Exhaust Particles Research Articles

Lysimachia mauritiana Lam. Extract Alleviates Airway Inflammation Induced by Particulate Matter Plus Diesel Exhaust Particles in Mice.

The respiratory-protective effects of Lysimachia mauritiana (LM) against airway inflammation were evaluated in a mouse model exposed to a fine dust mixture of diesel exhaust particles and particulate matter with a diameter of less than 10 µm (PM10D). To induce airway inflammation, PM10D was intranasally injected into BALB/c mice three times a day for 12 days, and LM extracts were given orally once per day. The immune cell subtypes, histopathology, and expression of inflammatory mediators were analyzed from the bronchoalveolar lavage fluid (BALF) and lungs. LM alleviated the accumulation of neutrophils and the number of inflammatory cells in the lungs and the BALF of the PM10D-exposed mice. LM also reduced the release of inflammatory mediators (MIP-2, IL-17, IL-1α, CXCL1, TNF-α, MUC5AC, and TRP receptor channels) in the BALF and lungs. Lung histopathology was used to examine airway inflammation and the accumulation of collagen fibers and inflammatory cells after PM10D exposure and showed that LM administration improved this inflammation. Furthermore, LM extract inhibited the MAPK and NF-κB signaling pathway in the lungs and improved expectoration activity through an increase in phenol red release from the trachea. LM alleviated PM10D-exposed neutrophilic airway inflammation by suppressing MAPK/NF-κB activation. This study indicates that LM extract may be an effective therapeutic agent against inflammatory respiratory diseases.

Diesel exhaust particles activate macrophages and IRF5 expression in atherosclerosis

Abstract Introduction Over 20% of global deaths related to cardiovascular disease have been attributed in part to air pollution, particularly fine particulate matter (PM2.5) (1). In highly trafficked urban areas, smaller ultrafine diesel exhaust particles (DEP) represent a significant proportion of PM2.5. DEP is associated with the progression of atherosclerosis and increased plaque susceptibility to rupture (2). We have previously shown that interferon regulatory factor 5 (IRF5) has a key role in necrotic core formation, a distinguishing feature of vulnerable atherosclerotic plaques, by rendering macrophages defective at efferocytosis (3). Pronounced elevation of IRF5 is also seen in symptomatic carotid plaques, particularly in the rupture-prone shoulder regions (4). Purpose We examined the effect of DEP on macrophage phenotype and IRF5 expression in atherosclerosis. Methods Bone marrow-derived macrophages (BMDMs) from C57BL/6 mice, differentiated with GM-CSF (to mimic inflammatory macrophages) or M-CSF (mimicking homeostatic resident macrophages) were incubated with PBS or DEP (10 µg/mL) in vitro for 18 hours. Expression of inflammatory cytokines (IL-6, IL-12α), macrophage polarisation markers CD11c (itgax, inflammatory) and CD206 (mrc1, resident anti-inflammatory) and IRF5 was quantified by real-time PCR. In addition, high fat-fed ApoE-/- mice were exposed to saline or DEP (35 µL at 1 mg/mL) twice weekly for 5 weeks by pulmonary administration. The pan-macrophage marker CD64, CD206 and IRF5 were quantified in paraffin-embedded sections of brachiocephalic artery lesions by immunohistochemistry. Results In M-CSF-differentiated murine macrophages incubated with DEP, significant fold increases in gene expression (relative to PBS control) were observed: IRF5 (1.4-fold), IL-6 (31.5-fold) and IL-12α (5.8-fold) while CD206 (0.8-fold) decreased (Figure 1a, n = 5, p<0.05, two-tailed paired t-tests). CD11c expression was unchanged. No statistically significant differences were detected in GM-CSF-differentiated macrophages. In the brachiocephalic arteries of DEP-exposed ApoE-/- mice we observed increases in CD64+ macrophages (28.2±7.4 vs 15.5±5.6) and IRF5 (16.6±3.6 vs 10.1±3.4) expression, while CD206 expression decreased (4.1±0.9 vs 11.0±1.2) in comparison to saline-exposed mice (Figure 1b mean±SD, n = 5, p<0.05, two-tailed unpaired t-tests, data expressed as % of intima area). Conclusion DEP promotes CD64+ macrophages and IRF5 expression in murine atherosclerosis, while inflammation and IRF5 is induced in vitro, but only in M-CSF-differentiated murine BMDMs. This suggests that DEP has no impact on inflammatory macrophages but could switch homeostatic resident macrophages to a more inflammatory phenotype via the activation of IRF5. Therefore, IRF5 is a promising candidate for further investigation into the initial macrophage response to inhaled particles that leads to the exacerbation of vascular disease.

Progranulin derivative attenuates lung neutrophilic infiltration from diesel exhaust particle exposure.

Air pollutants, such as diesel exhaust particles (DEPs), induce respiratory disease exacerbation with neutrophilic infiltration. Progranulin (PGRN), an epithelial cell and macrophage-derived secretory protein, is associated with neutrophilic inflammation. PGRN is digested into various derivatives at inflammatory sites and is involved in several inflammatory processes. PGRN and its derivatives likely regulate responses to DEP exposure in allergic airway inflammation. To investigate the role of PGRN and its derivatives in the regulation of responses to DEP exposure in allergic airway inflammation. A murine model of allergic airway inflammation was generated in PGRN-deficient mice, and they were simultaneously exposed to DEP followed by intranasal administration of full-length recombinant PGRN (PGRN-FL) and a PGRN-derived fragment (FBAC). Inflammatory status was evaluated by bronchoalveolar lavage fluid and histopathologic analyses. Human bronchial epithelial cells were stimulated with DEPs and house dust mites (HDMs), and the effect of FBAC treatment was evaluated by assessing various intracellular signaling molecules, autophagy markers, inflammatory cytokines, and intracellular oxidative stress. DEP exposure exaggerated neutrophilic inflammation, enhanced IL-6 and CXCL15 secretions, and increased oxidative stress in the murine model; this effect was greater in PGRN-deficient mice than in wild-type mice. The DEP-exposed mice with PGRN-FL treatment revealed no change in neutrophil infiltration and higher oxidative stress status in the lungs. On the contrary, FBAC administration inhibited neutrophilic infiltration and reduced oxidative stress. In human bronchial epithelial cells, DEP and HDM exposure increased intracellular oxidative stress and IL-6 and IL-8 secretion. Decreased nuclear factor erythroid 2-related factor 2 (Nrf2) expression and increased phosphor-p62 and LC3B expression were also observed. FBAC treatment attenuated oxidative stress from DEP and HDM exposure. FBAC reduced neutrophilic inflammation exaggerated by DEP exposure in a mouse model of allergic airway inflammation by reducing oxidative stress. PGRN and PGRN-derived proteins may be novel therapeutic agents in attenuating asthma exacerbation induced by air pollutant exposure.

Particle Size and Morphological Evaluation of Airborne Urban Dust Particles by Scanning Electron Microscopy and Bidimensional Empirical Mode Analysis

Airborne particles affect the health of the population. As particles decrease in size, they can penetrate deeper into the respiratory system, reaching the terminal bronchioles and alveoli. Particles as small as 0.1 µm in diameter may translocate into the bloodstream, potentially impacting various organs. Additionally, the smaller the particle size, the longer they remain suspended in the air, thereby increasing their deleterious damages. The aim of this work is to study the size distribution of airborne particles emitted from anthropogenic sources of air pollution, with a special emphasis on estimating the distribution of micro and nanoparticles considered the most harmful to health. The Bidimensional Empirical Mode Decomposition (BEMD) algorithm was used on micrographs of the particles obtained by Scanning Electron Microscopy (SEM). BEMD is a current empirical computational tool applied to image analysis that allows extracting non-linear heterogeneous oscillations of brightness. We studied ROFA (Residual Oil Fly Ash) from industrial sources and DEP (Diesel Exhaust Particles) from vehicular emissions as airborne particles. After collecting the particles on filters, micrographs were taken using SEM at different magnifications to which the BEMD algorithm was applied. Particle size and asymmetry distributions were obtained for each mode, allowing the identification of the most deleterious particles. The methodology employed herein is relatively simple and effective for inferring the impact of airborne particulate matter on health and the environment.

The Toxic Effects of Petroleum Diesel, Biodiesel, and Renewable Diesel Exhaust Particles on Human Alveolar Epithelial Cells.

The use of alternative diesel fuels has increased due to the demand for renewable energy sources. There is limited knowledge regarding the potential health effects caused by exhaust emissions from biodiesel- and renewable diesel-fueled engines. This study investigates the toxic effects of particulate matter (PM) emissions from a diesel engine powered by conventional petroleum diesel fuel (SD10) and two biodiesel and renewable diesel fuels in vitro. The fuels used were rapeseed methyl ester (RME), soy methyl ester (SME), and Hydrogenated Vegetable Oil (HVO), either pure or as 50% blends with SD10. Additionally, a 5% RME blend was also used. The highest concentration of polycyclic aromatic hydrocarbon emissions and elemental carbon (EC) was found in conventional diesel and the 5% RME blend. HVO PM samples also exhibited a high amount of EC. A dose-dependent genotoxic response was detected with PM from SD10, pure SME, and RME as well as their blends. Reactive oxygen species levels were several times higher in cells exposed to PM from SD10, pure HVO, and especially the 5% RME blend. Apoptotic cell death was observed in cells exposed to PM from SD10, 5% RME blend, the 50% SME blend, and HVO samples. In conclusion, all diesel PM samples, including biodiesel and renewable diesel fuels, exhibited toxicity.

Controllable generation of engine exhaust similar soot particles using an inverted nitrogen-diluted flame burner for calibration purpose

The calibration of vehicle engine exhaust PN analyzers has been a challenge due to the significant difference in properties between calibration particles and measured particles. In this study, an inverted nitrogen-diluted flame burner was designed to generate engine exhaust similar soot particles and evaluated for calibration use. The burner can produce reference-unimodal soot particles at 61–311 nm and total number concentration up to 108 #/cm3 by adjusting the flow rate of ethylene, nitrogen and air. Excellent stability of 0.91 % enables it to generate a fairly stable calibration particle flow. Mixing nitrogen in ethylene makes burner have a high degree of variability in generating smaller particles. The properties of size distribution, morphology, effective density indicate that the generated soot particles can simulate well with engine exhaust particles. TOA results indicate that the soot have high TC mass concentration of over 559.26 mg/m3 and EC/TC fraction of over 90 %.

Diesel exhaust particle inhalation in conjunction with high-fat diet consumption alters the expression of pulmonary SARS-COV-2 infection pathways, which is mitigated by probiotic treatment in C57BL/6 male mice

BackgroundBoth exposure to air pollutants and obesity are associated with increased incidence and severity of COVID-19 infection; however, the mechanistic pathways involved are not well-characterized. After being primed by the transmembrane protease serine 2 (TMPRSS2) or furin protease, SARS-CoV-2 uses the angiotensin-converting enzyme (ACE)-2 receptor to enter respiratory epithelial cells. The androgen receptor (AR) is known to regulate both TMPRSS2 and ACE2 expression, and neuropilin-1 (NRP1) is a proposed coreceptor for SARS-CoV-2; thus, altered expression of these factors may promote susceptibility to infection. As such, this study investigated the hypothesis that inhalational exposure to traffic-generated particulate matter (diesel exhaust particulate; DEP) increases the expression of those pathways that mediate SARS-CoV-2 infection and susceptibility, which is exacerbated by the consumption of a high-fat (HF) diet.MethodsFour- to six-week-old male C57BL/6 mice fed either regular chow or a HF diet (HF, 45% kcal from fat) were randomly assigned to be exposed via oropharyngeal aspiration to 35 µg DEP suspended in 35 µl 0.9% sterile saline or sterile saline only (control) twice a week for 30 days. Furthermore, as previous studies have shown that probiotic treatment can protect against exposure-related inflammatory outcomes in the lungs, a subset of study animals fed a HF diet were concurrently treated with 0.3 g/day Winclove Ecologic® Barrier probiotics in their drinking water throughout the study.ResultsOur results revealed that the expression of ACE2 protein increased with DEP exposure and that TMPRSS2, AR, NRP1, and furin protein expression increased with DEP exposure in conjunction with a HF diet. These DEP ± HF diet-mediated increases in expression were mitigated with probiotic treatment.ConclusionThese findings suggest that inhalational exposure to air pollutants in conjunction with the consumption of a HF diet contributes to a more susceptible lung environment to SARS-CoV-2 infection and that probiotic treatment could be beneficial as a preventative measure.

Spray combustion characteristics of boron slurry fuel in high particle loading conditions

Enhancing the energy density of hydrocarbon fuels is indeed crucial, especially in the context of addressing energy needs. Incorporating energetic particles as additives into conventional liquid fuels garners increased attention due to its potential to enhance energy density. Due to its high energy potential, boron is the most promising additive in several energetic particles. However, the study focusing on the boron-loaded slurry fuels are limited. Therefore, the present work focuses on the effect of boron loading on the spray combustion of boron-loaded slurry fuel, especially at higher loadings (10%, 20% & 30% boron + Jet A-1 fuel) using a swirl-stabilized spray combustor. The research scrutinizes the feed and exhaust particles' surface morphology, chemical composition and active boron content through diverse particle characterization techniques. Furthermore, the study investigates the influence of boron loading on the combustion characteristics of slurry fuel using methods such as colour flame imaging, spectroscopy, and BO2* Chemiluminescence imaging. The impact of boron loading on the positive thermal contribution of the slurry was examined by analyzing temperature measurements at various locations within the combustor. The BO2* chemiluminescence imaging and spectroscopy results indicate that the intensity of BO2 emission increases with a rise in particle loading. The temperature results reveal an increase in temperature compared to pure Jet A-1 for all the boron-loaded cases. In particular, JB10 and JB20 achieved nearly 90% and 85% of the theoretical temperature increase. The diffractogram and thermogravimetric results of the burnt particles collected show that the particles were burnt thoroughly for the boron-loaded cases.

Assessment of Cytotoxicity and Genotoxicity Induced by Diesel Exhaust Particles (DEPs) on Cell Line A549 and the Potential Role of Amide-Functionalized Carbon Nanotubes as Fuel Additive

Epidemiological studies have consistently linked air pollution to severe health risks. One strategy to reduce the impact of combustion products from engines is adding additives to the fuel. Potential benefits have been observed in terms of performance and emissions, as well as in decreasing fuel consumption. However, the associated emission of particulate matter into the environment may have unforeseen health effects. This study examines the effects of diesel exhaust particles (DEPs) from diesel fuel mixed with amide-functionalized carbon nanotubes (CNTF). The aim is to analyze the properties of DEPs and determine their toxic effects on lung cells. The DEPs were characterized using scanning and transmission electron microscopy, while the polycyclic aromatic hydrocarbons (PAHs) were analyzed through gas chromatography. Various assays were conducted to assess cell viability, apoptosis, oxidative stress, and DNA damage. The addition of CNTF to diesel fuel altered the morphology and size of the particles, as well as the quantity and composition of PAHs. At the cellular level, diesel DEPs induce higher levels of reactive oxygen species (ROS) production, DNA damage, apoptosis, and cytotoxicity compared to both CNTF and diesel–CNTF DEPs. These findings suggest that the nano-additives enhance energy efficiency by reducing pollutants without significantly increasing cell toxicity.

P07-10 Differential impact of renewable diesel exhaust particles on protein profiles in bronchoalveolar lavage fluid and plasma after instillation exposure in mice

P07-10 Differential impact of renewable diesel exhaust particles on protein profiles in bronchoalveolar lavage fluid and plasma after instillation exposure in mice

Modulation of miR-466d-3p on Wnt signaling pathway in response to DEPs-induced blood-brain barrier disruption

BackgroundDiesel exhaust particles (DEPs), a predominant component of ambient particulate matter (PM), are classified as ultrafine particles with the capacity to penetrate the cerebral blood-brain barrier (BBB). This penetration is implicated in the pathogenesis of central nervous system (CNS) disorders. The integrity of the BBB is inextricably linked to cerebrovascular homeostasis and the development of neurodegenerative disease, highlighting the importance of studying the effects and mechanisms of DEPs on BBB function damage. Methods and resultsUtilizing mouse cerebral microvascular endothelial cells (bEnd.3 cells) as an in vitro model of the BBB, we explored the detrimental effects of DEPs exposure on BBB permeability and integrity, with particular focus on inflammation, cell apoptosis, and miRNA expression profiles. Our findings revealed that exposure to DEPs at varying concentrations for 48 h resulted in the inhibition of bEND.3 cell proliferation, induction of cell apoptosis, and an upregulation in the secretion of inflammatory cytokines/chemokines and adhesion molecules. The BBB integrity was further compromised, as evidenced by a decrease in trans-epithelial electrical resistance(TEER), a reduction in cytoskeletal F-actin, and diminished tight junction (TJ) protein expression. Microarray analysis revealed that 23 miRNAs were upregulated and 11 were downregulated in response to a 50 μg/mL DEPs treatment, with miR-466d-3p being notably differentially expressed. Wnt3 was identified as a target of miR-466d-3p, with the Wnt signaling pathway being significantly enriched. We validated that miR-466d-3p expression was downregulated, and the protein expression levels of Wnt/β-catenin and Wnt/PCP signaling components were elevated. The modulation of the Wnt signaling pathway by miR-466d-3p was demonstrated by the transfection of miR-466d-3p mimic, which resulted in a downregulation of Wnt3 and β-catenin protein expression, and the mRNA level of Daam1, as well as an enhancement of TJ proteins ZO-1 and Claudin-5 expression. ConclusionsOur study further confirmed that DEPs can induce the disruption of BBB integrity through inflammatory processes. We identified alterations in the expression profile of microRNAs (miRNAs) in endothelial cells, with miR-466d-3p emerging as a key regulator of tight junction (TJ) proteins, essential for maintaining BBB integrity. Additionally, our findings primarily demonstrated that the Wnt/ β-catenin and Wnt/PCP signaling pathway can be activated by DEPs and are regulated by miR-466d-3p. Under the combined effects of Wnt/PCP and inflammation, there is an ultimate increase in BBB hyperpermeability.

Assessment of reactive-control compression ignition engine performance and emissions using spirulina microalgae biodiesel in conjunction with methanol as low-reactive fuel

AbstractDue to their numerous uses and great fuel economy, diesel engines have been around for millennia. Despite these benefits, diesel engines have been found to pollute the environment severely. Most of the problems were caused by these engines' combustion processes, engine loads, and exhaust particles. The RCCI engine used in the experiment has 20% lower fuel and 80% high reactive fuel. In this research, methanol, and algae biodiesel blends with dimethyl ether acted as lower and higher reactive fuels, respectively, and these fuels were used to analyze the performance and emission in the RCCI engine. Among the 80% of high reactive fuel, blends contain different proportions of algae biodiesel and diethyl ether such as 32B, 28B4ME, 24B8ME, 20B12ME, and 16B16ME. A single-cylinder, four-stroke RCCI engine with a speed of 1500 rpm is used for the experiment. In the tests, the brake power is varied from 1 to 5 kW with an interval of 1 kW. In the results, BTE, BSFC, and EGT engine performance as well as NOX, HC, CO2, and smoke emissions. According to the experimental findings, the fuel properties of 16B16ME show a calorific value of 34.7 /MJ kg-1 and BTE shows improvement for all additive added fuel and 16B16ME shows higher BTE of 32.5% than other fuel blends, Similarly NOx emission also reduced for 628 ppm for 16B16ME than other fuel blends. Therefore 16B16ME is a suitable blend than other blends in RCCI engine based on the experimental results achieved in the present research.

Air pollution amyloidogenesis is attenuated by the gamma-secretase modulator GSM-15606.

Chronic air pollution (AirPoll) is associated with accelerated cognitive decline and risk of Alzheimer's disease (AD). Correspondingly, wild-type and AD-transgenic rodents exposed to AirPoll have increased amyloid peptides and behavioral impairments. We examined the γ-secretase modulator GSM-15606 for potential AirPoll protection by its attenuating of amyloid beta (Aβ)42 peptide production. Male and female wild-type mice were fed GSM-15606 during an 8-week inhalation exposure to AirPoll subfractions, ambient nanoparticulate matter (nPM), and diesel exhaust particles (DEP). GSM-15606 decreased Aβ42 during nPM and DEP exposure without changing beta- or gamma-secretase activity or BACE1 and PS1 protein levels. DEP increased lateral ventricle volume by 25%. These enzyme responses are relevant to AD drug treatments, as well as to the physiological functions of the Aβ42 peptide. GSM-15606 attenuation of Aβ42 may benefit human exposure to AirPoll. Gamma-secretase modulator (GSM-15606) attenuates the amyloidogenic amyloid beta (Aβ)42 peptide during exposure to air pollution, which may be a mechanism by which air pollution increases Alzheimer's disease (AD) risk. AD drug treatments may also consider Aβ homeostasis among the chronic effects of GSM-15606 and other amyloid reduction treatments on secretase enzymes.

Long-term exposure to diesel exhaust particles induces concordant changes in DNA methylation and transcriptome in human adenocarcinoma alveolar basal epithelial cells

BackgroundDiesel exhaust particles (DEP), which contain hazardous compounds, are emitted during the combustion of diesel. As approximately one-third of the vehicles worldwide use diesel, there are growing concerns about the risks posed by DEP to human health. Long-term exposure to DEP is associated with airway hyperresponsiveness, pulmonary fibrosis, and inflammation; however, the molecular mechanisms behind the effects of DEP on the respiratory tract are poorly understood. Such mechanisms can be addressed by examining transcriptional and DNA methylation changes. Although several studies have focused on the effects of short-term DEP exposure on gene expression, research on the transcriptional effects and genome-wide DNA methylation changes caused by long-term DEP exposure is lacking. Hence, in this study, we investigated transcriptional and DNA methylation changes in human adenocarcinoma alveolar basal epithelial A549 cells caused by prolonged exposure to DEP and determined whether these changes are concordant.ResultsDNA methylation analysis using the Illumina Infinium MethylationEPIC BeadChips showed that the methylation levels of DEP-affected CpG sites in A549 cells changed in a dose-dependent manner; the extent of change increased with increasing dose reaching the statistical significance only in samples exposed to 30 µg/ml DEP. Four-week exposure to 30 µg/ml of DEP significantly induced DNA hypomethylation at 24,464 CpG sites, which were significantly enriched for DNase hypersensitive sites, genomic regions marked by H3K4me1 and H3K27ac, and several transcription factor binding sites. In contrast, 9,436 CpG sites with increased DNA methylation levels were significantly overrepresented in genomic regions marked by H3K27me3 as well as H3K4me1 and H3K27ac. In parallel, gene expression profiling by RNA sequencing demonstrated that long-term exposure to DEP altered the expression levels of 2,410 genes, enriching 16 gene sets including Xenobiotic metabolism, Inflammatory response, and Senescence. In silico analysis revealed that the expression levels of 854 genes correlated with the methylation levels of the DEP-affected cis-CpG sites.ConclusionsTo our knowledge, this is the first report of genome-wide transcriptional and DNA methylation changes and their associations in A549 cells following long-term exposure to DEP.

Using DPF to Control Particulate Matter Emissions from Ships to Ensure the Sustainable Development of the Shipping Industry

PM (particulate matter) emissions from ships are the main sources of marine atmosphere pollution. Controlling the emissions of particulate matter from ships is related to the sustainable development of the shipping industry. To reduce PM emissions from marine four-stroke diesel engines, DPFs are effective. Our results show that DPF had more than 90% capturing efficiency for both the number and mass emissions of PM, and the capturing efficiency for the accumulation mode was higher than that of the nuclear mode. DPF can also significantly reduce the chemical components of PM in marine diesel exhaust gas. The removal efficiencies for OC and EC were 89.7–91.6% and 84.8–92.8%, respectively, with each particle size range showing over 80% efficiency. SO42− was the ion with the highest content, followed by NH4+, NO3−, Na+, NO2−, and Cl−, with their reduced proportions remaining consistent with the removal efficiency of particulate matter. DPF can also effectively reduce PAH content and toxicity. The use of DPF can greatly improve the impact of ship emissions on the marine atmospheric environment. The appropriate DPF with the best performance can be selected according to the exhaust parameters and particle size distributions with different characteristics.

Epithelial-Mesenchymal Transition in Chronic Rhinosinusitis

Chronic rhinosinusitis (CRS) is characterized by prolonged inflammation of the nasal and paranasal sinus mucosa lasting over 12 weeks. CRS is divided into two main types based on the presence of nasal polyps: CRS without nasal polyps and CRS with nasal polyps. The condition is further classified into endotypes based on type 1, type 2, and type 3 inflammatory signatures, with differences in terms of disease severity, prognosis, and treatment response. Recent studies have emphasized the importance of the epithelial-mesenchymal transition (EMT) in CRS progression. In CRS, the EMT can be triggered by infections, allergens, hypoxia, and environmental pollutants. Specifically, EMT induction proceeds through the following mechanisms: viral and bacterial infections disrupt the epithelial barrier, house dust mites and other allergens activate the TGF-β and EGFR signaling pathways, hypoxia increases HIF-1α and other mesenchymal markers, and diesel exhaust particles and particulate matter cause oxidative stress. Maintaining the integrity of the epithelial barrier is essential for nasal mucosa homeostasis. In CRS, barrier damage activates repair processes that trigger the EMT, resulting in barrier dysfunction and tissue remodeling. Epithelial barrier dysfunction allows antigens and pathogens to penetrate, perpetuating inflammation and promoting the EMT. This disruption is a hallmark of CRS, emphasizing the importance of barrier integrity in the development of the disease. Key signaling pathways regulating the EMT in CRS include TGF-β, Wnt, HMGB1, AGE/ERK, TNF-α, and various miRNAs. These signaling pathways connect to various downstream pathways, such as the Smad2/3, GSK-3β/β-catenin, RAGE, and NF-κB pathways. This review focuses on the complex mechanisms of the EMT in CRS, emphasizing the role of epithelial barrier dysfunction and subsequent EMT processes in driving the disease’s development and progression. A deeper understanding of these EMT-driven mechanisms will help identify the potential therapeutic targets aimed at restoring epithelial integrity and reversing the EMT.

Calibrations, Validations, and Checks of a Dual 23 nm and 10 nm Diffusion Charger-Based Portable Emissions Measurement System (PEMS).

The upcoming Euro 7 vehicle exhaust emissions regulation includes particle number (PN) limits for all vehicles, not only those with direct fuel injection. It also sets the lower detection particle size of the PN methodology to 10 nm from 23 nm. Recently, a commercial diffusion charger-based PEMS added the possibility of switching the lower size between 23 nm and 10 nm. In this study, we assessed the dual PEMS in the calibration laboratory using diffusion flame soot or spark discharge graphite particles following the regulated procedures. Furthermore, we compared the dual PEMS with a laboratory grade system (LABS) using soot, graphite, and vehicle exhaust particles. To put the results into perspective, we added comparisons (validations) of two additional 23 nm PEMSs with LABSs over a three-year period. The results showed that the differences of the 23 nm PEMSs remained the same (around 35% underestimation) over the years and were similar to the dual PEMS. This difference is still well within the permissible tolerance from the regulation (50%). We argued that the reason is the calibration material used by the manufacturer (spark discharge graphite). We demonstrated that calibrating with combustion soot could reduce the differences. The 10 nm PEMS gave similar results but with much smaller differences, indicating that the calibration material is of less importance for the Euro 7 step. The results showed that the measurement uncertainty has not increased but rather decreased for the specific PEMS switching from 23 nm to 10 nm.

Immunological Effects of Diesel Particles in a Murine Model of Healthy Mice.

Introduction: Exposure to environmental pollutants such as diesel exhaust particles (DEP) increases the risk of respiratory disease exacerbation. However, the possible effects of these particles on the general population remain poorly understood. The present study aimed to assess the immunomodulatory and inflammatory effects of the inhalation of DEP in a model of healthy mice undergoing short-, mid- and long-term exposure. Materials and Methods: BALB/c ByJ mice were randomly divided into five experimental groups. The control group received three intranasal instillations of saline over 8 days while the other four groups received intranasal instillations of 150 µg of DEP 3 days per week for 8, 17, 26, and 53 days. Lung function assessment and flow cytometry were performed. Results: In lung tissue, intranasal exposure to DEP decreased total monocytes (p < 0.015 in all groups). At 26 days, a reduction in inflammatory monocytes and an increase in resident monocytes were observed, p = 0.001 and 0.0001, respectively. Eosinophils and neutrophils decreased at 26 days (p = 0.017 and p = 0.041, respectively). The intranasal challenges of DEP increased the total population of dendritic cells (DC) at 26 and 53 days (p = 0.017 and p = 0.022, respectively) and decreased the total and alveolar populations of macrophages (p < 0.003 for all groups compared to control), while interstitial macrophage populations increased over the time period (p = 0.0001 for all groups compared to control). Conclusions: Continuous DEP exposure triggers immune mechanisms that predispose healthy individuals to a pro-inflammatory and hyper-reactive microenvironment. This mouse model provides evidence of the capacity of DEP to increase DC, interstitial macrophages, and resident monocytes.

Measurement report: Vanadium-containing ship exhaust particles detected in and above the marine boundary layer in the remote atmosphere

Abstract. Each year, commercial ships emit over 1.67 Tg of particulate matter (PM) pollution into the atmosphere. These ships rely on the combustion of heavy fuel oil, which contains high levels of sulfur, large aromatic organic compounds, and metals. Vanadium is one of the metals most commonly associated with heavy fuel oil and is often used as a tracer for PM from ship exhaust. Previous studies have suggested that vanadium-containing PM has impacts on human health and climate due to its toxicological and cloud-formation properties, respectively; however, its distribution in the atmosphere is not fully understood, which limits our ability to quantify the environmental implications of PM emitted by ships. Here, we present data obtained from a Particle Analysis by Laser Mass Spectrometry (PALMS) instrument on the NASA DC-8 aircraft during the 2016–2018 Atmospheric Tomography Mission (ATom) and show that ∼ 1 % of the accumulation mode particles measured in the marine boundary layer of the central Pacific and Atlantic oceans contain vanadium. These measurements, which were made without targeting ship plumes, suggest that PM emitted by ships is widespread in the atmosphere. Furthermore, we observed vanadium-containing ship exhaust particles at altitudes up to 13 km, which demonstrates that not all ship exhaust particles are immediately removed via wet deposition processes. In addition, using laboratory calibrations, we determined that most vanadium-containing ship exhaust particles can contain up to a few weight percent of vanadium. This study furthers our understanding of both the chemical composition and distribution of PM emitted by ships, which will allow us to better constrain the climate, health, and air quality implications of these particle types in the future. We note that these data were collected prior to the 2020 International Maritime Organization (IMO) sulfur regulation and stand as a reference for understanding how ship emissions have evolved in light of these regulations.

Vehicle related non exhaust particle emissions – Euro 7 requirements

Vehicle related non exhaust particle emissions – Euro 7 requirements