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Environmental air pollutants pose significant threats to public health, especially the toxicity and diseases caused by the atmospheric fine particulate matters (PM 2.5 ). Since the health risks vary with both the concentrations and compositions of PM 2.5 which are determined by aerosol sources, how are their toxic effects relevant to the pollution level becomes an important issue, such as the haze episodes covering clean and polluted days. With the transition from non-pollution to pollution stage, daily PM 2.5 samples were collected from both the urban and industrial areas of Nanjing city, eastern China, covering a typical haze event in autumn-winter. Their unpropitious effects on human lung epithelial cells (A549) were compared by in vitro toxicity assays and chemical component analysis. Both air levels and cytotoxic effects of PM 2.5 varied with the transition of haze event. Although the concentration of PM 2.5 in air is of course the highest in pollution stage driven by local stable meteorological condition, unit mass of them posed higher toxicity (lower cell viability and higher IL-6) but induced lower cell oxidative (evidences of ROS and NQO1 mRNA expression) and inflammatory cytokine TNF-α responses than those particles during non-pollution stage. These patterns were explained by the metals and water-soluble components decreased with the haze development. Non-soluble particulate carbonaceous aerosol compositions might play a significant role in inducing cytotoxicity. Moreover, the regional pattern of episode pollution weakened the spatial variation within a city scale. Since the haze development intensified both the quantity and toxicity of PM 2.5 in air, the health risks of overall aerosol exposure were synthetically amplified during haze weather, so the increased air particles with higher toxic components from fuel combustion sources should be key targets of pollution control., (Copyright © 2020 Elsevier Inc. All rights reserved.)

[Display omitted] • Coal type affects particulate emission composition and cytotoxicity. • Water-soluble ions dominate PM 10 from honeycomb, anthracite, and industrial coals. • PM 10 from bituminous coal is dominated by carbonaceous components. • Heavy metals and water-soluble ions in PM 10 strongly correlated with cytotoxicity. • Limiting anthracite coal combustion is crucial in air quality for public health. Inhalable particles (PM 10 , particulate matters with an aerodynamic diameter < 10 μm) emitted from coal combustions is one of the most significant contributors to air pollution, endangering human health. The compositions of emissions and corresponding health risks of different types of coal sources are currently unclear. To address this, ten distinct types of coal were burnt, and original PM 10 samples were collected using dilution channel samplers. Subsequently, we performed a componential analysis on the collected samples and conducted in vitro cytotoxicity tests. Results showed that PM 10 from honeycomb, anthracite and industrial coals were dominated by water-soluble ions, while bituminous coal was dominated by carbonaceous components. Although heavy metal contents were lower than other investigated components in these PM 10 , they were still enriched in Fe, Pb and Zn. The NH 4 +, Cl- and SO 4 2- account for a large proportion of water-soluble ions. PM 10 induced obvious cytotoxicity to human lung cell A549, and the ability of anthracite coal to induce cellular TNF-α production was greater than that of honeycomb and bituminous coal. For IL-6, industrial coal elicited a stronger response than bituminous coal, followed by honeycomb and anthracite coal. Correlation analysis revealed that although heavy metals (Fe, Mn, Co, Ni, Cu) and water-soluble ions (K+, Ca2+, F-) accounted for less particle mass, they were strongly and significantly correlated with oxidative stress and inflammatory damage (r > 0.6, p < 0.05). Considering the actual coal consumption amount, our study identified restricting anthracite coal combustion should be a crucial focus for aerosol pollution control and public health protection policies. The results of the study not only increase the understanding of the chemical composition and cytotoxicity of PM 10 from the perspective of source emissions, but also provide targeted advice on the control of coal combustion, which is of great significance in environmental research, public health policy and air pollution control efforts. [ABSTRACT FROM AUTHOR]

Abstract Atmospheric fine particulate matters (PM 2.5) induce adverse human health effects through inhalation, and the harmful effects of PM 2.5 are determined not only by its air concentrations, but also by the particle components varied temporally. To investigate seasonal differences of the aerosol toxicity effects including cell viability and membrane damage, cell oxidative stress and responses of inflammatory cytokines, the human lung epithelial cells (A549) were exposed to PM 2.5 samples collected in both summer and winter by the in vitro toxicity bioassays. Toxicological results showed that, the PM 2.5 led to the cell viability decrease, cell membrane injury, oxidative stress level increase and inflammatory responses in a dose-dependent manner. Temporally, the cytotoxicity of winter PM 2.5 was higher than summer of this studied industrial area of Nanjing, China. According to the different contents of heavy metals accumulated in PM 2.5 , the transition metals such as Cu might be an important contributor to the aerosol cell toxicity. Highlights • In vitro toxicity of PM 2.5 showed seasonal differences. • PM 2.5 from different seasons showed varied metal components. • Transition metals in PM 2.5 contribute to the particle cell toxicity. • Health risks of PM 2.5 should consider composition and source effects. • Toxicity of winter PM 2.5 from Nanjing was higher than summer. [ABSTRACT FROM AUTHOR]

Environmental air pollutants pose significant threats to public health, especially the toxicity and diseases caused by the atmospheric fine particulate matters (PM 2.5). Since the health risks vary with both the concentrations and compositions of PM 2.5 which are determined by aerosol sources, how are their toxic effects relevant to the pollution level becomes an important issue, such as the haze episodes covering clean and polluted days. With the transition from non-pollution to pollution stage, daily PM 2.5 samples were collected from both the urban and industrial areas of Nanjing city, eastern China, covering a typical haze event in autumn-winter. Their unpropitious effects on human lung epithelial cells (A549) were compared by in vitro toxicity assays and chemical component analysis. Both air levels and cytotoxic effects of PM 2.5 varied with the transition of haze event. Although the concentration of PM 2.5 in air is of course the highest in pollution stage driven by local stable meteorological condition, unit mass of them posed higher toxicity (lower cell viability and higher IL-6) but induced lower cell oxidative (evidences of ROS and NQO1 mRNA expression) and inflammatory cytokine TNF-α responses than those particles during non-pollution stage. These patterns were explained by the metals and water-soluble components decreased with the haze development. Non-soluble particulate carbonaceous aerosol compositions might play a significant role in inducing cytotoxicity. Moreover, the regional pattern of episode pollution weakened the spatial variation within a city scale. Since the haze development intensified both the quantity and toxicity of PM 2.5 in air, the health risks of overall aerosol exposure were synthetically amplified during haze weather, so the increased air particles with higher toxic components from fuel combustion sources should be key targets of pollution control. ga1 • Stable atmosphere enables the continuous accumulation of local PM 2.5. • Haze development intensified both quantity and toxicity of PM 2.5 in air. • Regional haze pollution episode weakened the spatial variation within a city. • Trace metals and water-soluble contents in PM 2.5 decreased with haze development. • Non-soluble carbonaceous aerosol compositions might control the haze cytotoxicity. [ABSTRACT FROM AUTHOR]

Dust storm (DS) represent global air pollution and health issues considering the high morbidity and premature death rate every year. This study explores the characteristics, composition, and variations in inhalable particulate matters (PMs) as well as their corresponding in vitro toxicity to human lung epithelial cells (A549) during DS and normal days (ND) in the downtown (DT) and the north suburban (NS) of Nanjing city, eastern China. Results showed that compared to ND, concentrations of heavy metals (i.e., Cr, Cu, Ni, and Pb) bound in PMs were lower during the DS. Furthermore, the relationship of cytotoxicity with Ni and Pb levels in PMs was significant. However, the cytotoxicity difference was insignificant between NS and DT. This may be due to the long-range transport of components from natural sources mixed with local pollutants emitted from anthropogenic sources, offsetting the pollution difference between urban and suburban areas. During both periods, PM 2.5 toxicity was greater than PM 10 , while the potential of PM 10 to induce proinflammatory cytokines was comparable to PM 2.5. Results suggested that inflammation risk will increase significantly during DS due to a substantial increase in ambient air PM 10 concentration. [Display omitted] [ABSTRACT FROM AUTHOR]

Bioaerosols are a crucial part of atmospheric particulate matter (aerosols), combining physical and chemical aerosol properties with biological characteristics. They play a vital role in global ecosystems, climate change, air quality, and public health, and serve as an important pathway for transmitting respiratory infectious diseases. Major pandemics like H1N1, SARS, MERS, and COVID-19 have had far-reaching impacts on both human life and the global economy. Understanding the nexus 'sources-spatial and temporal distributions-influencing factors-health risks' of bioaerosols is crucial for developing strategies to mitigate pollution and prevent the spread of related epidemics. This review provides an overview of the primary sources of bioaerosols and their analysis methods, detailing the spatial and temporal distribution characteristics of their community structure across daily, annual, latitudinal gradient, vertical gradient, and urbanized environmental gradient variations. The study also elucidates the impact of land use types, meteorological conditions, climate change, and air quality on bioaerosols. It emphasizes the main exposure pathways, evaluation models, and constraints of pathogenic bioaerosols. Finally, this overview offers an outlook on the future development of bioaerosols and presents corresponding recommendations. [Display omitted] • The main source of pathogenic bioaerosols is anthropogenic. • The microbial indicator better tracks the migration of bioaerosols. • Bioaerosol fingerprints can more clearly specify their spatio-temporal distribution. • Urbanization and global warming may reduce the diversity of microbes in air. • Airborne pathogens are related to air pollution, climate change, and human activity. [ABSTRACT FROM AUTHOR]

Fine particulates in city air significantly impact human health, but the hazardous compositional mechanisms are still unclear. Besides the toxicity of environmental PM 2.5 to in vitro human lung epithelial cells (A549), the independent cytotoxicity of PM 2.5 -bound water-soluble (WS-PM 2.5) and water-insoluble (WIS-PM 2.5) fractions were also compared by cell viability, oxidative stress (reactive oxygen species, ROS), and inflammatory injury (IL-6 and TNF-α). The cytotoxicity of PM 2.5 varied significantly by sampling season and place, with degrees greater in winter and spring than in summer and autumn, related to corresponding trend of air PM 2.5 level, and also higher in industrial than urban site, although their PM 2.5 pollution levels were comparable. The PM 2.5 bound metals (Ni, Cr, Fe, and Mn) may contribute to cellular injury. Both WS-PM 2.5 and WIS-PM 2.5 posed significant cytotoxicity, that WS-PM 2.5 was more harmful than WIS-PM 2.5 in terms of decreasing cell viability and increasing inflammatory cytokines production. In particular, industrial samples were usually more toxic than urban samples, and those from summer were generally less toxic than other seasons. Hence, in order to mitigate the health risks of PM 2.5 pollution, the crucial targets might be components of heavy metals and soluble fractions, and sources in industrial areas, especially during the cold seasons. [Display omitted] • Both soluble and insoluble-PM 2.5 induced cytotoxicity with source differences. • PM 2.5 toxicity was higher for industrial than urban area and cold than warm season. • Soluble than insoluble-PM 2.5 induced stronger cytotoxicity and inflammation. • Transition metals Ni, Cr, Fe, Mn might contribute to the different PM 2.5 toxicity. • Spatial-temporal sources and solubility are important for PM 2.5 health risk assessment. [ABSTRACT FROM AUTHOR]