Versatile Aerosol Concentration Enrichment System Research Articles

Characterization of Endothelial to Mesenchymal Transition in Air Pollution Mediated Atherosclerosis: Insights from Trajectory Inference and Functional Analyses in Single cell RNA Sequencing Data

Background: Air pollution is the world’s leading environmental risk factor for atherosclerotic cardiovascular disease (ASCVD). Regressive transcriptional reprogramming and transition of cells to primordial states has been identified as a driver of atherosclerosis. Endothelial cell to mesenchymal cell transition (EndoMT) whereby an endothelial cell transforms to a mesenchymal-like cellular phenotype is one such mechanism. However its relevance to air pollution exposure remains uncharacterized. Methods: Male ApoE−/− mice were inhalationally exposed to concentrated particulate matter <2.5μ component (PM2.5) or filtered air (FA, controls) using a Versatile Aerosol Concentration Enrichment System (VACES, 5–6 h/day, 5 d/week for 36 weeks, n = 7/group. PM2.5 concentrations were 70-80 μg/m3 or ~10X ambient levels. Following euthanasia, single-cell RNA-sequencing of aortic cells was performed using the 10-X platform (CA). For all subsequent analyses, aortic cell samples were integrated. Unsupervised clustering (k-NN) and low-dimensional space visualization (UMAP) were performed with a supervised graph method (Minimum Spanning Tree and Principal Curves) to infer and visualize trajectory analysis of novel cell lineages (branching and cell ordering in pseudotime/pseudospace). Functional analyses were carried out by statistical enrichment analysis using Over Representation Analysis (ORA) and Gene Set Enrichment Analysis (GSEA) against databases of Gene Ontologies (GO), Biological Pathways, putative regulatory motifs, proteins, or disease annotations to find over-representation of terms and functions. Pseudotime distribution assessed along exposure groups and cell-types lineages were statistically compared using GLM models. Differential Expression Analysis within lineages and between groups were tested by GLM and GAM models and FDR correction, followed by functional analyses. Results: Comparison of the pseudotime lineage with lineage root node at the endothelial cells revealed a similarity between observed endothelial (EC) to vascular smooth muscle (VSMC) cell transition with the differential transition noted with PM2.5 from FA. This overlap suggests a potential exaggeration of EC to VSMC transition in response to PM2.5 exposure. Differential gene expression profiling upon PM2.5-exposure in EC revealed significant changes in GO terms related to cell differentiation, cell migration, and regulation of cell population proliferation. Specific genes with variable patterns of expression (4481) were identified along the EC to VSMC lineage. KEGG pathway analysis along the lineage revealed enriched pathways including PI3K/Akt signaling pathway, MAPK signaling pathway, and Rap1 signaling pathway which are all implicated in the development and progression of atherosclerosis. Conclusion: Single-cell analysis reveals that chronic exposure to PM2.5 results in the exaggeration of EC to VSMC transition consistent with the EndoMT paradigm that may help explain the acceleration of ASCVD in response to air pollution exposure. Additional analysis of cell specific pathways may provide improved understanding of mechanisms progression of atherosclerosis in response to environmental exposures. NIH: 1R35ES031702-01, R01 HL155450, 3R35ES031702-02S1; Burroughs Wellcome Fund: 1060485. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Unveiling the Molecular Characteristics, Origins, and Formation Mechanism of Reduced Nitrogen Organic Compounds in the Urban Atmosphere of Shanghai Using a Versatile Aerosol Concentration Enrichment System.

Reduced nitrogen-containing organic compounds (NOCs) in aerosols play a crucial role in altering their light-absorption properties, thereby impacting regional haze and climate. Due to the low concentration levels of individual NOCs in the air, the utilization of accurate detection and quantification technologies becomes essential. For the first time, this study investigated the diurnal variation, chemical characteristics, and potential formation pathways of NOCs in urban ambient aerosols in Shanghai using a versatile aerosol concentration enrichment system (VACES) coupled with HPLC-Q-TOF-MS. The results showed that NOCs accounted over 60% of identified components of urban organic aerosols, with O/N < 3 compounds being the major contributors (>70%). The predominance of the positive ionization mode suggested the prevalence of reduced NOCs. Higher relative intensities and number fractions of NOCs were observed during nighttime, while CHO compounds showed an opposite trend. Notably, a positive correlation between the intensity of NOCs and ammonium during the nighttime was observed, suggesting that the reaction of ammonium to form imines may be a potential pathway for the formation of reduced NOCs during the nighttime. Seven prevalent types of reduced NOCs in autumn and winter were identified and characterized by an enrichment of CH2 long-chain homologues. These NOCs included alkyl, cyclic, and aromatic amides in CHON compounds, as well as heterocyclic or cyclic amines and aniline homologue series in CHN compounds, which were associated with anthropogenic activities and may be capable of forming light-absorbing chromophores or posing harm to human health. The findings highlight the significant contributions of both primary emissions and ammonium chemistry, particularly amination processes, to the pollution of reduced NOCs in Shanghai's atmosphere.

Quantification and Characterization of Fine Plastic Particles as Considerable Components in Atmospheric Fine Particles.

The negative effects of air pollution, especially fine particulate matter (PM2.5, particles with an aerodynamic diameter of ≤2.5 μm), on human health, climate, and ecosystems are causing significant concern. Nevertheless, little is known about the contributions of emerging pollutants such as plastic particles to PM2.5 due to the lack of continuous measurements and characterization methods for atmospheric plastic particles. Here, we investigated the levels of fine plastic particles (FPPs) in PM2.5 collected in urban Shanghai at a 2 h resolution by using a novel versatile aerosol concentration enrichment system that concentrates ambient aerosols up to 10-fold. The FPPs were analyzed offline using the combination of spectroscopic and microscopic techniques that distinguished FPPs from other carbon-containing particles. The average FPP concentrations of 5.6 μg/m3 were observed, and the ratio of FPPs to PM2.5 was 13.2% in this study. The FPP sources were closely related to anthropogenic activities, which pose a potential threat to ecosystems and human health. Given the dramatic increase in plastic production over the past 70 years, this study calls for better quantification and control of FPP pollution in the atmosphere.

Development and performance evaluation of online monitors for near real-time measurement of total and water-soluble organic carbon in fine and coarse ambient PM

In this study, we developed two online monitors for total organic carbon (TOC) and water-soluble organic carbon (WSOC) measurements in fine (dp < 2.5 μm) and coarse (2.5 μm < dp < 10 μm) particulate matter (PM), respectively. Their performance has been evaluated in laboratory and field tests to demonstrate the feasibility of using these monitors to measure near real-time concentrations, with consideration of their potential for being employed in long-term measurements. The fine PM collection setup was equipped with a versatile aerosol concentration enrichment system (VACES) connected to an aerosol-into-liquid-sampler (AILS), whereas two virtual impactors (VIs) in tandem with a modified BioSampler were used to collect coarse PM. These particle collection setups were in tandem with a Sievers M9 TOC analyzer to read TOC and WSOC concentrations in aqueous samples hourly. The average hourly TOC concentration measured by our developed monitors in fine and coarse PM were 5.17 ± 2.41 and 0.92 ± 0.29 μg/m³, respectively. In addition, our TOC readings showed good agreement and were comparable with those quantified using Sunset Lab EC/OC analyzer operating in parallel as a reference. Furthermore, we conducted field tests to produce diurnal profiles of fine PM-bound WSOC, which can show the effects of ambient temperature on maximum values in the nighttime chemistry of the winter, as well as on increased photochemical activities in afternoon peaks during the summer. According to our experimental campaign, WSOC mean values during the study period (3.07 μg/m³ for the winter and 2.7 μg/m³ for the summer) were in a comparable range with those of earlier studies in Los Angeles. Overall, our results corroborate the performance of our developed monitors in near real-time measurements of TOC and WSOC, which can be employed for future source apportionment studies in Los Angeles and other areas, aiding in understanding the health impacts of different pollution sources.

Subchronic exposure to PM2.5 induced renal function damage and intestinal microflora changes in rats

BackgroundExposure to inhalable environmental particulate matter with a diameter of 2.5 µm or smaller (PM2.5) is associated with decreased or impaired kidney function, but the underlying biological mechanisms are not fully understood. Gut microbiota is an emerging key player in the homeostasis regulation of the gut-kidney axis. Few studies have investigated its role in PM2.5 exposure-induced gut-kidney axis homeostasis abnormalities. MethodsIn this study, a versatile aerosol concentration enrichment system for medium- to long-term whole-body exposure was used to expose Sprague-Dawley rats to filtered air (FA) or concentrated ambient PM2.5 for 12 weeks. A correlation analysis of renal impairment and the intestinal microbiome was performed. ResultsThe urine flow rate calculation and renal function analysis showed that PM2.5 exposure significantly impaired renal function and increased the urine flow rate. The fecal microbiota analysis showed that renal impairment and increased urine flow rates were consistent with the reduced estimates of the fecal bacteria Chao1, observed-species, Shannon, and Simpson (richness and diversity indices). Pearson’s correlation analysis showed that the estimated bacterial richness and diversity were correlated with the urine flow rate and renal function. The linear discriminant analysis effect size (LEfSe) analysis revealed differences between animals exposed to PM2.5 and FA in 25 bacterial groups. Further correlation of a single bacterial taxon with the urine flow rate and renal function showed that the relative abundances of 30, 29, 21, and 50 distinct bacterial groups were significantly correlated with the urine flow rate, estimated glomerular filtration rate (eGFR), serum cystatin C (CysC), and beta-2 microglobulin (β2-MG), respectively. ConclusionSubchronic exposure to PM2.5 can cause intestinal ecological disorders, which may, in turn, lead to decreased kidney function or the development of impaired kidney function.

Design, optimization, and evaluation of a wet electrostatic precipitator (ESP) for aerosol collection

In this study, we developed, optimized, and evaluated in lab and field experiments a wet electrostatic precipitator (ESP) for the collection of ambient PM2.5 (particulate matter with aerodynamic diameter <2.5 μm) into ultrapure water by applying an electrostatic charge to the particles. We operated the wet ESP at different flow rates and voltages to identify the optimal operating conditions. According to our experimental measurements, a flow rate of 125 lpm and an applied positive voltage of 11 kV resulted in a lower ozone generation of 133 ppb and a particle collection efficiency exceeding 80–90% in all size ranges. For the field tests, the wet ESP was compared with the versatile aerosol concentration enrichment system (VACES) connected to a BioSampler, a PTFE filter sampler, and an OC/EC analyzer (Sunset Laboratory Inc., USA) as a reference. The chemical analysis results indicated the wet ESP concentrations of metal and trace elements were in very good agreement with those measured by the VACES/BioSampler and PTFE filter sampler. Moreover, our results showed comparable total organic carbon (TOC) concentrations measured by the wet ESP, BioSampler, and OC/EC analyzer, while somewhat lower TOC concentrations were measured by the PTFE filter sampler, possibly due to the limitations of extracting water-insoluble organic carbon (WIOC) from a dry substrate in the latter sampler. The comparable TOC content in the wet ESP and BioSampler samples differs from previous findings that showed higher TOC content in BioSampler samples compared to those collected by dry ESP. The results of the Dithiothreitol (DTT) assay showed comparable DTT activity in the VACES/BioSampler and wet ESP PM samples while slightly lower in the PTFE filter samples. Overall, our results suggest that the wet ESP could be a promising alternative to other conventional sampling methods.

Endothelial mesenchymal transition with air pollution mediated atherosclerosis: insights from single cell RNA sequencing and trajectory inference analysis

Background: Atherosclerotic cardiovascular disease (ASCVD) is the major leading cause of global morbidity and mortality. There is an increasing realization that non-traditional risk factors in the environment may powerfully modulate ASCVD. Air pollution is the world’s leading environmental risk factor implicated extensively in ASCVD with prior studies from our lab and others demonstrating that the fine particulate matter aspect ≤2.5μm (PM 2.5 ) may worsen ASCVD. Recent insights into ASCVD have suggested a fundamental role for endothelial-to-mesenchymal cell transition (EMT) in atherosclerosis. We hypothesize that EMT may play a role in the deleterious effects of PM 2.5 -mediated atherosclerotic progression. Methods: Male ApoE -/- mice (n=7/group) were exposed to PM 2.5 or filtered air (FA, as controls) using a versatile aerosol concentration enrichment system (VACES) for 36 weeks (5h/day, 6d/wk). Concentrations of PM 2.5 averaged 7-10x ambient levels. Animals were euthanized at the end of exposure, followed by assessment of vascular function using myography with derivation of concentration-response curves to acetylcholine (ACh 10 -10 to 10 -4 ). scRNA-sequencing was done using 10x platform. Cell characterization analysis, unsupervised k-nearest neighbor learning algorithm, and Uniform Manifold and Approximation Projection (UMAP) were performed. We used a supervised graph method and UMAP to infer and visualize trajectory of novel cell lineage with lineage root node at endothelial cells. Results. Endothelium-dependent relaxation was impaired in aortas of PM 2.5 -exposed mice (dAUC: FA: 241.2 ± 19.04; PM 2.5 : 125.4 ± 39.21; p=0.0047). Our scRNA-sequencing data revealed 12 unique cell cluster groups in FA and 2 more cluster groups in PM 2.5 . This included an unannotated cell type and a dendritic cell population. Cell lineage inference of FA-exposed mice showed evolution into 2 lineages (vascular smooth muscle cells and monocytes); PM 2.5 -exposed mice diverged into 4 lineages, notably exhibiting differentiation and activation of more fibroblasts and lymphocytes, and an unknown population that had fibroblast-like properties. Importantly, the overlap of biomarkers between the unannotated population and fibroblast cells are mesenchymal cell biomarkers (Col1a1, Col1a2, Mgp, Col1a3, Dcn). This trajectory inference reflected a quasi-continuous transformation along cell lineages, with intermediate cell phenotypes between the annotated populations. Significantly augmented GO terms in EC upon PM 2.5 exposure include upregulation of endothelial cell migration, blood vessel endothelial cell migration, and deregulation of cell population proliferation. Conclusion: Chronic exposure to PM 2.5 results in EMT that may help explain abnormalities in endothelial function and acceleration of ASCVD noted with exposure. Further analysis of cell specific pathways may provide renewed understanding of the mechanisms underlying environmental exposures and progression of atherosclerosis. NIH/NIEHS-R35ES031702 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Ambient particulate matter exposure causes visual dysfunction and retinal neuronal degeneration

PM2.5 pollution is related to neurotoxic and vascular effects in eye diseases such as glaucoma. This study investigates the adverse effects of PM2.5 exposure on visual function and retinal neurons. A versatile aerosol concentration enrichment system was used to expose mice to either control air or PM2.5 polluted air. Six months after PM2.5 exposure, visual function was measured by electroretinography (ERG). Hematoxylin and eosin staining and immunofluorescence staining were used for histopathological analysis. Protein markers of apoptosis, astrocytic reactivity, inflammatory cytokines, lipid peroxidation, protein nitration and DNA damage response were quantified with ELISA, western blot or detected using immunofluorescence and immunohistochemistry. After six months of exposure, PM2.5-exposed mice responded poorly to light stimuli compared with those exposed to the control air. PM2.5 exposure caused retinal thinning and reduction in the expression of retinal ganglion cell-selective marker RNA-binding protein with multiple splicing (RBPMS). Further, positive TUNEL staining was observed in the inner nucleus and outer nuclear layers of the retinae after exposure to PM2.5, which was accompanied by the activation of apoptosis signaling molecules p53, caspase-3 and Bax. PM2.5 induced the release of inflammatory cytokines including tumor necrosis factor-α and cleaved interleukin-1β. Furthermore, increased levels of 8-OHdG and γ-H2AX in the mouse retinea were indicative of DNA single and double strand breaks by PM2.5 exposure, which activated PARP-1 mediated DNA damage and repair. In conclusion, this study demonstrates sub-chronic systemic exposure to concentrated PM2.5 causes visual dysfunction and retinal neuronal degeneration. Data availabilityThe datasets during and/or analyzed during the current study available from the corresponding author on reasonable request.

Accurate observation of black and brown carbon in atmospheric fine particles via a versatile aerosol concentration enrichment system (VACES).

Carbonaceous aerosols (CAs) are major components of fine particulate matter (PM2.5) that dramatically influence the energy budget of Earth. However, accurate assessment of the climatic impacts of CAs is still challenging due to the large uncertainties remaining in the measurement of their optical properties. In this respect, a modified versatile aerosol concentration enrichment system integrated into optical instruments (VACES-OPTS) was set up to increase particle concentration and amplify signal-noise ratio during optical measurement. Based on the novel technique, this study was able to lower the detection limit of CAs by an order of magnitude under high temporal resolution (2 h) and small sampling flow (6 L min-1). Besides, stable and reliable optical data were obtained for absorption apportionment and source identification of black carbon (BC) and brown carbon (BrC). In the field application of the new system, high absorption coefficient of CAs in Shanghai, China was witnessed. Further analysis of the contribution of black carbon BC and BrC to light absorption revealed that BrC could account for over 15% of the total absorption at 370 nm. According to the potential source contribution function model (PSCF) classification, CAs with strong light absorption in urban Shanghai originated not only from highly polluted inland China but also from active marine ship emissions.

Impacts of missing OH reactivity and aerosol uptake of HO2 radicals on tropospheric O3 production during the AQUAS-Kyoto summer campaign in 2018

Gaining quantitative information about the HOx cycle involved in ozone (O3) production is important for reduction of tropospheric O3. In this study, we evaluated the impacts of both the missing OH reactivity and the heterogeneous loss of HO2 due to ambient aerosol uptake on the photochemical O3 production potential and regime analysis during the Air QUAlity Study (AQUAS)-Kyoto summer campaign in 2018. We examined the missing OH reactivity, which was 50% of the averaged total OH reactivity (9.8 ± 3.8 (1σ) s−1), and the uptake loss rate of HO2 on ambient aerosols of 0.0017 ± 0.0015 s−1. The real-time uptake loss rate of HO2 was measured by employing a versatile aerosol concentration enrichment system (VACES). The O3 production potential increased by a factor of two when the missing OH reactivity was considered and decreased by ∼20% when the HO2 loss due to aerosol uptake was considered. In addition, the missing OH reactivity and the HO2 loss due to aerosol uptake decreased the relative sensitivity of the O3 production rate to volatile organic compounds (VOCs) and increased that to NOx (= NO + NO2). Consequently, the NOx limited regime period, the period in which the relative sensitivity of the O3 production rate to NOx was higher than that to VOCs, was expanded by a few hours. Finally, the effect of aerosol uptake on O3 production was anti-correlated with the NO concentration and peaked around noon when the NO concentration was the minimum. It is concluded that aerosols likely affect tropospheric O3 production in suburban and rural areas, where the concentrations of NOx, particularly NO, are very low ([NO] < 0.3 ppb).

Concentrated ambient fine particles exposure affects ovarian follicle development in mice

BackgroundAmbient fine particles (PM2.5) are known to cause various reproductive and developmental diseases. However, the potential mechanisms of PM2.5 exposure induced female reproductive damage remain unclear. MethodsFour weeks old female C57BL/6 J mice were exposed to filtered air (FA, n = 10) or concentrated ambient PM2.5 (CAP, n = 10) using a versatile aerosol concentration enrichment system. After 9 weeks of the exposure, mice were sacrificed under sevoflurane anesthesia and tissue samples were collected. Immunohistochemical analysis, enzyme-linked immunosorbent assay, quantitative polymerase chain reaction, and RNA-sequencing were performed to analyze the effects of PM2.5 exposure on follicle development and elucidate its potential mechanisms. ResultsChronic PM2.5 exposure resulted in follicular dysplasia. Compared to the FA-exposed group, follicular atresia in the CAP-exposed mice were significantly increased. Further studies confirmed that CAP induced apoptosis in granulosa cells, accompanied by a distortion of hormone homeostasis. In addition, RNA-sequencing data demonstrated that CAP exposure induced the alteration of ovarian gene expressions and was associated with inflammatory response. ConclusionsChronic exposure to CAP can induce follicular atresia, which was associated with hormone modulation and inflammation.

Exposure to environmentally relevant concentrations of ambient fine particulate matter (PM2.5) depletes the ovarian follicle reserve and causes sex-dependent cardiovascular changes in apolipoprotein E null mice

BackgroundFine particulate matter (PM2.5) exposure accelerates atherosclerosis and contains known ovotoxic chemicals. However, effects of exposure to PM2.5 on the finite ovarian follicle pool have hardly been investigated, nor have interactions between ovarian and cardiovascular effects. We hypothesized that subchronic inhalation exposure to human-relevant concentrations of PM2.5 results in destruction of ovarian follicles via apoptosis induction, as well as accelerated recruitment of primordial follicles into the growing pool. Further, we hypothesized that destruction of ovarian follicles enhances the adverse cardiovascular effects of PM2.5 in females.ResultsHyperlipidemic apolipoprotein E (Apoe) null ovary-intact or ovariectomized female mice and testis-intact male mice were exposed to concentrated ambient PM2.5 or filtered air for 12 weeks, 5 days/week for 4 h/day using a versatile aerosol concentration enrichment system. Primordial, primary, and secondary ovarian follicle numbers were decreased by 45%, 40%, and 17%, respectively, in PM2.5-exposed ovary-intact mice compared to controls (P < 0.05). The percentage of primary follicles with granulosa cells positive for the mitosis marker Ki67 was increased in the ovaries from PM2.5-exposed females versus controls (P < 0.05), consistent with increased recruitment of primordial follicles into the growing pool. Exposure to PM2.5 increased the percentages of primary and secondary follicles with DNA damage, assessed by γH2AX immunostaining (P < 0.05). Exposure to PM2.5 increased the percentages of apoptotic antral follicles, determined by TUNEL and activated caspase 3 immunostaining (P < 0.05). Removal of the ovaries and PM2.5-exposure exacerbated the atherosclerotic effects of hyperlipidemia in females (P < 0.05). While there were statistically significant changes in blood pressure and heart rate variability in PM2.5-compared to Air-exposed gonad-intact males and females and ovariectomized females, the changes were not consistent between exposure years and assessment methods.ConclusionsThese results demonstrate that subchronic PM2.5 exposure depletes the ovarian reserve by increasing recruitment of primordial follicles into the growing pool and increasing apoptosis of growing follicles. Further, PM2.5 exposure and removal of the ovaries each increase atherosclerosis progression in Apoe-/- females. Premature loss of ovarian function is associated with increased risk of osteoporosis, cardiovascular disease and Alzheimer’s disease in women. Our results thus support possible links between PM2.5 exposure and other adverse health outcomes in women.

Lifetime exposure of ambient PM2.5 elevates intraocular pressure in young mice

Epidemiological studies suggest that ambient particulate matter exposure may be a new risk factor of glaucoma, but it lacks solid experimental evidence to establish a causal relationship. In this study, young mice (4 weeks old) were exposed concentrated ambient PM2.5 (CAP) for 9 months, which is throughout most of the life span of a mouse under heavy pollution. CAP was introduced using a versatile aerosol concentration enrichment system which mimics natural PM2.5 exposure. CAP exposure caused a gradual elevation of intraocular pressure (IOP) and an increase in aqueous humor outflow resistance. In the conventional outflow tissues that regulates IOP, inducible nitric oxide synthase (iNOS) was up-regulated and 3-nitrotyrosine (3-NT) formation increased. At the cellular level, PM2.5 exposure increased the transendothelial electrical resistance of cells that control IOP (AAP cells). This is accompanied by increased reactive oxygen species (ROS), iNOS and 3-NT levels. Peroxynitrite scavenger MnTMPyP successfully treated the IOP elevation and restored it to normal levels by reducing 3-NT formation in outflow tissues. This study provides the novel evidence that in young mice, lifetime whole-body PM2.5 exposure has a direct toxic effect on intraocular tissues, which imposes a significant risk of IOP elevation and may initiate the development of ocular hypertension and glaucoma. This occurs as a result of protein nitration of conventional aqueous humor outflow tissues.

Characterizing the Chemical Profile of Incidental Ultrafine Particles for Toxicity Assessment Using an Aerosol Concentrator.

Incidental ultrafine particles (UFPs) constitute a key pollutant in industrial workplaces. However, characterizing their chemical properties for exposure and toxicity assessments still remains a challenge. In this work, the performance of an aerosol concentrator (Versatile Aerosol Concentration Enrichment System, VACES) was assessed to simultaneously sample UFPs on filter substrates (for chemical analysis) and as liquid suspensions (for toxicity assessment), in a high UFP concentration scenario. An industrial case study was selected where metal-containing UFPs were emitted during thermal spraying of ceramic coatings. Results evidenced the comparability of the VACES system with online monitors in terms of UFP particle mass (for concentrations up to 95 µg UFP/m3) and between filters and liquid suspensions, in terms of particle composition (for concentrations up to 1000 µg/m3). This supports the applicability of this tool for UFP collection in view of chemical and toxicological characterization for incidental UFPs. In the industrial setting evaluated, results showed that the spraying temperature was a driver of fractionation of metals between UF (<0.2 µm) and fine (0.2–2.5 µm) particles. Potentially health hazardous metals (Ni, Cr) were enriched in UFPs and depleted in the fine particle fraction. Metals vaporized at high temperatures and concentrated in the UF fraction through nucleation processes. Results evidenced the need to understand incidental particle formation mechanisms due to their direct implications on particle composition and, thus, exposure. It is advisable that personal exposure and subsequent risk assessments in occupational settings should include dedicated metrics to monitor UFPs (especially, incidental).

PM1.0-Nitrite Heterogeneous Formation Demonstrated via a Modified Versatile Aerosol Concentration Enrichment System Coupled with Ion Chromatography.

Particulate nitrite is a critical source of hydroxyl radicals; however, it lacks high-resolution methods due to its low abundance and stability to explore its formation mechanism. In this study, a modified versatile aerosol concentration enrichment system (VACES) coupled with ion chromatography (IC) was used to measure particulate NO2- hourly online and achieve a lowered detection limit of 10-3 μg m-3. VACES-IC was used to observe a high- and low-concentration events of PM1.0-NO2- in Shanghai, corresponding to the ambient-level concentrations of 0.34 and 0.05 μg m-3, respectively. The morning peak concentrations of NO2- even exceeded 3σ (standard deviation) in the high-concentration event due to the reduction of NO2 by aerosol SO32- based on kinetics and regression analysis. This implies that controlling SO2 emissions would be an effective strategy to decrease morning NO2- concentrations, correspondingly reducing the kinetic formation of SO42- by 20.8-34.8%. However, after sunrise, NO2- formation was primarily attributed to NO2 hydrolysis at pH 4.97-6.14. In the low-concentration event, NO2 hydrolysis also accounted for an overwhelming proportion (∼90%) of NO2- formation. This work estimates the contribution of different paths to particulate NO2- formation based on newly established high-resolution measurements.

A semicontinuous study on the ecotoxicity of atmospheric particles using a versatile aerosol concentration enrichment system (VACES): development and field characterization

Abstract. Oxidative stress can be used to evaluate not only adverse health effects but also adverse ecological effects, but limited research uses eco-toxicological assay to assess the risks posed by particle matters to non-human biomes. One important reason might be that the concentration of toxic components of atmospheric particles is far below the high detection limit of eco-toxic measurement. To solve the rapid detection problem, we extended a versatile aerosol concentration enrichment system (VACES) for ecotoxicity aerosol measurement and firstly used VACES to provide a comparison of ecotoxicity between non-concentrated and concentrated aerosols in ambient air. In this study, the total concentration (number or mass), the concentration of chemical components and the ecotoxicity were all increased by approximately 7 to 10 times in VACES, making the detection of ecotoxicity above the baseline. The comparison of ecotoxicity data and PM2.5 concentration showed that low concentration was not matched with ecotoxicity, although high concentration corresponded to higher ecotoxicity. In addition, the higher saturation temperature in VACES caused a loss of particulate matter, of which nitrate accounted for about 18 %.

Subchronic exposure to concentrated ambient PM2.5 perturbs gut and lung microbiota as well as metabolic profiles in mice.

Exposure to ambient fine particular matter (PM2.5) are linked to an increased risk of metabolic disorders, leading to enhanced rate of many diseases, such as inflammatory bowel disease (IBD), cardiovascular diseases, and pulmonary diseases; nevertheless, the underlying mechanisms remain poorly understood. In this study, BALB/c mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CPM) for 2 months using a versatile aerosol concentration enrichment system(VACES). We found subchronic CPM exposure caused significant lung and intestinal damage, as well as systemic inflammatory reactions. In addition, serum and BALFs (bronchoalveolar lavage fluids) metabolites involved in many metabolic pathways in the CPM exposed mice were markedly disrupted upon PM2.5 exposure. Five metabolites (glutamate, glutamine, formate, pyruvate and lactate) with excellent discriminatory power (AUC=1, p<0.001) were identified to predict PM2.5 exposure related toxicities. Furthermore, subchronic exposure to CPM not only significantly decreased the richness and composition of the gut microbiota, but also the lung microbiota. Strong associations were found between several gut and lung bacterial flora changes and systemic metabolic abnormalities. Our study showed exposure to ambient PM2.5 not only caused dysbiosis in the gut and lung, but also significant systemic and local metabolic alterations. Alterations in gut and lung microbiota were strongly correlated with metabolic abnormalities. Our study suggests potential roles of gut and lung microbiota in PM2.5 caused metabolic disorders.

Characterization of organic compounds and oxidative potential of aqueous PM2.5 suspensions collected via an aerosol-into-liquid collector for use in toxicology studies

Abstract In this study, we investigated the organic constituents and toxicological characteristics of PM2.5 liquid suspensions collected by the means of a modified versatile aerosol concentration enrichment system (VACES)/aerosol-into-liquid collector tandem technology. Filter and slurry PM2.5 samples were collected during warm (spanning from mid-August 2019 to early-September 2019) and cold (from mid-December 2019 to early-January 2020) seasons at an urban site in central Los Angeles. The collected samples were chemically analyzed for their total organic carbon (TOC) as well as individual organic species, including polycyclic aromatic hydrocarbons (PAHs), hopanes and steranes, n-alkanes, and organic acids. In addition, the oxidative potential of PM2.5 samples was quantified by means of the 2′,7′-dichlorodihydrofluorescein (DCFH) in vitro assay. Overall, our findings revealed a very good agreement between the mass fractions of organic compounds in the collected PM2.5 slurries and filters, judging by the average slurry-to -filter ratios of 1.17 ± 0.15, 1.13 ± 0.14, 1.13 ± 0.15, and 1.16 ± 0.22 for PAHs, hopanes and steranes, n-alkanes, and organic acids, respectively. Moreover, comparable (Pvalue = 0.2) oxidative potential levels were observed between the collected filters and PM2.5 liquid suspensions. The aqueous PM suspensions collected by the VACES/aerosol-into-liquid collector exhibited slightly higher (although not statistically significant) capture of some semi-volatile organic compounds (SVOCs), probably due to less sampling artifacts and better preservation of these SVOCs collected directly into aqueous suspensions compared to the filter samplers. The outcomes of this study confirm the efficient collection of PM-bound organic species in aqueous slurries by the aerosol-into-liquid collector, further corroborating the ability of this sampler to be used as an attractive alternative to filter samplers for collection of PM2.5 for toxicological studies.

Evaluation of a high flow rate electrostatic precipitator (ESP) as a particulate matter (PM) collector for toxicity studies

In this study, we investigated the performance of an electrostatic precipitator (ESP) operating at high flow rates (i.e., 50–100 lpm) as a fine particulate matter (PM2.5) collector for toxicological studies. The ESP optimum configuration (i.e., flow rate of 75 lpm and applied voltage of +12 kV) was determined based on maximum particle collection efficiencies and minimum ozone emissions associated with the instrument using different laboratory-generated aerosols. This configuration resulted in particle collection efficiencies above 80% for almost all particles in the size range of 0.015–2.5 μm while the ozone concentration was 17 ppb. The ESP was then deployed to our sampling site in central Los Angeles to evaluate its performance using ambient particles under the optimum configuration. Chemical composition and oxidative potential of PM2.5 samples collected on the foils placed inside the ESP tube were compared with those collected concurrently on filters and aerosol slurries using the versatile aerosol concentration enrichment system (VACES) operating in parallel. Our results demonstrated that the ESP was more efficient in preserving labile inorganic ions and total organic carbon (TOC) compared to filters. PM samples collected on ESP substrates also showed higher intrinsic oxidative potential compared to the filters, which might be the result of better preservation of redox active semi-volatile organic compounds on the ESP substrates. However, the TOC concentrations and intrinsic oxidative potential of PM samples collected on ESP substrates were somewhat lower than the aerosol slurries collected by the VACES, probably due to deficiency of water-insoluble compounds in extracted PM samples from ESP substrates. In conclusion, while particle collection for toxicological purposes by the ESP is somewhat inferior to a direct aerosol-into-liquid collection, the ESP performs equally well, if not better, than conventional filter samplers and can be utilized as a simple and adequately efficient PM collector for toxicological studies.

Semi-volatile components of PM2.5 in an urban environment: Volatility profiles and associated oxidative potential

The volatility profiles of PM2.5 semi-volatile compounds and relationships to the oxidative potential of urban airborne particles were investigated in central Los Angeles, CA. Ambient and thermodenuded fine (PM2.5) particles were collected during both warm and cold seasons by employing the Versatile Aerosol Concentration Enrichment System (VACES) combined with a thermodenuder. When operated at 50 °C and 100 °C, the VACES/thermodenuder system removed about 50% and 75% of the PM2.5 vol concentration, respectively. Most of the quantified PM2.5 semi-volatile species including organic carbon (OC), water soluble organic carbon (WSOC), polycyclic aromatic hydrocarbons (PAHs), organic acids, n-alkanes, and levoglucosan, as well as inorganic ions (i.e., nitrate, sulfate, and ammonium) exhibited concentration losses in the ranges of 40–66% and 67–92%, respectively, as the thermodenuder temperature increased to 50 °C and 100 °C. Species in the PM2.5 such as elemental carbon (EC) and inorganic elements (including trace metals) were minimally impacted by the heating process – thus can be considered refractory. On average, nearly half of the PM2.5 oxidative potential (as measured by the dichlorodihydrofluorescein (DCFH) alveolar macrophage in vitro assay) was associated with the semi-volatile species removed by heating the aerosols to only 50 °C, highlighting the importance of this quite volatile compartment to the ambient PM2.5 toxicity. The fraction of PM2.5 oxidative potential lost upon heating the aerosols to 100 °C further increased to around 75–85%. Furthermore, we document statistically significant correlations between the PM2.5 oxidative potential and different semi-volatile organic compounds originating from primary and secondary sources, including OC (Rwarm, and Rcold) (0.86, and 0.74), WSOC (0.60, and 0.98), PAHs (0.88, and 0.76), organic acids (0.76, and 0.88), and n-alkanes (0.67, and 0.83) in warm and cold seasons, respectively, while a strong correlation between oxidative potential and levoglucosan, a tracer of biomass burning, was observed only during the cold season (Rcold = 0.81).