New health index derived from oxidative potential and cell toxicity of fine particulate matter to assess its potential health effect.

Toxicological data and exposure levels of fine particulate matters (PM2.5) are necessary to better understand their health effects. Simultaneous measurements of PM2.5 oxidative potential (OP) and cell toxicity in urban areas (Beijing, China and Gwangju, Korea) reveal their dependence on chemical composition. Notably, acids (Polar), benzocarboxylic acids, and Pb were the chemical components that affected both OP and cell toxicity. OP varied more significantly among different locations and seasons (winter and summer) than cell toxicity. Using the measured OP, cell toxicity, and PM2.5 concentration, a health index was developed to better assess the potential health effects of PM2.5. The health index was related to the sources of PM2.5 derived from the measured chemical components. The contributions of secondary organic aerosols and dust to the proposed health index were more significant than their contributions to PM2.5 mass. The developed regression equation was used to predict the health effect of PM2.5 without further toxicity measurements. This new index could be a valuable health metric that provides information beyond just the PM2.5 concentration level.

Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE-/- mice exposed to diesel exhaust particles.

Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the in vivo effects of diesel exhaust particles (DEP) on the heart and the molecular mechanisms of DEP-induced heart dysfunction have not been investigated. In the current study, we attempted to identify the proteomic signatures of heart fibrosis caused by diesel exhaust particles (DEP) in CVDs-prone apolipoprotein E knockout (ApoE-/-) mice model using tandem mass tag (TMT)-based quantitative proteomic analysis. DEP exposure induced mild heart fibrosis in ApoE-/- mice compared with severe heart fibrosis in ApoE-/- mice that were treated with CVDs-inducing peptide, angiotensin II. TMT-based quantitative proteomic analysis of heart tissues between PBS- and DEP-treated ApoE-/- mice revealed significant upregulation of proteins associated with platelet activation and TGFß-dependent pathways. Our data suggest that DEP exposure could induce heart fibrosis, potentially via platelet-related pathways and TGFß induction, causing cardiac fibrosis and dysfunction.

Metal contents and size distributions of brake and tire wear particles dispersed in the near-road environment.

Traffic related non-tailpipe particulate matter emissions can rival the continuously decreasing tailpipe emissions in modern fleets. Non-tailpipe emissions have become the dominating source of traffic emissions in California already. This study measured ambient PM2.5 and PM10 concentrations at near road environments for two major highways in California, I-5 in Anaheim and I-710 in Long Beach. A total of 51 elements were measured from filter samples collected over four-hour intervals for a two-week period in the winter of 2020 before the statewide lockdown by the COVID-19 pandemic. Iron was the most abundant element in ΔPM10 (differences between downwind and upwind sites), contributing to 30 % and 24 % of total measured elements in ΔPM10 at the I-5 and I-710 locations, respectively. Iron correlated highly with other brake wear markers (e.g., titanium, copper, barium, manganese, and zirconium) with coefficient of determination (r2) ranging from 0.67 to 0.90 in both PM2.5 and PM10. Silicon was the second most abundant element, contributing to 21 % of total measured elements in ΔPM2.5 and ΔPM10. Silicon showed strong correlations with crustal elements such as calcium (r2 = 0.90), aluminum (r2 = 0.96), and potassium (r2 = 0.72) in ΔPM2.5, and the correlations were even higher in ΔPM10. Barium had a weak correlation with zinc, a commonly used maker for tire wear, with r2 = 0.63 and r2 = 0.11 for ΔPM10 at the I-5 and I-710 locations respectively. Barium showed a positive correlation with crosswind speed and could serve as a good brake wear PM marker. Hourly PM2.5 concentrations of iron and zinc showed cyclic peaks from 0800 to 1000 h at I-5 during weekdays. Particle mass distributions showed peaks near ~7 µm, while particle number distributions showed peaks near 2.1 µm and 6.5 µm, respectively. This is consistent with brake wear and road dust size ranges previously reported.

Comparison of the sources and oxidative potential of PM2.5 during winter time in large cities in China and South Korea.

Regional air pollution is rising in Northeast Asia due to increasing energy consumption resulting from a growing population and intensifying industrialization. This study analyzes the sources of air pollution using fine particulate matter (PM2.5) sampling from the atmosphere over Korea and China. We then use this analysis to further investigate the relationship between organic compounds (source tracers) and the oxidative potential of PM2.5. The PM2.5 concentration during winter measured at a measurement stations in Korea showed no significant variation year-to-year. The PM2.5 concentrations measured during winter at a site near Beijing, China were 62.45 µg/m3 in 2018 and 33.07 µg/m3 in 2020. The sources, as determined from PMF, were analyzed at a site in Korea, the sources as secondary nitrate (34.10 %), secondary sulfate (20.20 %), coal combustion (4.01 %), vehicle emission (8.55 %), cooking and biomass burning (18.39 %), dust (8.45 %), and SOA (6.29 %) were identified. At a site in China, secondary nitrate (17.54 %), secondary sulfate (12.03 %), coal combustion (15.53 %), vehicle emission (12.43 %), cooking and biomass burning (9.25 %), dust (26.40 %), secondary organic aerosol (6.82 %) were identified. Our results show secondary organic carbon had a positive association with oxidative potential in Korea while primary organic carbon presented higher correlation with oxidative potential in China. Further, the ECMWF Reanalysis v5 (ERA5) wind field during the high PM2.5 events demonstrated airflow from the west coast of China resulting in high polar organic compounds at the Korean monitoring site. The results further support that aged PM2.5, which contains secondary products, leads to increased oxidative potential. The results presented explain the high concentrations of secondary products and the impact on the biological activities of PM2.5, supporting additional actions to address the impacts of long-range transport of PM2.5.

Diesel exhaust particles induce human umbilical vein endothelial cells apoptosis by accumulation of autophagosomes and caspase-8 activation.

Diesel exhaust particles (DEP) are risk factors for endothelial cells (ECs) dysfunction. However, the mechanism by which DEP induce ECs apoptosis remains unclear. Here, we investigated how DEP induce death of human umbilical vein ECs (HUVECs), with a focus on the autophagy-mediated apoptotic pathway. DEP induced dose-dependent HUVECs death and exposure to the IC50 concentration of DEP (70 µg/ml) led to apoptosis. DEP phosphorylated Beclin-1 (Ser93) and increased protein levels of p62 and LC3BII and the number of LC3B puncta, indicating autophagy initiation. DEP increased expression of pro- and mature forms of cathepsin D, which increases lysosomal activity. However, DEP suppressed expression of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor proteins (STX17, VAMP8, SNAP29, YKT6, and STX7) to inhibit autolysosome formation, resulting in accumulation of autophagosomes. LC3B, p62, and caspase-8 form a tertiary complex in accumulated autophagosomes, which is known to serve as a platform for caspase-8 activation. Indeed, DEP activates caspase-8 and pretreatment with a caspase-8 inhibitor suppressed DEP-induced apoptosis. Furthermore, depletion of p62 decreased caspase-8 and caspase-3 activation and inhibited the DEP-induced apoptosis. Taken together, these findings demonstrated that DEP induced HUVECs apoptosis by inhibiting autophagosome maturation and identified caspase-8 as a novel mediator of DEP-induced ECs apoptosis.

Transcriptional analysis of gasoline engine exhaust particulate matter 2.5-exposed human umbilical vein endothelial cells reveals the different gene expression patterns related to the cardiovascular diseases.

Particulate matter (PM) causes several diseases, including cardiovascular diseases (CVDs). Previous studies compared the gene expression patterns in airway epithelial cells and keratinocytes exposed to PM. However, analysis of differentially expressed gene (DEGs) in endothelial cells exposed to PM2.5 (diameter less than 2.5 µm) from fossil fuel combustion has been limited. Here, we exposed human umbilical vein endothelial cells (HUVECs) to PM2.5 from combustion of gasoline, performed RNA-seq analysis, and identified DEGs. Exposure to the IC50 concentrations of gasoline engine exhaust PM2.5 (GPM) for 24 h yielded 1081 (up-regulation: 446, down-regulation: 635) DEGs. The most highly up-regulated gene is NGFR followed by ADM2 and NUPR1. The most highly down-regulated gene is TNFSF10 followed by GDF3 and EDN1. Gene Ontology enrichment analysis revealed that GPM regulated genes involved in cardiovascular system development, tube development and circulatory system development. Kyoto Encyclopedia of Genes and Genomes and Reactome pathway analyses showed that genes related to cytokine-cytokine receptor interactions and cytokine signaling in the immune system were significantly affected by GPM. We confirmed the RNA-seq data of some highly altered genes by qRT-PCR and showed the induction of NGFR, ADM2 and IL-11 at a protein level, indicating that the observed gene expression patterns were reliable. Given the adverse effects of PM2.5 on CVDs, our findings provide new insight into the importance of several DEGs and pathways in GPM-induced CVDs.

Comparison of physical and chemical characteristics and oxidative potential of fine particles emitted from rice straw and pine stem burning.

Agricultural burning and forest fires are common in Northeast Asia and contribute to the elevation of fine particulate pollution, which greatly affects air quality. In this study, chemical and physical attributes, as well as the oxidative potential of fine particles produced from rice straw and pine stem burning in a laboratory-scale chamber were determined. The burning of rice straw generated notably lower emissions of fine particles and elemental carbon (EC) than did the burning of pine stems. The longer retention of ultrafine particles was observed for rice straw burning likely caused by this material's longer period of initial flaming combustion. Organic carbon (OC), OC/EC, K+/OC, K+/EC, Zn, and alkanoic acid were higher in the fine particles of rice straw burning, while EC, K+/Cl-, Fe, Cr, Al, Cu, and levoglucosan were higher for pine stem burning particles. Chemical data were consistent with a higher hygroscopic growth factor and cloud formation potential and lower amount of agglomerated soot for rice straw burning particles. Rice straw burning particles displayed an oxidative potential seven times higher than that of pine stems.

Assessment of PM2.5-bound nitrogen-containing organic compounds (NOCs) during winter at urban sites in China and Korea.

In this study, ambient fine particles (PM2.5) were collected in two urban cities in China and Korea (Beijing and Gwangju, respectively) simultaneously in January 2018. Analysis of the nonpolar and semipolar organic matter (OM) using atmospheric pressure photoionization (APPI) Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR MS) revealed that compounds containing only C, H, and O (CHO) and those containing C, H, O, and N (CHON) accounted for more than 90% of the total intensity of the OM peaks. Higher proportions of CHON compounds were observed during days with abnormally high PM2.5 concentrations at both sites than on regular or non-event days. The proportion of CHON species at the Beijing site was not correlated with secondary ionic species (i.e., NO3-, SO42-, and NH4+) or gaseous components (i.e., O3, NO2, and SO2). In contrast, the proportion of CHON species at the Gwangju site was positively correlated with the concentrations of particulate nitrate and ammonium ions, assuming that ambient ammonium nitrate plays a role in the atmospheric formation of nitrogen-containing organic compounds (NOCs) at the Gwangju site and that Gwangju is more strongly influenced by secondary aerosols than Beijing is. In particular, a significant proportion of the compounds observed at the Beijing site contained only C, H and N (CHN), while negligible amounts of CHN were detected at the Gwangju site. The CHN species in Beijing were identified as quinoline compounds and the corresponding -CH2 homologous series using complementary GC × GC-TOF MS analysis. These results suggest that NOCs and their -CH2 homologous series from primary emissions may be significant contributors to nonpolar and semipolar OM during winter in Beijing, while NOCs with high oxidation states, likely formed via ambient-phase nitrate-mediated reactions, may be the dominant OM constituents in Gwangju.

Application of various cytotoxic endpoints for the toxicity prioritization of fine dust (PM2.5) sources using a multi-criteria decision-making approach.

Fine dust (PM2.5) is generated from various sources, and many studies have reported on the sources of PM2.5. However, the current research on PM2.5 toxicity based on its sources is insufficient. In this study, we developed a framework for the prioritization of fine dust (PM2.5) sources on the basis of the multi-endpoint toxicities using the multi-criteria decision-making method (MCDM). To obtain the multi-endpoint toxicities of PM2.5 sources, cell mortality, reactive oxygen species (ROS), inflammation and mutagenicity were measured for diesel exhaust particles (DEP), gasoline exhaust particles (GEP), rice straw burning particles (RBP), coal combustion particles (CCP) and tunnel dust particles (TDP). The integrative toxicity score (ITS) of the PM2.5 source was calculated using MCDM, which consist of four steps: (1) defining the decision-making matrix, (2) normalization and weighting, (3) calculating the ITS (linear aggregation) and (4) a global sensitivity analysis. The indicator of cell mortality had the highest weight (0.3780) followed by inflammation (0.2471), ROS (0.2178) and mutagenicity (0.1571). Additionally, the ITS based on the sources contributing to PM2.5 resulted in the following order: DEP (0.89), GEP (0.44), RBP (0.40), CCP (0.23) and TDP (0.06). The relative toxicity index (RTI), which represents the ratio of toxicity due to the difference in sources, increases as the contribution of the highly toxic sources increases. The RTI over 1 is closely associated with an increased contribution from highly toxic sources, such as diesel exhaust, gasoline exhaust and biomass burning. It is necessary to investigate the toxicity of various PM2.5 sources and PM2.5 risk based on the sources.

Differential toxicities of fine particulate matters from various sources.

Fine particulate matters less than 2.5 µm (PM2.5) in the ambient atmosphere are strongly associated with adverse health effects. However, it is unlikely that all fine particles are equally toxic in view of their different sizes and chemical components. Toxicity of fine particles produced from various combustion sources (diesel engine, gasoline engine, biomass burning (rice straw and pine stem burning), and coal combustion) and non-combustion sources (road dust including sea spray aerosols, ammonium sulfate, ammonium nitrate, and secondary organic aerosols (SOA)), which are known major sources of PM2.5, was determined. Multiple biological and chemical endpoints were integrated for various source-specific aerosols to derive toxicity scores for particles originating from different sources. The highest toxicity score was obtained for diesel engine exhaust particles, followed by gasoline engine exhaust particles, biomass burning particles, coal combustion particles, and road dust, suggesting that traffic plays the most critical role in enhancing the toxic effects of fine particles. The toxicity ranking of fine particles produced from various sources can be used to better understand the adverse health effects caused by different fine particle types in the ambient atmosphere, and to provide practical management of fine particles beyond what can be achieved only using PM mass which is the current regulation standard.

Oxidative potential of fine ambient particles in various environments.

The oxidative potential (OP) and chemical characteristics of fine particles collected from urban, roadside, rural, and industrial sites in Korea during spring, summer, fall, and winter seasons and an urban site in the Philippines during dry and wet seasons were examined. Significant differences in the OP of fine particles among sites and seasons were found. The industrial site yielded the highest OP activity (both mass and volume-normalized OP) among the sites, suggesting the strongest reactive oxygen species (ROS)-generating capability of industry source-dominant PM2.5. Seasonal data show that OP activities increased during the spring and summer possibly due to increased heavy metals caused by dust events and secondary organic aerosols formed by strong photochemical activity, respectively. The strength of the OP association with the chemical components highlights the influence of organic carbon and transition metals on the OP of ambient fine particles. The two OP assays (dithiothreitol (DTT) and electron spin resonance (ESR)) having different ROS-generating mechanisms were found to have different sensitivities to the chemical components facilitating a complementary analysis of the OP of ambient fine particles. Multiple linear regression model equations (OP as a function of chemical components) which were dependent on the sites were derived. A comparison of the daily OP and hazard index (HI) (the ratio of the measured mass concentration to the reference mass concentration of fine particles) suggests that the HI may not be sufficient to accurately estimate the health effects of fine particles, and a direct or indirect measurement of toxicity such as OP should be required in addition to the concentration level.