Particulate Matter Components Research Articles

Secondary organic aerosols derived from intermediate-volatility n-alkanes adopt low-viscous phase state

Abstract. Secondary organic aerosol (SOA) derived from n-alkanes, as emitted from vehicles and volatile chemical products, is a major component of anthropogenic particulate matter, yet the chemical composition and phase state are poorly understood and thus poorly constrained in aerosol models. Here we provide a comprehensive analysis of n-alkane SOA by explicit gas-phase chemistry modeling, machine learning, and laboratory experiments to show that n-alkane SOA adopts low-viscous semi-solid or liquid states. Our study underlines the complex interplay of molecular composition and SOA viscosity: n-alkane SOA with a higher carbon number mostly consists of less functionalized first-generation products with lower viscosity, while the SOA with a lower carbon number contains more functionalized multigenerational products with higher viscosity. This study opens up a new avenue for analysis of SOA processes, and the results indicate few kinetic limitations of mass accommodation in SOA formation, supporting the application of equilibrium partitioning for simulating n-alkane SOA formation in large-scale atmospheric models.

Diel variations of airborne microbes and antibiotic resistance genes in Response to urban PM2.5 chemical properties during the heating season

Among the components of fine particulate matter (PM2.5), the contributions of airborne microorganisms and antibiotic resistance genes (ARGs) to health risks have been overlooked. Airborne microbial dynamics exhibit a unique diurnal cycle due to environmental influences. However, the specific roles of PM2.5 chemical properties resulting from fossil fuel combustion in driving circadian fluctuations in microbial populations and ARGs remain unclear. This study explored the interactions between toxic components and microbial communities during the heating period to understand the variations in ARGs. Bacterial and fungal communities showed a higher susceptibility to diel variations in PM2.5 compared to their chemical properties. Mantel tests revealed that chemical properties and microbial community interactions contribute differently to ARG variations, both directly and indirectly, during circadian fluctuations. Our findings highlight that, during the daytime, the enrichment of pathogenic microorganisms and ARGs increases the risk of PM2.5 toxicity. Conversely, during the nighttime, the utilization of water-soluble ions by the fungal community increased, leading to a significant increase in fungal biomass. Notably, Aspergillus exhibited a significant correlation with mobile genetic elements and ARGs, implying that this genus is a crucial driver of airborne ARGs. This study provides novel insights into the interplay between the chemical composition, microbial communities, and ARGs in PM, underscoring the urgent need for a comprehensive understanding of effective air pollution control strategies.

Key drivers of the oxidative potential of PM2.5 in Beijing in the context of air quality improvement from 2018 to 2022

The mass concentration of atmospheric particulate matter (PM) has been continuously decreasing in the Beijing-Tianjin-Hebei region. However, health endpoints do not exhibit a linear correlation with PM mass concentrations. Thus, it is urgent to clarify the prior toxicological components of PM to further improve air quality. In this study, we analyzed the long-term oxidative potential (OP) of water-soluble PM2.5, which is generally considered more effective in assessing hazardous exposure to PM in Beijing from 2018 to 2022 based on the dithiothreitol assay and identified the crucial drivers of the OP of PM2.5 based on online monitoring of air pollutants, receptor model, and random forest (RF) model. Our results indicate that dust, traffic, and biomass combustion are the main sources of the OP of PM2.5 in Beijing. The complex interactions of dust particles, black carbon, and gaseous pollutants (nitrogen dioxide and sulfur dioxide) are the main factors driving the OP evolution, in particular, leading to the abnormal rise of OP in Beijing in 2022. Our data shows that a higher OP is observed in winter and spring compared to summer and autumn. The diurnal variation of the OP is characterized by a declining trend from 0:00 to 14:00 and an increasing trend from 14:00 to 23:00. The spatial variation in OP of PM2.5 was observed as the OP in Beijing is lower than that in Shijiazhuang, while it is higher than that in Zhenjiang and Haikou, which is primarily influenced by the distribution of black carbon. Our results are of significance in identifying the key drivers influencing the OP of PM2.5 and provide new insights for advancing air quality improvement efforts with a focus on safeguarding human health in Beijing.

Ferruginous components of particulate matters in subway environments, α-Fe2O3 or Fe3O4, exacerbates allergies

The respiratory effects of particulate matter (PM) in subway station platforms or tunnels have attracted considerable research attention. However, no studies have characterized the effects of subway PM on allergic immune responses. In this study, iron oxide (α-Fe2O3 and Fe3O4) particles—the main components of subway PM—were intratracheally administered to BALB/c mice where ovalbumin (OVA) induced allergic pulmonary inflammation. Iron oxide particles enhanced OVA-induced eosinophil recruitment around the bronchi and mucus production from airway epithelium. The concentrations of type 2 cytokines, namely, interleukin (IL)-5 and IL-13, in bronchial alveolar lavage fluids were increased by iron oxide particles. Iron oxide particles also increased the number of type 2 innate lymphoid cells and CD86+ cells in the lung. Moreover, phagocytosis of particles in lung cells was confirmed by Raman spectroscopy. In a subsequent in vitro study, bone marrow-derived antigen-presenting cells (APCs) isolated from NC/Nga mice were exposed to iron oxide particles and OVA. They were also exposed to outdoor ambient PM: Vehicle Exhaust Particulates (VEP) and Urban Aerosols (UA) as references. Iron oxide particles promoted the release of lactate dehydrogenase, C-X-C motif chemokine ligand 1 and IL-1α from APCs, which tended to be stronger than those of VEP. These results suggest that iron oxide particles enhance antigen presentation in the lungs, promoting allergic immune response in mice; iron oxide particles-induced death and inflammatory response of APCs can contribute to allergy exacerbation. Although iron oxide particles do not contain various compounds like VEP, iron oxide alone may have sufficient influence.

An assessment of inorganic components in condensable particulate matter as a function of surface aggregation, spatial suspension state and particle size

Experimental studies assessed the removal efficiency and fine-size distribution of CPM coupled with compositional analysis across air pollution control device systems (APCDs) at an ultra-low emission (ULE) power plant. The findings indicated total CPM emissions were reduced to a minimum of 0.418mg/m3 at the Wet Electrostatic Precipitator (WESP). The Wet Flue Gas Desulfurization (WFGD) showed the highest removal efficiency (98%) across all particle sizes, notably in the ultra-micron range. Selective Catalytic Reduction (SCR) demonstrated a mere 34% overall efficiency, with a negative removal rate in the ultra-fine particle range. The WESP effectively removed CPM only in sub-micron and ultra-micron sizes, but significantly increased water-soluble ions formation in ultra-fine spatially suspended CPM (CPMspa), leading to overall negative efficiency. Thus, the removal efficiency of the ultra-fine particle range was most affected among the three particle size ranges when the flue gas went through the APCDs. Major metal elements and water-soluble ions were more readily removed by APCDs due to their surface aggregation, while the removal of trace elements like Hg and Se was limited. Reducing SO42-/NH4+ formation in SCR, and optimizing WESP spray system operations based on flue gas components are essential steps in controlling CPM concentration in ULE power plants.

Particulate black carbon mass concentrations and the episodic source identification driven by atmospheric blocking effects in Astana, Kazakhstan

Black carbon (BC) is a component of fine particulate matter (PM2.5) that is a key contributor to adverse human health effects and climate forcing. To date, BC mass concentrations and possible sources in Kazakhstan have not been studied. Thus, understanding the temporal variations of BC for a large developing region with a complex climate is useful. In this study, measurements of fine particulate BC mass concentrations in Astana were made from June 2020 to October 2021 by measuring light absorption of PM2.5 on filters. The mean BC concentration was 2.56 ± 1.29 μg m−3 with maximum and minimum monthly mean BC concentrations being 4.56 ± 2.03 μg m−3 and 1.12 ± 0.42 μg m−3 in January 2021 and June 2020, respectively. Temporal analyses of BC, SO2, PM10, NOx, CO, meteorological and atmospheric stability parameters were performed. Aggregated pollutant ‘episodic loadings’ during the heating and non-heating periods were identified. Their relationships with blocking anticyclones and cyclones were investigated by examining the reversal of meridional gradients at 500 hPa geopotential height (GPH) maps and identifying Omega (Ω) and Rex blocking types. Astana has some of the highest BC concentrations of cities worldwide. Seasonal BC source location identification using Conditional Bivariate Probability Function (CBPF) analysis implicated combined heat and power (CHP) plant emissions as the major BC source in Astana. Significant increases in BC concentrations were observed during the cold season due to numerous sources, generally poorer atmospheric dispersion and blocking events. The Concentration Weighted Trajectory (CWT) analysis results showed that the distribution of the 75th percentile of BC during episodic periods actively controlled by blockings exceeding than the entire measurement period, which may reflect cross-border transport and adjacent countries.

Fine particulate matter (PM2.5) induces testosterone disruption by triggering ferroptosis through SIRT1/HIF-1α signaling pathway in male mice

Fine particulate matter (PM2.5), a significant component of air pollution particulate matter, is inevitable and closely associated with increasing male reproductive disorder. However, the testicular targets of PM2.5 and its toxicity related molecular mechanisms are still not fully understood. In this study, the conditional knockout (cKO) mice and primary Leydig cells were used to explore the testicular targets of PM2.5 and the related underlying mechanisms. First, apparent the structure impairment of seminiferous tubules, Leydig cells vacuolization, decline of serum testosterone and sperm quality reduction were found in male wild-type (WT) and Sirt1 knockout mice after exposure to PM2.5. Enrichment analyses revealed that differentially expressed genes (DEGs) were enriched in steroid hormone biosynthesis, ferroptosis, and HIF-1 signaling pathway in the mice testes after exposure to PM2.5, which were subsequently verified by the molecular biological analyses. Notably, similar enrichment analyses results were also observed in primary Leydig cells after treatment with PM2.5. In addition, Knockdown of Sirt1 significantly increased PM2.5-induced expression and activation of HIF-1α, which was in parallel to the changes of cellular iron levels, oxidative stress indicators and the ferroptosis markers. In conclusion, this highlights that PM2.5 triggers ferroptosis via SIRT1/HIF-1α signaling pathway to inhibit testosterone synthesis in males. These findings provide a novel research support for the study that PM2.5 causes male reproductive injury.

Long-term evolution of carbonaceous aerosols in PM2.5 during over a decade of atmospheric pollution outbreaks and control in polluted central China

Against the backdrop of an uncertain evolution of carbonaceous aerosols in polluted areas over the long term amid air pollution control measures, this 11-year study (2011–2021) investigated fine particulate matter (PM2.5) and carbonaceous components in polluted central China. Organic carbon (OC) and elemental carbon (EC) averaged 16.5 and 3.4 μg/m3, constituting 16 and 3 % of PM2.5 mass. Carbonaceous aerosols dominated PM2.5 (35 and 27 %) during periods of excellent and good air quality, while polluted days witnessed other components as dominants, with a significant decrease in primary organic aerosols and increased secondary pollution. From 2011 to 2021, OC and EC decreased by 53 and 76 %, displaying a high-value oscillation phase (2011–2015) and a low-value fluctuation phase (post-2016). A substantial reduction in high OC and EC concentrations in 2016 marked a milestone in significant air quality improvement attributed to effective control measures, especially targeting OC and EC, evident from their decreased proportion in PM2.5. Primary OC (POC) in winter exhibited the most pronounced reduction (8 % per year), and the seasonal disparities in PM2.5 and carbonaceous components were reduced, showcasing the effectiveness of control measures. Contrary to the more pronounced reduction of EC, which decreased in proportion to PM2.5, secondary OC (SOC) in PM2.5 exhibited an increasing trend. Along with rising OC/EC, SOC/OC, and SOC/EC ratios, this indicates a growing prominence of secondary pollution compared to the decrease in primary pollution. SOC shows an increasing trend with NO2 rise (r = 0.53), without O3 promoting SOC. Positive correlations of SOC with SO2, CO (r = 0.41, 0.59), also highlight their influence on atmospheric conditions, oxidative capacity, and chemical reactions, indirectly impacting SOC formation. The implementation of precise precursor emission reduction measures holds the key to future efforts in mitigating SOC pollution and reducing PM2.5 concentrations, thereby contributing to improved air quality.

Enhanced Soil Carbon Stability through Alterations in Components of Particulate and Mineral-Associated Organic Matter in Reclaimed Saline–Alkali Drainage Ditches

Soil carbon content and stability are primarily influenced by the stabilization of particulate organic matter (POM) and mineral-associated organic matter (MAOM). Despite extensive research on the stabilization processes of POM and MAOM carbon components under various land-use types, the investigation into stabilization processes of soil carbon remains limited in saline–alkali soils. Therefore, we collected soil samples from different positions of saline–alkali drainage ditches at four reclamation times (the first, seventh, fifteenth, and thirtieth year) to determine their carbon content and physicochemical properties. Moreover, POM and MAOM fractions were separated from soil samples, and Fourier transform infrared spectra (FTIR) were used to investigate changes in their chemical composition. The results showed that with increasing reclamation time, the soil total carbon and soil organic carbon (SOC) contents significantly increased from 14 to 15 and 2.9 to 5.5 g kg−1, respectively. In contrast, soil inorganic carbon content significantly decreased from 11 to 9.6 g kg−1. Notably, the changes in soil carbon components following the increasing reclamation time were primarily observed in the furrow sole at a depth of 20–40 cm. While the SOC content of the POM fraction (SOCPOM) decreased significantly, the SOC content of the MAOM fraction (SOCMAOM) increased significantly. These alterations were largely dominated by drainage processes after reclamation instead of a possible conversion from SOCPOM to SOCMAOM. FTIR results revealed that MAOM was greatly influenced by the reclamation time more than POM was, but the change in both POM and MAOM contributed to an increase in soil carbon stability. Our findings will deepen the comprehension of soil carbon stabilization processes in saline–alkali drainage ditches after reclamation and offer a research framework to investigate the stability processes of soil carbon components via alterations in POM and MAOM fractions.

Assessment major NOx sources to nitrate of TSP around the Danjiangkou reservoir using isotopes and a Bayesian isotope mixing model

Nitrate (NO3−) is a key component of atmospheric particulate matter. However, studies quantifying NO3− formation and sources in water source areas remain scarce. This study employs NO3− concentration, dual isotopic analyses (δ15N, δ18O), and SIAR and PSCF models to elucidate NO3− formation mechanisms and apportion sources in the Danjiangkou Reservoir area. The result showed that the concentration of NO3− (0.52 μg m−3-2.39 μg m−3), δ15N–NO3- (−2.3‰-4.2‰) and δ18O–NO3- (64.2‰–96.6‰) values varied seasonally in total suspended particulate matter (TSP). The contribution of the NO2 + ·OH pathway was the highest in summer (84%), while the main contributions came from the N2O5 + H2O and NO3 + VOCs pathways in winter (75%). The SIAR model revealed that the contributions of coal combustion and traffic emissions were 34% and 23%, respectively, indicating that fossil fuel release contributed most. Moreover, the contribution of biomass combustion sources was 31%, and soil emission sources had the least (12%). Considering liquefied petroleum gas, gasoline, and diesel vehicles as traffic emission sources, their contribution to NO3− in TSP increased to 50%. The PSCF analysis indicated that external input areas were predominantly from central Henan Province, northern Hubei Province, and central Shaanxi Province. This study quantitatively analyzed the sources of NO3− in atmospheric particulate matter in water sources for the first time, indicating that controlling the emissions of nitrogen oxides from gasoline cars, heavy-duty diesel trucks, and ships could help alleviate haze pollution and enhance air quality in the Danjiangkou reservoir area.

Characteristics of number concentration, size distribution and components of particulate matter emitted from a typical large civil airport

Civil airports are recognized as significant contributors to fine particulate matter, especially ultra-fine particulate matter (UFP). The pollutants from airport activities have a notable adverse impact on global climate, urban air quality, and public health. However, there is a lack of practical observational studies on the characterization of integrated pollutant emissions from large civil airports. This study aims to focus on the combined emission characteristics of particulate number concentration (PNC), size distribution, and components at a large civil airport, especially UFP. The findings reveal that airport activities significantly contribute to elevated PNC levels during aircraft activity in downwind conditions (four times higher than background levels) and upwind conditions (7.5 times higher). UFP dominates the PNC around the airport. The particle size distribution shows two peaks occurring around 10-30 nm and 60-80 nm. Notably, particles within the ranges of 17-29 nm and 57-101 nm account for 65.9 % and 12.0 % of the total PNC respectively. Aircraft landing has the greatest impact on particles sized between 6 and 17 nm while takeoff affects particles sized between 29 and 57 nm resulting in a respective increase in PNC by factors of approximately 3.27 and 35.4-fold increase compared to background levels. Different aircraft types exhibit varying effects on PNC with A320 and A321 showing more pronounced effects during takeoff and landing.The presence of airports leads to roughly five-fold rise in elemental component concentrations with Si being highest followed by OC, Ca, Al, Fe, Ca2+, EC, and Mg2+. The OC/EC ratio under high aircraft activity in downwind conditions falls within range of approximately 2.5–3.5. These characteristic components and ratio can be considered as identifying species for civil airports. PMF model show about 75 % of the particulate emissions at the airport boundary were related to airport activities.

Effects of photo-oxidation and transition metals on the formation of reactive oxygen species from aromatic compounds using spectroscopic method

Particulate matter (PM) can cause adverse health effects by overproducing reactive oxygen species (ROS). Although the ability of PM to induce ROS generation depends on its composition and environmental factors. This study explores how photo-oxidation affects ROS generation from aromatic compounds (ACs, including catechol (CAT), phthalic acid (PA), and 4,4′-oxydibenzoic acid (4,4′-OBA)) and their mixtures with transition metals (TMs, including Fe(II), Mn(II), and Cu(II)) using Fourier-transform infrared (FTIR) and Ultraviolet-visible spectroscopy (UV–Vis). Results showed that photo-oxidation facilitated ROS generation from ACs. CAT-Fe(II)/Cu(II) showed synergistic effects, but 4,4′-OBA-Fe(II)/Cu(II) showed antagonistic effects. ACs-Mn(II) and PA-Fe(II)/Cu(II) exhibited synergistic effects first and then showed antagonistic effects. The different interactions were due to complexation between ACs and TMs. The photo-oxidized ACs-TMs significantly enhanced ROS generation compared with ACs-TMs. The study suggested the photo-oxidation mechanism involved that the transfer of π-electrons from the ground to an excited state in benzene rings and functional groups, leading to the breakage and formation of chemical bonds or easier π-electron transfer from ACs to TMs. The former could generate ROS directly or produce polymers that promoted ROS generation, while the latter promoted ROS generation by transferring π-electrons to dissolved oxygen quickly. Our study revealed that both interactions among components and photo-oxidation significantly influenced ROS generation. Future studies should integrate broader atmospheric factors and PM components to fully assess oxidative potential and health impacts.

Short-Term Effects of Primary and Secondary Particulate Matter on Ceramide Metabolism, Pro-Inflammatory Response, and Blood Coagulation.

Evidence of the precise biological pathway responsible for acute cardiovascular events triggered by particulate matter (PM) exposure from anthropogenic emissions is sparse. We investigated the associations of biomarkers relevant to the pathophysiology of atherothrombosis (ceramide metabolism, pro-inflammatory response, and blood coagulation) with primary and secondary components in particulate matter with aerodynamic diameters less than 2.5 μm (PM2.5). A total of 152 healthy participants were followed with four repeated clinical visits between September 2019 and January 2020 in Beijing. Exposure to ambient inorganic aerosols (sulfate, nitrate, ammonium, and chloride), as well as organic aerosols (OA) in PM2.5, was measured by a real-time aerosol chemical speciation monitor, and sources of OA were performed by positive matrix factorization. We found significant increases of 101.9-397.9% in ceramide indicators associated with interquartile-range increases in inorganic aerosols and OA prior to 72 h of exposure. Higher levels of organic and inorganic aerosols in PM2.5 were associated with increases of 3.1-6.0% in normal T cells regulated upon activation and expressed and secreted relevant to the pro-inflammatory response; increases of 276.9-541.5% were observed in D-dimers relevant to coagulation. Detrimental effects were further observed following OA exposure from fossil fuel combustion. Mediation analyses indicated that ceramide metabolism could mediate the associations of PM2.5 components with pro-inflammatory responses. Our findings expand upon the current understanding of potential pathophysiological pathways of cardiovascular events posed by ambient particulates and highlight the importance of reducing primary and secondary PM from anthropogenic combustions.

Effect of air pollutants on allergic inflammation in structural cells of nasal mucosa.

Air pollution is a growing global concern, and its effect on allergic inflammation has attracted the attention of many researchers. Particulate matter (PM) is a major component of ambient air pollution, and heavy metals are the primary toxic constituents of PM. As previous studies on the impact of air pollutants on allergic inflammation lacked physiological resemblance to actual atmospheric exposure, we built an experimental model to investigate the effects of aerosolized air pollutants on nasal epithelial cells and fibroblasts. We collected PM 2.5 samples from ambient 24 h air in Seoul from August 2020 to August 2022, and then conducted component analysis for metallic constituents. Primary nasal epithelial cells and nasal fibroblasts, obtained and cultured from the turbinate tissues of human participants, were treated with PM 2.5 and heavy metals were identified from component analysis to observe changes in cytokine expression. 3D-hybrid culture model, a co-culture of an air-liquid interface and nasal fibroblast spheroids, was built to observe the impact of air pollutants in the form of aerosols. Among the heavy metals, Si was the predominant component of PM 2.5 and Zn showed the highest correlation with the concentration of PM 2.5 in Seoul. PM 2.5, Zn, and Si increased the production of epithelial cell-derived cytokines, with which PM 2.5 and Zn exhibited similar trends with one another. Exposure of 3D-hybrid model to aerosolized PM 2.5 and Zn yielded elevated periostin, α-SMA, and fibronectin expressions from fibroblast spheroids, and those without epithelial barrier exhibited a similar increase in periostin expression. Ambient air pollutants in the form of aerosols lead to an increased expression of allergic inflammatory cytokines in both nasal epithelial cells and fibroblasts. Regulations on air pollution will help reduce the burden of allergic diseases worldwide in the future.

Single Droplet Tweezer Revealing the Reaction Mechanism of Mn(II)-Catalyzed SO2 Oxidation.

Sulfate aerosol is one of the major components of secondary fine particulate matter in urban haze that has crucial impacts on the social economy and public health. Among the atmospheric sulfate sources, Mn(II)-catalyzed SO2 oxidation on aerosol surfaces has been regarded as a dominating one. In this work, we measured the reaction kinetics of Mn(II)-catalyzed SO2 oxidation in single droplets using an aerosol optical tweezer. We show that the SO2 oxidation occurs at the Mn(II)-active sites on the aerosol surface, per a piecewise kinetic formulation, one that is characterized by a threshold surface Mn(II) concentration and gaseous SO2 concentration. When the surface Mn(II) concentration is lower than the threshold value, the reaction rate is first order with respect to both Mn(II) and SO2, agreeing with our traditional knowledge. But when surface Mn(II) concentration is above the threshold, the reaction rate becomes independent of Mn(II) concentration, and the reaction order with respect to SO2 becomes greater than unity. The measured reaction rate can serve as a tool to estimate sulfate formation based on field observation, and our established parametrization corrects these calculations. This framework for reaction kinetics and parametrization holds promising potential for generalization to various heterogeneous reaction pathways.

AhR Agonistic Components in Urban Particulate Matter Regulate Astrocytic Activation and Function.

Exposure to atmospheric particulate matter (PM) has been found to accelerate the onset of neurological disorders via the induction of detrimental neuroinflammatory responses. To reveal how astrocytes respond to urban atmospheric PM stimulation, a commercially available standard reference material (SRM1648a) was tested in this study on the activation of rat cortical astrocytes. The results showed that SRM1648a stimulation induced both A1 and A2 phenotypes in astrocytes, as characterized by the exposure concentration-dependent increases in Fkbp5, Sphk1, S100a10, and Il6 mRNA levels. Studying the functional alterations of astrocytes indicated that the neurotrophic factors of Gdnf and Ngf were transcriptionally upregulated due to astrocytic A2-type activation. SRM1648a also promoted autonomous motility of astrocytes and elevated the expressions of chemokines. The aryl hydrocarbon receptor (AhR) agonistic components, such as polycyclic aromatic hydrocarbons (PAHs), were recognized to greatly contribute to SRM1648a-induced effects on astrocytes, which was confirmed by the attenuation of PM-disturbed astrocytic effects via AhR blockage. This study, for the first time, uncovered the direct regulation of urban atmospheric PM on astrocytic activation and function and traced the containing bioactive components (e.g., PAHs) with AhR agonistic activity. The findings provided new knowledge on understanding the ambiguous neurological disturbance from ambient fine PM pollution.

Quantifying Multipollutant Health Impacts Using the Environmental Benefits Mapping and Analysis Program-Community Edition (BenMAP-CE): A Case Study in Atlanta, Georgia.

Air pollution risk assessments do not generally quantify health impacts using multipollutant risk estimates, but instead use results from single-pollutant or copollutant models. Multipollutant epidemiological models account for pollutant interactions and joint effects but can be computationally complex and data intensive. Risk estimates from multipollutant studies are therefore challenging to implement in the quantification of health impacts. Our objective was to conduct a case study using a developmental multipollutant version of the Environmental Benefits Mapping and Analysis Program-Community Edition (BenMAP-CE) to estimate the health impact associated with changes in multiple air pollutants using both a single and multipollutant approach. BenMAP-CE was used to estimate the change in the number of pediatric asthma emergency department (ED) visits attributable to simulated changes in air pollution between 2011 and 2025 in Atlanta, Georgia, applying risk estimates from an epidemiological study that examined short-term single-pollutant and multipollutant (with and without first-order interactions) exposures. Analyses examined individual pollutants (i.e., ozone, fine particulate matter, carbon monoxide, nitrogen dioxide (), sulfur dioxide, and particulate matter components) and combinations of these pollutants meant to represent shared properties or predefined sources (i.e., oxidant gases, secondary pollutants, traffic, power plant, and criteria pollutants). Comparisons were made between multipollutant health impact functions (HIF) and the sum of single-pollutant HIFs for the individual pollutants that constitute the respective pollutant groups. Photochemical modeling predicted large decreases in most of the examined pollutant concentrations between 2011 and 2025 based on sector specific (i.e., source-based) estimates of growth and anticipated controls. Estimated number of avoided asthma ED visits attributable to any given multipollutant group were generally higher when using results from models that included interaction terms in comparison with those that did not. We estimated the greatest number of avoided pediatric asthma ED visits for pollutant groups that include (i. e., criteria pollutants, oxidants, and traffic pollutants). In models that accounted for interaction, year-round estimates for pollutant groups that included ranged from 27.1 [95% confidence interval (CI): 1.6, 52.7; traffic pollutants] to 55.4 (95% CI: 41.8, 69.0; oxidants) avoided pediatric asthma ED visits. Year-round results using multipollutant risk estimates with interaction were comparable to the sum of the single-pollutant results corresponding to most multipollutant groups [e.g., 52.9 (95% CI: 43.6, 62.2) for oxidants] but were notably lower than the sum of the single-pollutant results for some pollutant groups [e.g., 77.5 (95% CI: 66.0, 89.0) for traffic pollutants]. Performing a multipollutant health impact assessment is technically feasible but computationally complex. It requires time, resources, and detailed input parameters not commonly reported in air pollution epidemiological studies. Results estimated using the sum of single-pollutant models are comparable to those quantified using a multipollutant model. Although limited to a single study and location, assessing the trade-offs between a multipollutant and single-pollutant approach is warranted. https://doi.org/10.1289/EHP12969.

Nontargeted Identification of Organic Components in Fine Particulate Matter Related to Lung Tumor Metastasis Based on an Adverse Outcome Pathway Strategy.

Emerging studies implicate fine particulate matter (PM2.5) and its organic components (OCs) as urgent hazard factors for lung cancer progression in nonsmokers. Establishing the adverse outcome pathway (AOP)-directed nontargeted identification method, this study aimed to explore whether PM2.5 exposure in coal-burning areas promoted lung tumor metastasis and how we identify its effective OCs to support traceability and control of regional PM2.5 pollution. First, we used a nude mouse model of lung cancer for PM2.5 exposure and found that the exposure significantly promoted the hematogenous metastases of A549-Luc cells in lung tissues and the adverse outcomes (AOs), with key events (KEs) including the changed expression of epithelial-mesenchymal transition (EMT) markers, such as suppression of E-cad and increased expression of Fib. Subsequently, using AOs and KEs as adverse outcome directors, we identified a total of 35 candidate chemicals based on the in vitro model and nontargeted analysis. Among them, tributyl phosphate (C12H27O4P), 2-bromotetradecane (C14H29Br), and methyl decanoate (C11H22O2) made greater contributions to the AOs. Finally, we clarified the interactions between these OCs and EMT-activating transcription factors (EMT-ATFs) as the molecular initiation event (MIE) to support the feasibility of the above identification strategy. The present study updates a new framework for identifying tumor metastasis-promoting OCs in PM2.5 and provides solid data for screening out chemicals that need priority control in polluted areas posing higher lung cancer risk.

Particulate matter from car exhaust alters function of human iPSC-derived microglia

BackgroundAir pollution is recognized as an emerging environmental risk factor for neurological diseases. Large-scale epidemiological studies associate traffic-related particulate matter (PM) with impaired cognitive functions and increased incidence of neurodegenerative diseases such as Alzheimer’s disease. Inhaled components of PM may directly invade the brain via the olfactory route, or act through peripheral system responses resulting in inflammation and oxidative stress in the brain. Microglia are the immune cells of the brain implicated in the progression of neurodegenerative diseases. However, it remains unknown how PM affects live human microglia.ResultsHere we show that two different PMs derived from exhausts of cars running on EN590 diesel or compressed natural gas (CNG) alter the function of human microglia-like cells in vitro. We exposed human induced pluripotent stem cell (iPSC)-derived microglia-like cells (iMGLs) to traffic related PMs and explored their functional responses. Lower concentrations of PMs ranging between 10 and 100 µg ml−1 increased microglial survival whereas higher concentrations became toxic over time. Both tested pollutants impaired microglial phagocytosis and increased secretion of a few proinflammatory cytokines with distinct patterns, compared to lipopolysaccharide induced responses. iMGLs showed pollutant dependent responses to production of reactive oxygen species (ROS) with CNG inducing and EN590 reducing ROS production.ConclusionsOur study indicates that traffic-related air pollutants alter the function of human microglia and warrant further studies to determine whether these changes contribute to adverse effects in the brain and on cognition over time. This study demonstrates human iPSC-microglia as a valuable tool to study functional microglial responses to environmental agents.

Role of circPSEN1 in carbon black and cadmium co-exposure induced autophagy-dependent ferroptosis in respiratory epithelial cells

Carbon black and cadmium (Cd) are important components of atmospheric particulate matter and cigarette smoke that are closely associated with the occurrence and development of lung diseases. Carbon black, particularly carbon black nanoparticles (CBNPs), can easily adsorbs metals and cause severe lung damage and even cell death. Therefore, this study aimed to explore the mechanisms underlying the combined toxicity of CBNPs and Cd. We found that the combined exposure to CBNPs and Cd promoted significantly greater autophagosome formation and ferroptosis (increased malonaldehyde (MDA), reactive oxygen species (ROS), and divalent iron ions (Fe2+) levels and altered ferroptosis-related proteins) compared with single exposure in both 16HBE cells (human bronchial epithelioid cells) and mouse lung tissues. The levels of ferroptosis proteins, transferrin receptor protein 1 (TFRC) and glutathione peroxidase 4 (GPX4), were restored by CBNPs-Cd exposure following treatment with a 3-MA inhibitor. Additionally, under CBNPs-Cd exposure, circPSEN1 overexpression inhibited increases in the autophagy proteins microtubule-associated protein 1 light chain 3 (LC3II/I) and sequestosome-1 (P62). Moreover, increases in TFRC and Fe2+, and decreases in GPX4were inhibited. Knockdown of circPSEN1 reversed these effects. circPSEN1 interacts with autophagy-related gene 5 (ATG5) protein and upregulates nuclear receptor coactivator 4 (NCOA4), the co-interacting protein of ATG5, thereby degrading ferritin heavy chain 1 (FTH1) and increasing Fe2+ in 16HBE cells. These results indicated that the combined exposure to CBNPs and Cd promoted the binding of circPSEN1 to ATG5, thereby increasing autophagosome synthesis and ATG5-NCOA4-FTH1 axis activation, ultimately inducing autophagy-dependent ferroptosis in 16HBE cells and mouse lung tissues. This study provides novel insights into the toxic effects of CBNPs and Cd in mixed pollutants.