to deplete antioxidants from a model human respiratory tract lining fluid (RTLF). For comparison, the observed oxidative activity was compared with that of particles derived from industrial and vehicular sources. 相似文献16.
Corey A Cohn Richard Laffers Sanford R Simon Thomas O'Riordan Martin AA Schoonen 《Particle and fibre toxicology》2006,3(1):1-10
Background
Exposure to ambient particulate matter has been associated with a number of adverse health effects. Particle characteristics such as size, surface area and chemistry seem to influence the negative effects of particles. In this study, combustion particles from vehicle exhaust and wood smoke, currently used in biological experiments, were analysed with respect to microstructure and chemistry. 相似文献17.
Michael Gasser Michael Riediker Loretta Mueller Alain Perrenoud Fabian Blank Peter Gehr Barbara Rothen-Rutishauser 《Particle and fibre toxicology》2009,6(1):30
Background
Fine particulate matter originating from traffic correlates with increased morbidity and mortality. An important source of traffic particles is brake wear of cars which contributes up to 20% of the total traffic emissions. The aim of this study was to evaluate potential toxicological effects of human epithelial lung cells exposed to freshly generated brake wear particles. 相似文献18.
Anne T Saber Nicklas R Jacobsen Jette Bornholdt Sanna L Kjær Marianne Dybdahl Lotte Risom Steffen Loft Ulla Vogel Håkan Wallin 《Particle and fibre toxicology》2006,3(1):4-8
Background
Particulate air pollution has been associated with lung and cardiovascular disease, for which lung inflammation may be a driving mechanism. The pro-inflammatory cytokine, tumor necrosis factor (TNF) has been suggested to have a key-role in particle-induced inflammation. 相似文献19.
Karin S Hougaard Keld A Jensen Pernille Nordly Camilla Taxvig Ulla Vogel Anne T Saber Håkan Wallin 《Particle and fibre toxicology》2008,5(1):1-15
Background
Results from epidemiological studies indicate that particulate air pollution constitutes a hazard for human health. Recent studies suggest that diesel exhaust possesses endocrine activity and therefore may affect reproductive outcome. This study in mice aimed to investigate whether exposure to diesel exhaust particles (DEP; NIST 2975) would affect gestation, postnatal development, activity, learning and memory, and biomarkers of transplacental toxicity. Pregnant mice (C57BL/6; BomTac) were exposed to 19 mg/m3 DEP (~1·106 particles/cm3; mass median diameter ? 240 nm) on gestational days 9–19, for 1 h/day.Results
Gestational parameters were similar in control and diesel groups. Shortly after birth, body weights of DEP offspring were slightly lower than in controls. This difference increased during lactation, so by weaning the DEP exposed offspring weighed significantly less than the control progeny. Only slight effects of exposure were observed on cognitive function in female DEP offspring and on biomarkers of exposure to particles or genotoxic substances.Conclusion
In utero exposure to DEP decreased weight gain during lactation. Cognitive function and levels of biomarkers of exposure to particles or to genotoxic substances were generally similar in exposed and control offspring. The particle size and chemical composition of the DEP and differences in exposure methods (fresh, whole exhaust versus aged, resuspended DEP) may play a significant role on the biological effects observed in this compared to other studies. 相似文献20.
Solenne Taront Audrey Dieudonné Simon Blanchard Pascale Jeannin Philippe Lassalle Yves Delneste Philippe Gosset 《Particle and fibre toxicology》2009,6(1):9