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Physicochemical properties of nanoparticles are important in regulating nanoparticle toxicity; however, the contribution of nanoparticle charge remains unclear. The objective of this study was to investigate the pulmonary effects of inhalation of charged soot nanoparticles. We established a stably charged nanoparticle generation system for whole-body exposure in BALB/c mice, which produced positively charged, negatively charged, and neutral soot nanoparticles in a wide range of concentrations. After a 7-day exposure, pulmonary toxicity was assessed, together with proteomics analysis. The charged soot nanoparticles on average carried 1.17-1.35 electric charges, and the sizes for nanoparticles under different charging conditions were all fixed at 69 ~ 72 nm. We observed that charged soot nanoparticles induced cytotoxic LDH and increased lung permeability, with the release of 8-isoprostane and caspase-3 and systemic IL-6 in mice, especially for positively charged soot nanoparticles. Next, we observed that positive-charged soot nanoparticles upregulated Eif2, Eif4, sirtuin, mammalian target of rapamycin (mTOR), peroxisome proliferator-activated receptors (PPAR), and HIPPO-related signaling pathways in the lungs compared with negatively charged soot nanoparticles. HIF1α, sirt1, E-cadherin, and Yap were increased in mice's lungs by positively charged soot nanoparticle exposure. In conclusion, carbonaceous nanoparticles carrying electric ions, especially positive-charged, are particularly toxic when inhaled and should be of concern in terms of pulmonary health protection.

Fine particulate matter (PM2.5) has been linked to cardiopulmonary disease and systemic effects in humans. However, few studies have investigated the particle bioreactivity in Chinese megacities during haze episodes. The objective of this study was to determine the contributions of chemical components in PM2.5 to particle bioreactivity in Chinese megacities during haze episodes. PM2.5 samples were collected in 14 megacities across China from 23 December 2013 to 16 January 2014. Average PM2.5 concentrations ranged 88.92~199.67 μg/m3. Organic carbon (OC), elemental carbon (EC), anions, and cations per unit of PM2.5 were linked to cellular bioreactivity (i.e., reactive oxygen species (ROS) as assessed by dichlorodihydrofluorescein diacetate (DCFH) and inflammation as assessed by interleukin (IL)-6 in A549 cells). The contributions of chemicals in PM2.5 to ROS and inflammation were examined by the Pearson correlation coefficient and random forests. These results indicated that OC, Ca2+, SO42−, Cl−, F−, K+, and NO3− contributed to ROS production, whereas OC, Cl−, EC, K+, F−, Na+, and Ca2+ contributed to inflammation. In conclusion, PM2.5-contained OC and acidic ions are important in regulation of oxidative stress and inflammation during haze episodes. Our findings suggest that severe haze PM2.5 events cause deterioration in air quality and may adversely affect human health.

Exposure to road dust particulate matter (PM) causes adverse health impacts on the human airway. However, the effects of road dust on the upper airway epithelium in humans remain unclear. We investigated the involvement of the epidermal growth factor receptor (EGFR) after PM with an aerodynamic diameter of < 2.5 μm (PM2.5)-induced E-cadherin disruption of human pharyngeal epithelial cells. First, we collected road dust PM2.5 from 10 Chinese cities, including Wuhan, Nanjing, Shanghai, Guangzhou, Chengdu, Beijing, Lanzhou, Tianjin, Harbin, and Xi'an. Human pharyngeal FaDu cells were exposed to road dust PM2.5 at 50 μg/mL for 24 h, cytotoxicity (cell viability and lactate dehydrogenase (LDH)) was assessed, and expressions of the proinflammatory interleukin (IL)-6 and high-mobility group box 1 (HMGB1) protein, receptor for advanced glycation end products (RAGE), occludin, E-cadherin, EGFR, and phosphorylated (p)-EGFR were determined. The E-cadherin gene was then knocked down to investigate EGFR activation in FaDu cells. Exposure to road dust PM2.5 resulted in a decrease in cell viability and increases in LDH and IL-6. Our data suggested that PM2.5 could decrease expressions of occludin and E-cadherin and increase expressions of EGFR and p-EGFR, which was confirmed by E-cadherin-knockdown. Our results showed a negative association between the alterations in E-cadherin and total elemental components in correlation analysis, especially S, Cl, K, Ti, Mn, Fe, Cu, Zn, and Pb. Exposure to metals in PM2.5 from road dust may lead to loss of the barrier function of the upper airway epithelium and activation of the EGFR. Our study showed the adverse effects of road dust PM2.5 on pharyngeal epithelial cells of the human upper airway.

Particle morphology can affect the performance of an electrostatic precipitator air–liquid interface (ESP-ALI) cell exposure system and the resulting cell toxicity. In this study, three types of monodisperse aerosols – spherical sucrose particles, nonspherical align soot aggregates, and nanosilver aggregates/agglomerates – were selected to evaluate the collection efficiency at flow rates ranging from 0.3 to 1.5 lpm. To quantify the particle morphology, the fractal dimensions (Df) of the tested aerosols were characterized. The penetration of fine particles (dp = 100–250 nm) under different operating conditions was correlated with a characteristic exponential curve using the dimensionless drift velocity (Vc/Vavg,r) as the scaling parameter. For nanoparticles (NPs, dp nm) with different particle morphologies, the particle penetrations in the ESP-ALI were similar, but their diffusion losses were not negligible. In contrast, for fine particles, the collection efficiency of soot nanoaggregates (Df = 2.29) was higher than that of spherical sucrose particles. This difference might be due to the simultaneous influences of the electric field-induced and flow field-induced alignment. Furthermore, based on Zhibin and Guoquan’s Deutsch model, a quadratic equation was applied to fit the experimental data and to predict the performance of the ESP-ALI.

Introduction Angiotensin-converting enzyme 2 (ACE2) provides an adhesion site for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Patients with COPD could have severe outcomes after SARS-CoV-2 infection. The objective of this study was to investigate ACE2 regulation by air pollution during the development of COPD. Methods Sprague Dawley rats were exposed to unconcentrated traffic-related air pollution for 3 and 6 months. We examined lung injury markers, oxidative stress, inflammation, emphysema, ACE2 and angiotensin II receptor type 1 (AT1) and 2 (AT2) in the lungs after exposure. Results Lung injury occurred due to an increase in permeability and lactate dehydrogenase cytotoxicity was observed after 6 months of exposure to fine particulate matter of, Short-term exposure to PM1 increases ACE2 overexpression in lungs. Long-term exposure to PM1 decreases the ACE2 overexpression in emphysema. Air pollution may be a risk for #SARSCoV2 adhesion during the development of COPD. https://bit.ly/2Vfykur

This study investigated the hourly inorganic aerosol chemistry and its impact on atmospheric visibility over an urban area in Central Taiwan, by relying on measurements of aerosol light extinction, inorganic gases, and PM

Acute exposure to fresh traffic-related air pollutants (TRAPs) can be high for road users, including motorbike drivers, cyclists, and pedestrians. However, evaluating the toxicity of fresh traffic emissions from on-road vehicles is challenging since pollution properties can change dynamically within a short distance and time. This study demonstrated a mobile platform equipped with an On-Board Diagnostic II (OBDII) system, a tailor-made portable emission measurement system, and an electrostatic air-liquid interface exposure system with human monocytic THP-1 cells to characterize on-road tailpipe emissions under real driving conditions. High number concentrations up to 10

Characterizing engineered nanoparticles (ENPs) in complex environmental matrices remains a challenging task. This work presents a two-dimensional size analysis method by combining differential mobility analyzer (DMA) and single-particle inductively coupled plasma-mass spectrometry (spICP-MS) with a new atomizer (ATM)-enabled sample introduction that is relatively easy to operate. The tailing of electrical mobility size distributions was solved by heating the aerosol flow, where water-shelled gold nanoparticles (AuNPs) were dehydrated, effectively eliminating the tailing. The improved method has a good sizing performance and can resolve the size fractions of mixed 30 nm and 50 nm AuNPs. It can reliably analyze 7.8 × 10

This study applied positive matrix factorization (PMF) to identify the sources of size-resolved submicrometer (10-1000 nm) particles and quantify their contributions to impaired visibility based on the particle number size distributions (PNSDs), aerosol light extinction (b

Removing submicron particles in the size range from 0.1 to 1.0 µm from gas streams is difficult because they cannot be efficiently captured neither through inertial separation nor by diffusion utilized in air pollution control devices. Electrostatic agglomeration is an effective and practical method for improving the removal efficiency of fine particulate matters. For optimizing the performance of electrostatic agglomerators, in addition to the intensity and frequency of an alternating electric field and the particle residence time, an electrostatic aerosol particle agglomerator was designed and established to experimentally evaluate the influence of particle charges on its performance in this study. The results demonstrate that the performance of the electrostatic aerosol agglomerator can be greatly improved in terms of increasing the particle charges from 9 to 19 (e−/particle). Combined with the low frequency of an AC electric field, the agglomeration efficiency can be further enhanced. The highest agglomeration efficiency of 40.2% is achieved in the submicron size range at AC frequency of 45 Hz. Furthermore, the oscillating distance (cm/Hz) is proposed and estimated for correlating the agglomeration efficiency under various testing conditions. It was found that the agglomeration efficiency can be described by a simple power-law equation using this parameter.

INTRODUCTION Coronavirus disease 2019 (COVID-19) emerged in Wuhan, China in late 2019, and soon unfolded as a global outbreak accompanied by declarations of a public health emergency of international concern (PHEIC) and later a pandemic from the World Health Organization (WHO). COVID-19 has resulted in 2,626,321 confirmed cases and 181,938 reported deaths worldwide (as of 14 April 2020). The underlying virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a highly contagious novel coronavirus that transmits as an aerosol and threatens people of all ages, from infant to geriatric, while those with cardiovascular disease are recognized as particularly susceptible to more severe symptoms from SARS-CoV-2 infection. WHO recommends using a mask to limit the COVID-19 outbreak; however, SARS-CoV-2 transmission models and its removal efficiency by wearing a mask remain unclear. Furthermore, differences in the field-specific definitions/terminologies related to transmission and mask usage tend to cause confusion and misunderstanding among both experts and the public.

Electrospray-differential mobility analysis coupled with aerosol particle mass analysis (ES-DMA/APM) was demonstrated for the development of a metal–organic framework (MOF) nanocarrier system. A successful quantification of ibuprofen loading in UiO-66-NH2 (i.e., the representative drug molecule and MOF, respectively) achieved based on the aerosol particle mass of MOF measured by ES-DMA/APM (≈55 mg of ibuprofen/g of UiO-66-NH2). The structural stability of UiO-66-NH2 versus ibuprofen release was successfully quantified over a 7-day period in an acidic phosphate buffer solution. The methodology provides a proof-of-concept scheme for controlled release studies of different types of active pharmaceutical ingredients from a variety of MOF-based nanocarrier systems.

Traffic emission is responsible for most small-sized particulate matter (PM) air pollution in urban areas. Several recent studies have indicated that traffic-related PM may aggravate kidney disease. Furthermore, exposure to particulate air pollution may be related to the risk of chronic kidney disease (CKD). However, the underlying molecular mechanisms have not been adequately addressed. In the present study, we studied the mechanisms of renal damage that might be associated with exposure to PM. In a real world of whole-body exposure to traffic-related PM model for 3-6 months, PM in urban ambient air can affect kidney function and induce autophagy, endoplasmic reticulum (ER) stress and apoptosis in kidney tissues. Exposure to traffic-related diesel particulate matter (DPM) led to a reduction in cell viability in human kidney tubular epithelial cells HK-2. DPM increased mitochondrial reactive oxygen species (ROS) and decreased the mitochondrial membrane potential. Furthermore, DPM induced ER stress and activated the unfolded protein response (UPR) pathway. Eventually, DPM exposure induced caspase pathways and triggered apoptosis. In addition, DPM induced autophagy through the inhibition of the Akt/mTOR pathway. Autophagy inhibition resulted in significantly increased cytotoxicity and apoptosis. These findings suggest that air pollution in urban areas may cause nephrotoxicity and autophagy as a protective role in PM-induced cytotoxicity.

Virtual impactors can be used as aerosol concentrators as well as particle size classifiers. The flow field and particle trajectory inside a linear slit-type virtual impactor were investigated using a commercial computational fluid dynamics software package. Effects of flow and slit geometry, including the inlet flow (Qin), the ratio of minor to total flow (r), and the configuration of the taper-lip slit nozzle and the collection slit nozzle, were studied. A new modified Stokes number (Stkc) for the virtual impactor was proposed to predict the d50 at different r values. Stkc,500.5 was found to be retained at approximately 0.9 under different Qin or r values, and it can be considered the characteristic performance parameter for the slit virtual impactor. The numerical simulation results show that the particle loss starts increasing when Stkc0.5 is larger than 2.0 due to a particle-crossing phenomenon. The range of the maximum concentration factor (CFmax) is influenced by the particle-crossing phenomenon. An expression was also developed to predict the size range of particles with the maximum CF under different inlet flow rates. Regarding the geometrical configuration, the arc-lip nozzle could postpone particle-crossing and lessen the internal losses of coarse particles, whereas it increased particle losses near d50. However, the divergent collection slit nozzle could effectively decrease particle losses on the wall of the nozzle without this side effect. The designing guidelines of a linear-slit virtual impactor are briefly summarized based on these findings.

A custom-built steam-based aerosol collector (SBAC) was developed to improve the detection limits in aerosol chemical analysis. The SBAC was coupled with wet chemical analytical instruments to characterize the chemical composition of ambient particulate matter with high-time resolution. The particulate matter was mixed with a jet of steam and formed large droplets because of the supersaturation condition in the cooling chamber. The enlarged droplets were subsequently collected using an inertial aerosol separator and delivered to selected instruments for chemical analysis. Experiments were subsequently conducted to evaluate our custom-built SBAC under various sampling flow rates. In particular, particle growth and particle collection efficiency experiments were conducted, and the SBAC was compared with a filter-based sampler. Sample solutions were collected, extracted, and analyzed to determine the influence of sampling flow rate, particle size, and aerosol chemical concentration on the SBAC's collection efficiency. The SBAC was found to provide data with a higher time resolution, to exhibit an improved detection limit, and to effectively perform aerosol chemical analysis compared with the filter-based samplers, although the effect of flow rate on SBAC performance is complicated and further experiments on this aspect are warranted. This paper contributes to the literature by providing guidelines for designing a SBAC for aerosol chemical analysis.

We investigated the effects of antibiotics, drugs, and metals on lung and intestinal microbiomes after sub-chronic exposure of low-level air pollution in ageing rats. Male 1.5-year-old Fischer 344 ageing rats were exposed to low-level traffic-related air pollution via whole-body exposure system for 3 months with/without high-efficiency particulate air (HEPA) filtration (gaseous vs. particulate matter with aerodynamic diameter of ≤2.5 µm (PM

Human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) were shown to have potential for immunoregulation and tissue repair. The objective of this study was to investigate the effects of hUC-MSCs on emphysema in chronic obstructive pulmonary disease (COPD). The C57BL/6JNarl mice were exposed to cigarette smoke (CS) for 4 months followed by administration of hUC-MSCs at 3 × 106 (low dose), 1 × 107 (medium dose), and 3 × 107 cells/kg body weight (high dose). The hUC-MSCs caused significant decreases in emphysema severity by measuring the mean linear intercept (MLI) and destructive index (DI). A decrease in neutrophils (%) and an increase in lymphocytes (%) in bronchoalveolar lavage fluid (BALF) were observed in emphysematous mice after hUC-MSC treatment. Lung levels of interleukin (IL)-1β, C-X-C motif chemokine ligand 1 (CXCL1)/keratinocyte chemoattractant (KC), and matrix metalloproteinase (MMP)-12 significantly decreased after hUC-MSC administration. Significant reductions in tumor necrosis factor (TNF)-α, IL-1β, and IL-17A in serum occurred after hUC-MSC administration. Notably, the cell viability of lung fibroblasts improved with hUC-MSCs after being treated with CS extract (CSE). Furthermore, the hUC-MSCs-conditioned medium (hUC-MSCs-CM) restored the contractile force, and increased messenger RNA expressions of elastin and fibronectin by lung fibroblasts. In conclusion, hUC-MSCs reduced inflammatory responses and emphysema severity in CS-induced emphysematous mice.

Aerosol type plays a critical role in the relationship between aerosol optical depth (AOD) and particulate matter (PM) mass concentration. Here, we present a mathematical formulation of how PM...

Background: Air pollution has been linked to emphysema in chronic obstruction pulmonary disease (COPD). However, the underlying mechanisms in the development of emphysema due to air pollution remain unclear. The objective of this study was to investigate the role of components of the Hippo signaling pathway for E-cadherin-mediated contact inhibition of proliferation in the lungs after air pollution exposure. E-Cadherin-mediated contact inhibition of proliferation via the Hippo signaling pathway was investigated in Sprague-Dawley (SD) rats whole-body exposed to air pollution, and in alveolar epithelial A549 cells exposed to diesel exhaust particles (DEPs), E-cadherin-knockdown, and high-mobility group box 1 (HMGB1) treatment. Underlying epithelial differentiation, apoptosis, and senescence were also examined, and the interaction network among these proteins was examined. COPD lung sections were used to confirm the observations in rats. Results: Expressions of HMGB1 and E-cadherin were negatively regulated in the lungs and A549 cells by air pollution, and this was confirmed by knockdown of E-cadherin and by treating A549 cells with HMGB1. Depletion of phosphorylated (p)-Yap occurred after exposure to air pollution and E-cadherin-knockdown, which resulted in decreases of SPC and T1α. Exposure to air pollution and E-cadherin-knockdown respectively downregulated p-Sirt1 and increased p53 levels in the lungs and in A549 cells. Moreover, the protein interaction network suggested that E-cadherin is a key activator in regulating Sirt1 and p53, as well as alveolar epithelial cell differentiation by SPC and T1α. Consistently, downregulation of E-cadherin, p-Yap, SPC, and T1α was observed in COPD alveolar regions with particulate matter (PM) deposition. Conclusions: Our results indicated that E-cadherin-mediated cell-cell contact directly regulates the Hippo signaling pathway to control differentiation, cell proliferation, and senescence due to air pollution. Exposure to air pollution may initiate emphysema in COPD patients.

The deterioration of visibility due to air pollutants and relative humidity has been a serious environmental problem in eastern Asia. In most previous studies, chemical compositions of atmospheric particles were provided using filter-based offline analyses, which were unable to provide long-term and in-situ measurements that resolve sufficient temporal variations of air pollution and meteorology, hindering the resolution of the relationship between air quality and visibility. Here, we present a year-long continuously measured data from a comprehensive suite of online instruments to investigate diurnal and seasonal impacts of the aerosol chemical compositions in PM

The significance of this work is that ambient PM

Epidemiological studies identified the relationship between air pollution and pulmonary tuberculosis. Effects of lung-deposited dose of particulate matter (PM) on culture-positive pulmonary tuberculosis remain unclear. This study investigates the association between lung-deposited dose of PM and pulmonary tuberculosis pleurisy. A case-control study of subjects undergoing pleural effusion drainage of pulmonary tuberculosis (case) and chronic heart failure (control) was conducted. Metals and biomarkers were quantified in the pleural effusion. The air pollution exposure was measured and PM deposition in the head, tracheobronchial, alveolar region, and total lung region was estimated by Multiple-path Particle Dosimetry (MPPD) Model. We performed multiple logistic regression to examine the associations of these factors with the risk of tuberculosis. We observed that 1-μg/m3 increase in PM10 was associated with 1.226-fold increased crude odds ratio (OR) of tuberculosis (95% confidence interval (CI): 1.023-1.469, p

Quantifying aerosol compositions (e.g., type, loading) from remotely sensed measurements by spaceborne, suborbital and ground-based platforms is a challenging task. In this study, the first and second-order spectral derivatives of aerosol optical depth (AOD) with respect to wavelength are explored to determine the partitions of the major components of aerosols based on the spectral dependence of their particle optical size and complex refractive index. With theoretical simulations from the Second Simulation of a Satellite Signal in the Solar Spectrum (6S) model, AOD spectral derivatives are characterized for collective models of aerosol types, such as mineral dust (DS) particles, biomass-burning (BB) aerosols and anthropogenic pollutants (AP), as well as stretching out to the mixtures among them. Based on the intrinsic values from normalized spectral derivatives, referenced as the Normalized Derivative Aerosol Index (NDAI), a unique pattern is clearly exhibited for bounding the major aerosol components; in turn, fractions of the total AOD (fAOD) for major aerosol components can be extracted. The subtlety of this NDAI method is examined by using measurements of typical aerosol cases identified carefully by the ground-based Aerosol Robotic Network (AERONET) sun–sky spectroradiometer. The results may be highly practicable for quantifying fAOD among mixed-type aerosols by means of the normalized AOD spectral derivatives.

Vehicle emissions are an important source of particulate matter (PM) in urban areas and have well-known adverse health effects on human health. Oxidative potential (OP) is used as a quantification metric for indexing PM toxicity. In this study, by using a liquid spot sampler (LSS) and the dithiothreitol (DTT) assay, the diurnal OP variation was assessed at a ground-level urban monitoring station. Besides, since the monitoring station was adjacent to the main road, the correlation between OP and traffic volume was also evaluated. PM components, including metals, water-soluble inorganic aerosols (WSIAs), black carbon (BC), and polycyclic aromatic hydrocarbons (PAHs), were also simultaneously monitored. The daytime and evening mean ± std volume-normalized OP (OPv) were 0.46 ± 0.27 and 0.48 ± 0.26 nmol/min/m3, and exhibited good correlations with PM1.0 and BC; however, these concentrations were only weakly correlated with mass-normalized OP (OPm). The mean ± std OPm was higher in the daytime (41.3 ± 13.8 pmol/min/μg) than in the evening (36.1 ± 11.5 pmol/min/μg). According to the PMF analysis, traffic emissions dominated the diurnal OP contribution. Organic matter and individual metals associated with non-exhaust traffic emissions, such as Mn, Fe, and Cu, contributed substantially to OP. Diurnal variations of PAH concentrations suggest that photochemical reactions could enhance OP, highlighting the importance of atmospheric aging on PM toxicity.

Fine particulate matter (PM

Traffic-related air pollutants (TRAPs) pose a serious health hazard for residents and commuters in urban areas. In this study, a real-time mobile monitoring system was deployed in Taipei, a typical East Asian city with an overlap of high population density, traffic, and special structures (e.g., viaducts), to capture the on-road TRAPs at different times of the day. In general, black carbon, ultrafine particles (UFPs), CO concentrations, and lung deposition surface area (LDSA) were positively correlated with traffic flow, and for PM2.5, a more independent fluctuating concentration was observed. During rush-hour periods, the mean concentrations of UFPs, PM2.5, and LDSA were 6.12 × 104 ± 3.83 × 104 cm−3, 23 ± 8 μg/m3, and 2.29 × 102 ± 1.20 × 102 μm2/cm3, respectively. Additionally, the UFP number concentration and LDSA were two times higher along the high-traffic commuting route than along the lower traffic route. Pollutants tended to accumulate at sites near viaducts and high buildings and were significantly influenced by vehicle composition. In this study, the ratio of LDSA to total particle surface area concentration was used as an indicator of the degree of particle irregularity, which was directly related to aging during transport.

Exposure to road dust particulate matter (PM) causes adverse health impacts on the human airway. However, the effects of road dust on the upper airway epithelium in humans remain unclear. We investigated the involvement of the epidermal growth factor receptor (EGFR) after PM with an aerodynamic diameter of2.5 μm (PM

In urban areas, traffic emission is a growing concern for ambient air quality and public health. Ultrafine particles (UFP) and black carbon (BC), a fraction of ambient particulate matter (PM), are both closely related to traffic emissions. Characterizing their physical and chemical properties is a crucial step in assessing health effects and air pollution policies. This study set up a traffic-influenced site in Taipei urban area to continuously measure different aerosol properties of PM2.5 and PM1.0. The particle size distributions (PSD) have shown that the geometric mean diameter (GMD) and the total particle number concentration (PNC) of UFPs displayed an opposite diurnal variation and were strongly affected by traffic flux. In addition, the ratio of surface area concentrations directly measured by Nanoparticle Surface Area Monitor (NSAM, TSI 3550) and estimated by the measurements using Scanning Mobility Particle Sizer (SMPS, TSI 3938) is proposed as a new indicator to quantify the irregular morphology of UFPs. It was found that the ratio is well correlated with BC and exhibits peaks in daily rush hour, suggesting that most BC have a non- spherical shape in the urban environment.

Toxicological studies have demonstrated the associations between fine particle (PM2.5) components and various cytotoxic endpoints. However, few studies have investigated the toxicological effects of source-specific PM2.5 at the individual level. To investigate the potential impact of source-specific PM2.5 on cytotoxic effects, we performed repeated personal PM2.5 monitoring of 48 adult participants in Hong Kong during the winter and summer of 2014–2015. Quartz filters were analyzed for carbonaceous aerosols and water-soluble ions in PM2.5. Teflon filters were collected to determine personal PM2.5 mass and metal concentrations. The toxicological effects of personal PM2.5 exposure—including cytotoxicity, inflammatory response, and reactive oxygen species (ROS) production—were measured using A549 cells in vitro. Personal PM2.5 samples collected in winter were more effective than those collected in summer at inducing cytotoxicity and the expression of proinflammation cytokine IL-6. By contrast, summer personal PM2.5 samples induced high ROS production. We performed a series of statistical analyses, Spearman correlation and a source apportionment approach with a multiple linear regression (MLR) model, to explore the sources contributing most significantly to personal PM2.5 bioreactivity. Secondary inorganic species and transition metals were discovered to be weak-to-moderately associated with cytotoxicity (rs: 0.26–0.55; p

Toxicity attributable to the particle charge remains unclear. The objective of this study was to investigate pulmonary effects of the electric charge of particles. We established a stably charged aerosol particle generation system for whole-body exposure in BALB/c mice, which produced positively, negatively, and neutrally charged soot particles in a wide range of numbers and mass concentrations. The charged soot particles on average carried 1.16~1.35 electric charges, and the mode sizes for particles under different charging statuses were all fixed at 69.6~71.8 nm. After inhalation, the positively and negatively charged soot particles arrested the body weight increase in mice. Pulmonary cytotoxicity of lactate dehydrogenase, oxidative stress 8-isoprostane, and the benzo(a)pyrene diolepoxide protein adduct occurred in dose-dependent manners by negatively charged soot particles. We further observed that positively and negatively charged soot particles induced systemic interleukin-6 production in dose-dependent responses in mice. Our findings suggest that inhalation of particles carrying negative electric ions could cause lung toxicity that should be of concern in terms of pulmonary health protection.

Background: Inter-alpha-trypsin inhibitor heavy chain 4 (ITIH4) is considered a type II acute-phase protein; however, the role of ITIH4 in the lungs after exposure to fine particulate matter (PM2.5) remains unclear. The objective of this study was to investigate the role of ITIH4 in the lungs in response to PM2.5 exposure.Results: ITIH4 expression in bronchoalveolar lavage fluid (BAL) of 47 healthy subjects and of SD rats exposed to PM2.5 was determined, and the underlying anti-apoptotic and matrix-stabilizing pathways in A549 cells by diesel exhaust particles (DEPs) were also investigated. First, we observed that an interquartile range (IQR) increase in PM2.5 accounted for a decrease of 2.673 ng/mL in ITIH4, an increase of 1.104 pg/mL in 8-isoprostane, and an increase of 6.918 pg/mL in interleukin (IL)-6 in human BAL. Increases in 8-isoprostane and IL-6 in the lungs and decreases in ITIH4 in the BAL, lungs, and serum were observed after PM2.5 exposure. ITIH4 was correlated with lung lysates and BAL samples (r=0.377, pr=-0.420, p2.5. ITIH4 expression decreased after DEP exposure in a dose-dependent manner. A decrease in sirtuin 1 (Sirt1) and increases in phosphorylated extracellular signal-regulated kinase (p-ERK) and caspase-3 were observed after DEP exposure. Conclusions: In conclusion, PM2.5 decreased ITIH4 in the lungs, which was associated with alveolar epithelial cell senescence and apoptosis. ITIH4 could be a vital protein in regulating alveolar destruction, and its deficiency occurs due to PM2.5.

Cigarette smoke (CS) has been reported to induce oxidative stress and inflammatory process in the lungs. However, the role of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) in the regulation of pulmonary inflammation remains unclear. The objective of this study is to investigate the effects of hUC-MSCs on lung inflammation in the acute CS-induced pulmonary inflammation animal model. Eight-week-old male C57BL/6 mice were intravenously administered 3 × 106, 1 × 107, and 3 × 107 cells/kg of hUC-MSCs as well as normal saline alone (control) after 3 days of CS exposure. Mice exposed to high-efficiency particulate air (HEPA)-filtered room air served as the CS control group. High-dose (3 × 107 cells/kg) hUC-MSC administration significantly decreased tumor necrosis factor (TNF)-α in the bronchoalveolar lavage fluid (BALF) of CS-exposed mice (p < 0.05). The chemokine (CXC motif) ligand 1/keratinocyte chemoattractant (CXCL1/KC) in BALF were significantly reduced by low-dose (3 × 106 cells/kg) and high-dose (3 × 107 cells/kg) hUC-MSC (p < 0.05). Medium-dose hUC-MSC administration decreased interleukin (IL)-1β in lung of mice, and TNF-α and caspase-3 were decreased in the lung of CS-exposed mice by medium- and high-dose MSC (p < 0.05). Low-dose hUC-MSCs significantly elevated serum CXCL1/KC and IL-1β in CS-exposed mice (p < 0.05). Our results suggest that high-dose hUC-MSCs reduced pulmonary inflammation and had antiapoptotic effects in acute pulmonary inflammation.

The aim of this study is to assess the offshore wind and solar power and to determine whether the future power supply in Taiwan will be stable. The estimated annual offshore wind and solar power generation for 2030 are 11343 GWh and 11367 GWh, respectively. Based on these results, it appears that the annual power supply can easily help balance the total power demand. However, the power demand is high during the summer peak months, and power generation may be insufficient during peak summer hours by 2030. Specifically, in 2024, the peak hourly percent reserve margin (PRM) in summer will be negative (-0.9%). If the installation of offshore wind turbines and solar panels is delayed, then the problem of insufficiency will be even more severe. However, if the offshore wind and solar photovoltaic projects are completed on schedule, and the first, second, and third nuclear power plants (NPPs) extend their service to 2030, then the hourly PRM could reach 15% during the summer peak hours from 2025 to 2030 and 5–11% in the other years. Moreover, if the fourth NPP opens, then the estimated summer peak hourly PRM would increase by 6–7%.

This study investigated the effects of pollution emissions on the bioreactivity of PM2.5 during Asian dust periods. PM2.5 during the sampling period were 104.2 and 85.7 μg m−3 in Xi'an and Beijing, respectively, whereas PM2.5 which originated from the Tengger Desert was collected (dust background). Pollution conditions were classified as non-dust days, pollution episode (PE), dust storm (DS)-1, and DS-2 periods. We observed a significant decrease in cell viability and an increase in LDH that occurred in A549 cells after exposure to PM2.5 during a PE and DS-1 in Xi'an and Beijing compared to Tengger Desert PM2.5. Positive matrix factorization was used to identify pollution emission sources. PM2.5 from biomass and industrial sources contributed to alterations in cell viability and LDH in Xi'an, whereas vehicle emissions contributed to LDH in Beijing. OC, EC, Cl−, K+, Mg2+, Ca, Ti, Mn, Fe, Zn, and Pb were correlated with cell viability and LDH for industrial emissions in Xi'an during DS. OC, EC, SO42−, S, Ti, Mn, and Fe were correlated with LDH for vehicle emissions in Beijing during DS. In conclusion, the dust may carry pollutants on its surface to downwind areas, leading to increased risks of particle toxicity.

The pressure drop of glass-fiber and cellulose filter media loaded with oil-coated particles was investigated. The focus of this study was to develop a model describing the pressure drop of fibrous filter media under the above particle loading condition. A set of experimental data collected during previous work was used for this modelling. For the cases where the coated particles possessed an oil volumetric percentage below 50%, the filter was divided into two layers: One layer collected all test particles while the other layer remained clean, and the pressure drop of the first layer was estimated using a modified Bergman model, whereas that of the second was calculated with the Davies equation. The total filter pressure drop is the summation of the layers’ pressure drops. For the cases where the coated particles possessed an oil volumetric percentage above 50%, a power-law equation with two parameters (viz., the exponent, n, and the critical volume, Vcr) was applied to fit the experimental data. The correlations of the above parameters with the solid-core diameter fraction (X) of the particles and the viscosity of the coating oil were calculated for the glass-fiber and cellulose filter media.