Evidence links air pollution to dementia, yet its role in Lewy body dementia (LBD) remains unclear. In this work, we showed in a cohort of 56.5 million individuals across the United States that fine particulate matter (PM _2.5 ) exposure raises LBD risk. Mechanistically, we found that PM _2.5 exposure led to brain atrophy in wild-type mice, an effect not seen in α-synuclein (αSyn)–deficient mice. PM _2.5 exposure generated a highly pathogenic αSyn strain, PM _2.5 –induced preformed fibril (PM-PFF), with enhanced proteinase K resistance and neurotoxicity, resembling αSyn LBD strains. PM _2.5 samples from China, the United States, and Europe consistently induced proteinase-resistant αSyn strains and in vivo pathology. Transcriptomic analyses revealed shared responses between PM _2.5 -exposed mice and LBD patients, underscoring PM _2.5 ’s role in LBD and stressing the need for interventions to reduce air pollution and its associated neurological disease burden.

The physical and chemical properties as well as the oxidative potential (OP) of water soluble components of coal combustion fine particles were examined. A laboratory-scale pulverized-coal burning system was used to produce coal combustion particles at different burning temperatures of 550 °C, 700 °C, 900 °C, and 1,100 °C. Few studies have reported the effects of burning temperature on both the chemistry and toxicity of coal combustion particles. The highest mass emission factor of particulate matter less than 2.5 µm (PM_2.5) was found to be produced at 700 °C (3.51 g/kg), owing to strong elemental carbon (EC) emission and ash formation (ions and elements) resulting from the incomplete combustion of tar and char, and mineral fragmentation. The highest organic carbon in PM_2.5 was found at 550 °C. At a temperature higher than 700 °C, the fraction of carbonaceous species decreased while the fractions of ions and elements increased owing to ash formation. Sulfate was found to be the dominant ionic species, followed by sodium, calcium, and magnesium. The highest emission of elements (Al, As, Ba, Cd, Co, Cu, Fe, Mn, Ni, Pb, Sr, Ti, V, and Zn) and the highest fractions of Fe and Al were observed at 700 °C. Intrinsic OP activities obtained from dithiothreitol (DTT) and electron spin resonance (ESR) assays showed the highest values at 550 °C, suggesting that fine particles from low-temperature coal combustion had the highest reactive oxygen species generation capability (potentially toxic) among various tested burning temperatures. The results of principal component analysis suggested a correlation between OP-DTT activity and OC, EC, Cd, Co, V, and Zn, while OP-ESR activity was associated with chloride, nitrate, Ba, Pb, Sr, and Ti. © 2018 American Association for Aerosol Research

We performed simultaneous measurements of chemical compositions of fine particles in Beijing, China and Gwangju, Korea to better understand their sources during winter haze period. We identified PM_2.5 events in Beijing, possibly caused by a combination of multiple primary combustion sources (biomass burning, coal burning, and vehicle emissions) and secondary aerosol formation under stagnant conditions and/or dust sources under high wind speeds. During the PM_2.5 events in Gwangju, the contribution of biomass burning and secondary formation of nitrate and organics to the fine particles content significantly increased under stagnant conditions. We commonly observed the increases of nitrogen-containing organic compounds and biomass burning inorganic (K⁺) and organic (levoglucosan) markers, suggesting the importance of biomass burning sources during the winter haze events (except dust event cases) at both sites. Pb isotope ratios indicated that the fraction of Pb originated from possibly industry and coal combustion sources increased during the PM_2.5 events in Gwangju, relative to nonevent days.

To reduce fine particulate matter (PM_2.5) level, the sources of PM_2.5 in terms of the composition thereof needs to be identified. In this study, the experimental burning of ten types of biomass that are typically used in Republic of Korea, collected at the regional area were to investigate the indicated organic speciation and the results obtained therefrom were applied to the chemical mass balance (CMB) model for the study area. As a result, the organic molecular markers for the biomass burning were identified as they were varying according to chemical speciation of woods and herbaceous plants and depending upon the hard- and soft characteristics of specimens. Based on the source profile from biomass burning, major sources of PM_2.5 in the study area of the present study appeared as sources of biomass burning, the secondary ions, secondary particulate matters, which is including long-distance transport, wherein the three sources occupied most over 84% of entire PM_2.5. In regard to the subject area distinguished into residential area and on roads, the portion of the biomass burning appeared higher in residential area than on roads, whereas the generation from vehicles of gasoline engine and burning of meats in restaurants, etc. appeared higher on roads comparing to the residential area.

Toxicological data and exposure levels of fine particulate matters (PM_2.5) are necessary to better understand their health effects. Simultaneous measurements of PM_2.5 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 PM_2.5 concentration, a health index was developed to better assess the potential health effects of PM_2.5. The health index was related to the sources of PM_2.5 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 PM_2.5 mass. The developed regression equation was used to predict the health effect of PM_2.5 without further toxicity measurements. This new index could be a valuable health metric that provides information beyond just the PM_2.5 concentration level.

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.