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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., 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 © 2023. Published by Elsevier Ltd.)

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.)

Air pollution is a serious environmental issue. As a key aerosol component, PM 2.5 associated toxic trace metals pose significant health risks by inhalation and ingestion, but the evidences and mechanisms were insufficient and not well understood just by their total environmental concentrations. To accurately assess the potential risks of airborne metals, a series of in vitro physiologically based tests with synthetic human lung and gastrointestinal fluids were conducted to assess both the bioaccessibility and bioavailability of various PM 2.5 bound metals in the respiratory and digestive systems from both urban and industrial areas of Nanjing city. Moreover, the chemical acellular toxicity test [dithiothreitol (DTT) assay] and source analysis were performed. Generally, the bioaccessibility and bioavailability of investigated metals were element and body fluid dependent. Source oriented metals in PM 2.5 showed diverse bioaccessibility in different human organs. The PM 2.5 induced oxidative potential was mainly contributed by the bioaccessible/bioavailable transition metals such as Fe, Ni and Co from metallurgic dust and traffic emission. Future researches on the toxicological mechanisms of airborne metals incorporating the bioaccessibility, bioavailability and toxicity tests are directions., (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., (Copyright © 2020 Elsevier Inc. All rights reserved.)

The atmospheric fine particulate matters (PM 2.5 ) induce significant negative effects on human health, such as in the form of oxidative stress and pro-inflammatory response. Organic pollutants are important harmful and toxic compositions in PM 2.5 , risks of which usually show temporal and spatial variations. To investigate the toxic effects of airborne organic pollutants on human lung epithelial cells A549, the PM 2.5 samples were collected monthly from both urban and industrial areas during a whole year in Nanjing, eastern China. After exposure to organic components extracted from these PM 2.5 , the cell viability, lactate dehydrogenase content, oxidative stress index level and inflammatory factor expression level were measured. Supported by the concentrations of polycyclic aromatic hydrocarbons (PAHs) and n-alkanes, results showed that, organic components of PM 2.5 from cold season (winter and spring) typically influenced cell membrane, cell oxidation and inflammatory damage, while the urban samples of warm season (summer and autumn) impacted cell viability more prominently. Spatially, the toxicity of samples from industrial sources was generally stronger than that from urban source, but urban samples induced much stronger damage to cell membranes than industrial one. The correlations between the PAHs, n-alkanes contents and toxicity parameters indicated that, the airborne organic components derived from motor vehicle exhaust and coal combustion were possibly the key toxic sources., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

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., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The concentration and loading distribution of trace metals (Cu, Zn, Pb, Co, Ni, Cr, and Mn) and major elements (Al, Ca, Fe, and Mg) in different particle size fractions (2000-280, 280-100, 100-50, 50-10, 10-2, and <2 μm) of surface soils from highly urbanized areas in Hong Kong were studied. The enrichment of Pb, Cu, and Zn in the urban soils was strongly influenced by anthropogenic activities, and Pb accumulated in fine particles was mainly derived from past vehicular emissions as shown by Pb isotopic signatures. Trace metals primarily accumulated in clay, fine silt, and very fine sand fractions, and might pose potential health risks via the inhalation of resuspended soil particles in the air (PM10 or PM2.5), and ingestion of adhered soils through the hand-to-mouth pathway. The mobility, bioavailability, and human bioaccessibility of Pb and Zn in bulk soils correlated significantly with metal concentrations in fine silt and/or very fine sand fractions., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Although air quality guidelines generally use the atmospheric concentration of fine particulate matter (PM 2.5) as a metric for air pollution evaluation and management, the fact cannot be ignored that different particle toxicities are unequal and significantly related to their sources and chemical compositions. Therefore, judging the most harmful source and identifying the toxic component would be helpful for optimizing air quality standards and prioritizing targeted PM 2.5 control strategies to protect public health more effectively. Since the combustions of fuels, including oil, coal, and biomass, are the main anthropogenic sources of environmental PM 2.5 , their discrepant contributions to health risks of mixed ambient aerosol pollution dominated by the respective emission intensity and unequal toxicity of chemical components need to be identified. In order to quantify the differences between these combustion primary emissions, 10 types of PM 2.5 from each typical source group, i.e., vehicle exhaust, coal combustion, and plant biomass (domestic biofuel) burning, were collected for comparative study with toxicological mechanisms. In total, 30 types of individual combustion samples were intercompared with representative urban ambient air PM 2.5 samples, whose chemical characteristics and biological effects were investigated by component analysis (carbon, metals, soluble ions) and in vitro toxicity assays (cell viability, oxidative stress, inflammatory response) of human lung adenocarcinoma epithelial cells (A549). Carbonaceous fractions were plenteous in automobile exhaust and biomass burning, while heavy metals were more plentiful in PM 2.5 from coal combustion and automobile exhaust. The overall ranking of mass-normalized cytotoxicity for source-specific PM 2.5 was automobile exhaust > coal combustion > domestic plant biomass burning > ambient urban air, possibly with differential toxicity triggers, and showed that the carbonaceous fractions (organic carbon, OC; elemental carbon, EC) and redox-active transition metals (V, Ni, Cr) assisted by water-soluble ions (Ca 2+ , Mg 2+ , F - , Cl -) might play important roles in inducing cellular reactive organic species (ROS) production, causing oxidative stress and inflammation, resulting in cell injury and apoptosis, and thus damaging human health. Coupled with the source apportionment results of typical urban ambient air PM 2.5 in eastern China, reducing toxic PM 2.5 from these anthropogenic combustions will be greatly beneficial to public health. In addition to the air pollution control measures that have been implemented, like strengthening the vehicle emission standards, switching energy from coal to gas and electricity, and controlling the open incineration of agricultural straws, further methods could be considered, especially by preferentially reducing the diesel exhaust, lessening the coal combustion by replacement with low-ash clean coals, and depressing the rural crop straw biomass burning emissions. [ABSTRACT FROM AUTHOR]

Fine particulate matter (PM 2.5) is detrimental to the human respiratory system. However, the toxicity of PM 2.5 and its associated potentially harmful species, notably novel pollutants like environmentally persistent free radicals (EPFRs), remains unclear. Therefore, one-year site monitoring and ambient air PM 2.5 sampling in the Nanjing urban area was designed to investigate the relationships between chemical compositions (carbon fractions, metallic elements, and water-soluble ions) and EPFRs, and change in cytotoxicity with varying PM 2.5 components. Oxidative stress (reactive oxygen species, ROS), inflammatory injury (IL-6 and TNF-α), and membrane injury (LDH) of human lung epithelial cells (A549) induced by PM 2.5 were analyzed using in vitro cytotoxicity test. Both the composition and toxicity of PM 2.5 from different seasons were compared. The average daily exposure of urban PM 2.5 associated EPFRs load in Nanjing were 2.29 × 1011 spin m−3. Their exposure concentration and cytotoxic damage ability were stronger in the cold season than warm. The particle compositions of metals and carbon fractions were significantly positively correlated with EPFRs. The airborne EPFRs, organic carbon (OC), and heavy metal Cu, As, and Pb may pose principal cell damage ability, which is worthy of further study interlinking aerosol pollution and health risks. [Display omitted] • PM 2.5 pollution in typical urban area is accompanied by the associated EPFRs exposure. • The overall exposure risk of bulk PM 2.5 is related to both aerosol level and compositions. • PM 2.5 loaded EPFRs were significantly positively correlated with metallic elements and carbon fractions. • Airborne EPFRs, organic carbon, and heavy metals may be pivotal cytotoxic components. • Cytotoxicity and pollution of PM 2.5 and EPFRs are higher in cold than warm season. [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]