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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]

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. [Display omitted] • PM 2.5 could directly enhance β-hexosaminidase release by basophilic cells. • Degranulation of basophil cells exposed to PM 2.5 show regional and seasonal variations. • PM 2.5 shows the strong pro-inflammation effect on basophilic cells. • Airborne heavy metals and water-soluble ions correlate positively with cell inflammatory response. • PM 2.5 -induced cellular inflammation was driven by anthropogenic sources. [ABSTRACT FROM AUTHOR]

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. ga1 • Bioaccessibility and bioavailability of airborne metals were compared sequentially. • Metals dissolved in respiratory–digestive systems were element and fluid dependent. • Source-dependent PM 2.5 metals pose varied bioaccessibility/bioavailability in organs. • Bioaccessible/bioavailable transition metals induce PM 2.5 oxidative potential. • Metal bioaccessibility/bioavailability explain aerosol toxicity and health risks. [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]

Organic pollutants are important harmful components in atmospheric fine particulate matters (PM 2.5), health risks of which varied with temporal and spatial distributions. To clarify the characteristics of atmospheric organic pollution, the concentrations, sources, and human health risks of typical organic compositions in PM 2.5 samples from both industrial and urban areas of Nanjing in eastern China were investigated monthly for a year. Results showed that, the concentrations of PM 2.5 -bound polycyclic aromatic hydrocarbons (PAHs) and n-alkanes were higher in winter and spring than those in summer and autumn. The organic pollution was slightly higher in industrial than urban area, though the PAHs in autumn and the n-alkanes in warm season (summer and autumn) were higher in urban area. With regards to the pollutant sources, the atmospheric PAHs were dominated by motor vehicle exhaust in the urban area, and combined with coal combustion emission in the industrial area. Airborne n-alkanes were mainly from biological source accompanied by fossil fuel combustion in industrial area. The PM 2.5 -bound PAHs indicated higher risks to adults in industrial area than in urban area with the seasonal patterns: winter > spring > autumn > summer. More attention should be paid to the health risks of exposure to organic pollutants accumulated in PM 2.5 during cold season. Controlling vehicle emissions might be the key measure for alleviating atmospheric PAHs and n-alkanes pollution in megacities, while coal purification can be an effective control method in industrial areas. • Organic pollutants are typical harmful components in PM 2.5 • Concentrations, sources, and health risks of PM 2.5 show spatio-temporal patterns. • PAHs and n-alkanes pollution were serious in cold season and industrial area. • Vehicle emission is a key target for alleviating particulate organic pollution. • Coal purification can be an effective pollution control method in industrial area. [ABSTRACT FROM AUTHOR]