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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]

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]

Abstract: A semi-static solution culture method was used to study the effects of Ca2+ supply and interaction of Cd–Pb on the subcellular distribution of Cd and Pb in earthworm Eisenia fetida. The subcellular distribution of Cd and Pb was shown to be metal specific. About 80% of the Cd was distributed in the cytosol (fraction G), and only about 20% of total Cd was found in the tissue and cell membrane (fraction E) and the microsomes (fraction F). Nearly 50% of the Pb was rich in the tissue and cell membrane (fraction E). The supply of Ca2+ ions significantly decreased Cd concentration in the cytosol (fraction G) and the whole tissue of the E. fetida. At the subcellular level, the addition of Pb2+ ions significantly decreased the Cd percentage associated with fraction G from 83.7% to 58.4% and increased fraction E from 10.7% to 34.0%, respectively. [Copyright &y& Elsevier]

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]