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As an emerging atmospheric pollutant, airborne environmentally persistent free radicals (EPFRs) are formed during many combustion processes and pose various adverse health effects. In health-oriented air pollution control, it is vital to evaluate the health effects of atmospheric fine particulate matter (PM 2.5 ) from different emission sources. In this study, various types of combustion-derived PM 2.5 were collected on filters in a partial-flow dilution tunnel sampling system from three typical emission sources: coal combustion, biomass burning, and automobile exhaust. Substantial concentrations of EPFRs were determined in PM 2.5 samples and associated with significant potential exposure risks. Results from in vitro cytotoxicity and oxidative potential assays suggest that EPFRs may cause substantial generation of reactive oxygen species (ROS) upon inhalation exposure to PM 2.5 from anthropogenic combustion sources, especially from automobile exhaust. This study provides important evidence for the source- and concentration-dependent health effects of EPFRs in PM 2.5 and motivates further assessments to advance public health-oriented PM 2.5 emission control., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

PM 2.5 pollution is a widespread environmental and health problem, particularly in China. Besides leading to well-known diseases in the respiratory system, PM 2.5 can also alter immune function to induce or aggravate allergic diseases. To determine whether there are temporal and spatial differences in the allergic responses to PM 2.5 , monthly samples were collected from four regions (urban, industrial, suburban, and rural areas) through a whole year in Nanjing city, China. Inorganic chemical components (metals and water-soluble ions) of PM 2.5 were analyzed, and the rat basophil cells (RBL-2H3) exposed to PM 2.5 were assessed through quantitative measures of degranulation (β-hex and histamine) and pro-inflammation cytokine (IL-4 and TNF-α) expression. The highest levels of β-hex were measured in winter and spring PM 2.5 from urban and industrial areas, or autumn PM 2.5 from suburban and rural areas. With respect to histamine, autumn PM 2.5 samples were most potent irrespective of the location. Autumn and winter PM 2.5 induced higher levels of IL-4 than spring and summer samples. However, spring and autumn PM 2.5 caused higher levels of TNF-α. The concentrations of water-soluble ions (NH 4 + , K + and Cl - ), as well as heavy metals (Pb and Cr), were directly and statistically correlated to the inflammation observed in vitro. In general, the differences between regional and seasonal PM 2.5 in stimulating cell degranulation may depend on endotoxin and airborne allergen content of PM 2.5 . The heavy metals and water-soluble ions in PM 2.5 were mostly anthropogenic, which increased the particles' mass-based cellular inflammatory potential, therefore, their health risks, e.g. from vehicular exhaust, coal, and biomass combustion, cannot be ignored., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

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.)

Atmospheric fine particulate matter (PM 2.5 ) can harm human health, but the chemical composition and toxicity of PM 2.5 pollution might vary with weather conditions. In order to investigate the impacts of snowfall weather on aerosol characteristics and toxicity by changing particle sources and components, the daily PM 2.5 samples were collected before, during, and after a snowfall event in urban, industrial, suburban, and rural areas of Nanjing city in eastern China, for both chemical composition analysis and cytotoxicity tests. After 24 h exposure to these PM 2.5 , the cell activity, oxidative stress indicators and inflammatory factor expression levels of human lung epithelial cells A549 were measured by ELISA, and DNA damage was determined by comet assay. Although the concentrations of PM 2.5 in the air were reduced during snowfall, they posed stronger cytotoxicity, genetic toxicity and inflammatory responses to A549 cells. Related to the elevated mass concentrations of some components accumulated in PM 2.5 during snowfall, As, Co, Cr, Sr, V, water-soluble Na + and Ca 2+ showed positive correlations with toxicity indicators. Therefore, snowfall will clean air by deposition, but also make the PM 2.5 components remaining in air mostly anthropogenic by covering ground soil/dust, thus increase the particle's mass-based cytotoxicity and their health risks still cannot be ignored, such as the heavy metals and water-soluble ions from automobile exhaust and coal combustion., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

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]