Environmentally persistent free radicals induce airway hyperresponsiveness in neonatal rat lungs

Background  

Increased asthma risk/exacerbation in children and infants is associated with exposure to elevated levels of ultrafine particulate matter (PM). The presence of a newly realized class of pollutants, environmentally persistent free radicals (EPFRs), in PM from combustion sources suggests a potentially unrecognized risk factor for the development and/or exacerbation of asthma.     

Impact of agglomeration state of nano- and submicron sized gold particles on pulmonary inflammation

Background

Traffic emissions including diesel engine exhaust are associated with increased respiratory and cardiovascular morbidity and mortality. Controlled human exposure studies have demonstrated impaired vascular function after inhalation of exhaust generated by a diesel engine under idling conditions.

Objectives

To assess the vascular and fibrinolytic effects of exposure to diesel exhaust generated during urban-cycle running conditions that mimic ambient 'real-world' exposures.

Methods

In a randomised double-blind crossover study, eighteen healthy male volunteers were exposed to diesel exhaust (approximately 250 μg/m³) or filtered air for one hour during intermittent exercise. Diesel exhaust was generated during the urban part of the standardized European Transient Cycle. Six hours post-exposure, vascular vasomotor and fibrinolytic function was assessed during venous occlusion plethysmography with intra-arterial agonist infusions.

Measurements and Main Results

Forearm blood flow increased in a dose-dependent manner with both endothelial-dependent (acetylcholine and bradykinin) and endothelial-independent (sodium nitroprusside and verapamil) vasodilators. Diesel exhaust exposure attenuated the vasodilatation to acetylcholine (P < 0.001), bradykinin (P < 0.05), sodium nitroprusside (P < 0.05) and verapamil (P < 0.001). In addition, the net release of tissue plasminogen activator during bradykinin infusion was impaired following diesel exhaust exposure (P < 0.05).

Conclusion

Exposure to diesel exhaust generated under transient running conditions, as a relevant model of urban air pollution, impairs vasomotor function and endogenous fibrinolysis in a similar way as exposure to diesel exhaust generated at idling. This indicates that adverse vascular effects of diesel exhaust inhalation occur over different running conditions with varying exhaust composition and concentrations as well as physicochemical particle properties. Importantly, exposure to diesel exhaust under ETC conditions was also associated with a novel finding of impaired of calcium channel-dependent vasomotor function. This implies that certain cardiovascular endpoints seem to be related to general diesel exhaust properties, whereas the novel calcium flux-related effect may be associated with exhaust properties more specific for the ETC condition, for example a higher content of diesel soot particles along with their adsorbed organic compounds.     

Effects of prenatal exposure to diesel exhaust particles on postnatal development, behavior, genotoxicity and inflammation in mice

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.     

Fibrin clot structure remains unaffected in young, healthy individuals after transient exposure to diesel exhaust

Exposure to urban particulate matter has been associated with an increased risk of cardiovascular disease and thrombosis. We studied the effects of transient exposure to diesel particles on fibrin clot structure of 16 healthy individuals (age 21- 44). The subjects were randomly exposed to diesel exhaust and filtered air on two separate occasions. Blood samples were collected before exposure, and 2 and 6 hours after exposure. There were no significant changes on clot permeability, maximum turbidity, lag time, fibre diameter, fibre density and fibrinogen level between samples taken after diesel exhaust exposure and samples taken after filtered air exposure. These data show that there are no prothrombotic changes in fibrin clot structure in young, healthy individuals exposed to diesel exhaust.     

Experimental exposure to diesel exhaust increases arterial stiffness in man

Introduction  

Exposure to air pollution is associated with increased cardiovascular morbidity, although the underlying mechanisms are unclear. Vascular dysfunction reduces arterial compliance and increases central arterial pressure and left ventricular after-load. We determined the effect of diesel exhaust exposure on arterial compliance using a validated non-invasive measure of arterial stiffness.     

Early-Life Exposure to Traffic-Related Air Pollutants Induced Anxiety-like Behaviors in Rats via Neurotransmitters and Neurotrophic Factors

Recent epidemiological studies have reported significantly increasing hospital admission rates for mental disorders such as anxiety and depression, not only in adults but also in children and adolescents, indicating more research is needed for evaluation of the etiology and possible reduction and prevention of these disorders. The aim of the present study was to examine the associations between perinatal exposure to traffic-related air pollutants and anxiety-like behaviors and alterations in neurological and immunological markers in adulthood using a rat model. Sprague Dawley pregnant rats were exposed to clean air (control), diesel exhaust (DE) 101 ± 9 μg/m³ or diesel exhaust origin secondary organic aerosol (DE-SOA) 118 ± 23 μg/m³ from gestational day 14 to postnatal day 21. Anxiety-related behavioral tests including open field tests, elevated plus maze, light/dark transition tests and novelty-induced hypophagia were performed on 10-week-old rats. The hippocampal expression of neurotransmitters, neurotrophic factors, and inflammatory molecular markers was examined by real-time RT-PCR. Anxiety-like behaviors were observed in both male and female rat offspring exposed to DE or DE-SOA. Moreover, serotonin receptor (5HT1A), dopamine receptor (Drd2), brain-derived neurotrophic factor and vascular endothelial growth factor A mRNAs were significantly decreased, whereas interleukin-1β, cyclooxygenase-2, heme oxygenase-1 mRNAs and microglial activation were significantly increased in both male and female rats. These findings indicate that brain developmental period exposure to traffic-related air pollutants may induce anxiety-like behaviors via modulation of neurotransmitters, neurotrophic factors, and immunological molecular markers, triggering neuroinflammation and microglia activation in rats.     

Diesel exhaust particles modulate the tight junction protein occludin in lung cells in vitro

Background  

Using an in vitro triple cell co-culture model consisting of human epithelial cells (16HBE14o-), monocyte-derived macrophages and dendritic cells, it was recently demonstrated that macrophages and dendritic cells create a transepithelial network between the epithelial cells to capture antigens without disrupting the epithelial tightness. The expression of the different tight junction proteins in macrophages and dendritic cells, and the formation of tight junction-like structures with epithelial cells has been demonstrated. Immunofluorescent methods combined with laser scanning microscopy and quantitative real-time polymerase chain reaction were used to investigate if exposure to diesel exhaust particles (DEP) (0.5, 5, 50, 125 μg/ml), for 24 h, can modulate the expression of the tight junction mRNA/protein of occludin, in all three cell types.     

Towards a single brick solution for the abatement of NOx and soot from diesel engine exhausts

Nano-structured perovskite-type lanthanum ferrites La_1 − xA_xFe_1 − yB_yO₃ (where A = Na, K, Rb and B = Cu), prepared by the solution combustion synthesis (SCS) method and characterized by BET, XRD, FESEM, AAS and catalytic activity tests in microreactors as well as on an engine bench, proved to be effective in the simultaneous removal of soot and NO, the two prevalent pollutants in diesel exhaust gases in the temperature range 350–450 °C. The best compromise between soot and nitrogen oxide abatement was shown by the La-K-Cu-FeO₃ catalyst which displayed the highest catalytic activity towards carbon combustion and the highest NO conversion activity.     

Katalysatoren für den Umweltschutz

Catalysts for environmental protection. The main emitters of anthropogenic air pollution are internal combustion engines, power plants, and production processes. Components of exhaust gases which are regarded as pollutants are hydrocarbons (HC), carbon monoxide (CO), nitrogen oxides (NO_x), sulfur dioxide (SO₂), and dust. Three main types of catalyst are understood to improve the environment; namely automotive emission control, NO_x abatement and oxidation. To reduce the pollutants HC, CO, and NO_x in automobile exhaust gas, three-way catalysts are currently applied. The reduction of particle emissions in diesel exhaust gas is achieved by diesel filters and oxidation catalysts. Pollutants from power plants are mainly the inorganic components NO_x and SO₂. In the SCR process, NO_x is catalytically reduced to nitrogen and water. The DESONOX process is suited for the simultaneous catalytic abatement of NO_x and SO_x. Exhaust gases from production processes in many areas require after-treatment. Therefore catalyst formulations depend on process parameters and exhaust gas components. This overview presents and explains catalyst types, design, mode of operation, and processes.     

PM2.5 Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model

Air pollution-related particulate matter (PM) exposure reportedly enhances allergic airway inflammation. Some studies have shown an association between PM exposure and a risk for allergic rhinitis (AR). However, the effect of PM for AR is not fully understood. An AR mouse model was developed by intranasal administration of 100 μg/mouse PM with a less than or equal to 2.5 μm in aerodynamic diameter (PM_2.5) solution, and then by intraperitoneal injection of ovalbumin (OVA) with alum and intranasal challenging with 10 mg/mL OVA. The effects of PM_2.5 on oxidative stress and inflammatory response via the Nrf2/NF-κB signaling pathway in mice with or without AR indicating by histological, serum, and protein analyses were examined. PM_2.5 administration enhanced allergic inflammatory cell expression in the nasal mucosa through increasing the expression of inflammatory cytokine and reducing the release of Treg cytokine in OVA-induced AR mice, although PM_2.5 exposure itself induced neither allergic responses nor damage to nasal and lung tissues. Notably, repeated OVA-immunization markedly impaired the nasal mucosa in the septum region. Moreover, AR with PM_2.5 exposure reinforced this impairment in OVA-induced AR mice. Long-term PM_2.5 exposure strengthened allergic reactions by inducing the oxidative through malondialdehyde production. The present study also provided evidence, for the first time, that activity of the Nrf2 signaling pathway is inhibited in PM_2.5 exposed AR mice. Furthermore, PM_2.5 exposure increased the histopathological changes of nasal and lung tissues and related the inflammatory cytokine, and clearly enhanced PM_2.5 phagocytosis by alveolar macrophages via activating the NF-κB signaling pathway. These obtained results suggest that AR patients may experience exacerbation of allergic responses in areas with prolonged PM_2.5 exposure.     

Biomass Smoke Exposure Enhances Rhinovirus-Induced Inflammation in Primary Lung Fibroblasts

Biomass smoke is one of the major air pollutants and contributors of household air pollution worldwide. More than 3 billion people use biomass fuels for cooking and heating, while other sources of exposure are from the occurrence of bushfires and occupational conditions. Persistent biomass smoke exposure has been associated with acute lower respiratory infection (ALRI) as a major environmental risk factor. Children under the age of five years are the most susceptible in developing severe ALRI, which accounts for 940,000 deaths globally. Around 90% of cases are attributed to viral infections, such as influenza, adenovirus, and rhinovirus. Although several epidemiological studies have generated substantial evidence of the association of biomass smoke and respiratory infections, the underlying mechanism is still unknown. Using an in vitro model, primary human lung fibroblasts were stimulated with biomass smoke extract (BME), specifically investigating hardwood and softwood types, and human rhinovirus-16 for 24 h. Production of pro-inflammatory mediators, such as IL-6 and IL-8, were measured via ELISA. Firstly, we found that hardwood and softwood smoke extract (1%) up-regulate IL-6 and IL-8 release (p ≤ 0.05). In addition, human rhinovirus-16 further increased biomass smoke-induced IL-8 in fibroblasts, in comparison to the two stimulatory agents alone. We also investigated the effect of biomass smoke on viral susceptibility by measuring viral load, and found no significant changes between BME exposed and non-exposed infected fibroblasts. Activated signaling pathways for IL-6 and IL-8 production by BME stimulation were examined using signaling pathway inhibitors. p38 MAPK inhibitor SB239063 significantly attenuated IL-6 and IL-8 release the most (p ≤ 0.05). This study demonstrated that biomass smoke can modulate rhinovirus-induced inflammation during infection, which can alter the severity of the disease. The mechanism by which biomass smoke exposure increases inflammation in the lungs can be targeted and inhibited via p38 MAP kinase pathway.     

Low temperature exhaust gas fuel reforming of diesel fuel

The application of exhaust gas assisted fuel reforming in diesel engines has been investigated. The process involves hydrogen generation by direct catalytic interaction of diesel fuel with engine exhaust gas. Using a laboratory reforming mini reactor incorporated in the exhaust system of a diesel engine, up to 16% hydrogen in the reactor product gas was achieved at a reactor inlet temperature of 290 °C. The results showed that such levels of hydrogen can be produced with appropriate control of the reaction parameters at temperatures typical of exhaust gas temperatures of diesel engines operating at part load without any requirement for external heat source or air and steam supply. The use of simulated reformed fuel was shown to be beneficial in terms of engine exhaust emissions and resulted in reduction of NO_X and smoke emissions.     

Volatile Dose and Exposure Time Impact Perception in Neighboring Plants

Volatiles emitted from stressed plants can induce resistance in healthy neighbors. It remains unknown, however, how plants perceive volatiles and convert them into internal signals. We exposed lima bean (Phaseolus lunatus L.) to different concentrations of either of two volatiles, nonanal and methyl salicylate (MeSA), over 6 or 24 h. Plant resistance to the bacterial pathogen, Pseudomonas syringae, was increased significantly after exposure to a headspace with two concentrations of nonanal for 6 h, and the same pattern emerged after an exposure over 24 h. By contrast, exposure to a low concentration of MeSA over 6 h did not significantly reduce bacterial infections, whereas exposure to the same concentration over 24 h significantly enhanced resistance. The dose–response relation that was apparent after 6 h of MeSA exposure disappeared in the 24 h treatment, in which the three tested concentrations caused indistinguishable, high levels of resistance to P. syringae. A low concentration of a potentially resistance-enhancing volatile sufficed to cause resistance to pathogens in the receiver plant only after long exposure time. Plant-plant signaling appears to involve the accumulation of volatiles in the receiver.     

Diesel exhaust particles increase IL-1β-induced human β-defensin expression via NF-κB-mediated pathway in human lung epithelial cells

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.     

EVALUATION OF THE USE OF 1-NITROPYRENE,PYRENE, AND 1-HYDROXYPYRENE AS MARKERS OF DIESEL EXHAUST EXPOSURE IN UNDERGROUND MINING: RESULTS FROM THE BIOMODEM STUDY

The exposure to diesel exhaust was studied in underground mining of oil shale in Estonia. The purpose of this study was to evaluate different approaches to exposure assessment. Fifty men who drove diesel-powered excavators underground were compared with 50 surface workers who had no known occupational exposure to diesel exhaust. Samples of respirable air were analyzed for 1-nitropyrene and pyrene. Urine samples were collected at the start and after the first and the last shift of the same week, and were analyzed for 1-hydroxypyrene. Although ambient monitoring of 1-nitropyrene indicated a relatively high exposure of underground workers to diesel exhaust compared to surface workers (approximately 10-fold higher), only a small increase in the excretion of 1-hydroxypyerene was observed. Nonoccupational exposures such as smoking, recent consumption of grilled food, and recent proximity to an open fire had a greater impact on urinary excretion of 1-hydroxypyrene than occupational exposure to diesel exhaust.     

Oxidation of propane over a diesel exhaust catalyst

The oxidation of propane, over a concentration range of 0.30 to 1.04 mole % in air was investigated over a commercial diesel exhaust catalyst consisting of CuO, Cr₂O₃ and Pd supported on Al₂O₃. The rate of reaction was correlated by a first order, irreversible rate function; the resulting pre-exponential factor and activation energy were 3.15 × 10⁷ cc/g-sec and 21.3 kcal/gmole, respectively. At high temperatures the reaction rate became influenced by pore diffusion. A temperature of 675°K was required to obtain 50% propane conversion. It was concluded that this catayst is unsuitable for catalytic mufflers on diesel buses since the measured value of diesel exhaust temperatures at the cataytic muffler inlet is significantly less than 675°K.     

Pulsed ultraviolet light decontamination of virus-laden airstreams

Continuous ultraviolet germicidal irradiation (UVGI) has been extensively studied, but research on pulsed UVGI (PUVGI) is lacking and has primarily focused on disinfection of solid surfaces or liquids. This study addressed the gap in knowledge on the effectiveness of pulsed UVGI for disinfecting virus-laden calm air, with relevance to indoor rooms. Φ6 bacteriophage (a surrogate used to study communicable enveloped human respiratory viral pathogens such as influenza virus) was aerosolized by a Collison device into an enclosed test chamber, wherein the bioaerosol was exposed to PUVGI. The spectral content and performance of a pulsed white light lamp with a substantial UVC component were defined. Pulsed UV exposure of 10 to 30 s resulted in a two-log reduction in viable recovered virus from filter membranes and cyclone-based samplers. The small differences in Φ6 survival, after 10 to 30 s of exposure, emphasized the difficulty of complete eradication. However, exposure to 10 s of PUVGI resulted in significant reduction of virus viability. The dose–response displayed clear regimes of fast and slow exponential decay. Susceptibility factor for the fast-decay regime of aerosolized Φ6 (Z = 0.24 m²/J) was similar to those reported for influenza A virus aerosols at similar relative humidity. Our study demonstrated the potency of PUVGI against a viral bioaerosol. This has potential implications for the control of infectious bioaerosols in the healthcare setting.

© 2017 American Association for Aerosol Research     

The effects of fuel characteristics and engine operating conditions on the elemental composition of emissions from heavy duty diesel buses

The effects of fuel characteristics and engine operating conditions on elemental composition of emissions from twelve heavy duty diesel buses have been investigated. Two types of diesel fuels – low sulfur diesel (LSD) and ultra low sulfur diesel (ULSD) fuels with 500 ppm and 50 ppm sulfur contents respectively and 3 driving modes corresponding to 25%, 50% and 100% power were used. Elements present in the tailpipe emissions were quantified by inductively coupled plasma mass spectrometry (ICPMS) and those found in measurable quantities included Mg, Ca, Cr, Fe, Cu, Zn, Ti, Ni, Pb, Be, P, Se, Ti and Ge. Multivariate analyses using multi-criteria decision making methods (MCDM), principal component analysis (PCA) and partial least squares (PLS) facilitated the extraction of information about the structure of the data. MCDM showed that the emissions of the elements were strongly influenced by the engine driving conditions while the PCA loadings plots showed that the emission factors of the elements were correlated with those of other pollutants such as particle number, total suspended particles, CO, CO₂ and NO_x. Partial least square analysis revealed that the emission factors of the elements were strongly dependent on the fuel parameters such as the fuel sulfur content, fuel density, distillation point and cetane index. Strong correlations were also observed between these pollutants and the engine power or exhaust temperature. The study provides insights into the possible role of fuel sulfur content in the emission of inorganic elements from heavy duty diesel vehicles.