Airborne environmentally persistent free radicals (EPFRs) in PM2.5 from combustion sources: Abundance, cytotoxicity and potential exposure risks.

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 (PM2.5) from different emission sources. In this study, various types of combustion-derived PM2.5 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 PM2.5 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 PM2.5 from anthropogenic combustion sources, especially from automobile exhaust. This study provides important evidence for the source- and concentration-dependent health effects of EPFRs in PM2.5 and motivates further assessments to advance public health-oriented PM2.5 emission control.

A novel g-C3N4-SH@konjac glucomannan composite aerogel for patulin removal from apple juice and its photocatalytic regeneration.

Patulin (PAT) is a hazardous mycotoxin frequently occurs in fruit industry. A reusable g-C3N4-SH@KG composite aerogel for PAT removal in a novel "dark adsorption-light regeneration" mode was prepared by thiol(-SH) functionalization and konjac glucomannan (KG) immobilization. The g-C3N4-SH@KG was characterized by SEM, FT-IR, XPS and UV-Vis DRS, and its PAT adsorption and photocatalytic regeneration behaviors and mechanisms were investigated. The g-C3N4-SH@KG exhibited good regeneration performance, maintaining 83% of PAT initial adsorption capacity (0.92 mg/g) after 5 "adsorption-regeneration" cycles. The adsorption process was endothermic and spontaneous. •OH and h+ generated by photocatalysis were the main substances that degraded PAT into two products and regenerated -SH. The g-C3N4-SH@KG could effectively remove PAT without negative impact on juice quality. The study provided a new strategy for the regeneration of thiol-functionalized PAT adsorbents, and a new idea for the application of non-selective photocatalysis in the control of food contaminations.

Nitrate and sodium nitroprusside alter the development of Asian black-spined toads' embryos by inducing nitric oxide production.

Nitrate is the most stable and abundant form of inorganic nitrogen in water. However, owing to human activities, the nitrate concentration in aquatic ecosystems has notably increased worldwide. One of the mechanisms underlying nitrate toxicity in vertebrates includes the functional inhibition of the sodium iodide symporter, resulting in thyroid dysfunction. In this study, we aimed to determine the alternative mechanisms underlying the toxicological effects of nitrates on the Asian black-spined toad (Duttaphrynus melanostictus). Embryos of D. melanostictus were exposed to sodium nitroprusside (SNP, positive control) or 100 mg/L nitrate-nitrogen (NO3-N) for 184 h. We observed that both SNP and NO3-N significantly decreased body mass and length and delayed developmental processes. Teratogenic symptoms, including tumors, hyperplasia, and abdominal edema, were also observed in embryos exposed to SNP and NO3-N. Furthermore, SNP and NO3-N significantly increased nitric oxide levels in the embryos, altering the thyroid hormone, nitrogen, cytochrome P450-mediated drug, and xenobiotic metabolism signaling pathways, as well as the pathway involved in chemical carcinogenesis. The similar toxicological effects of SNP and NO3-N suggested that nitrate toxicity resulted from the generation of nitric oxide. Therefore, the present study provides insights into an alternative mechanism underpinning nitrate toxicity, which is useful for the conservation of amphibians in nitrate-rich environments.

Insight into urban PM2.5 chemical composition and environmentally persistent free radicals attributed human lung epithelial cytotoxicity.

Fine particulate matter (PM2.5) is detrimental to the human respiratory system. However, the toxicity of PM2.5 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 PM2.5 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 PM2.5 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 PM2.5 were analyzed using in vitro cytotoxicity test. Both the composition and toxicity of PM2.5 from different seasons were compared. The average daily exposure of urban PM2.5 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.

Seasonal and areal variability in PM2.5 poses differential degranulation and pro-inflammatory effects on RBL-2H3 cells.

PM2.5 pollution is a widespread environmental and health problem, particularly in China. Besides leading to well-known diseases in the respiratory system, PM2.5 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 PM2.5, 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 PM2.5 were analyzed, and the rat basophil cells (RBL-2H3) exposed to PM2.5 were assessed through quantitative measures of degranulation (ß-hex and histamine) and pro-inflammation cytokine (IL-4 and TNF-α) expression. The highest levels of ß-hex were measured in winter and spring PM2.5 from urban and industrial areas, or autumn PM2.5 from suburban and rural areas. With respect to histamine, autumn PM2.5 samples were most potent irrespective of the location. Autumn and winter PM2.5 induced higher levels of IL-4 than spring and summer samples. However, spring and autumn PM2.5 caused higher levels of TNF-α. The concentrations of water-soluble ions (NH4+, 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 PM2.5 in stimulating cell degranulation may depend on endotoxin and airborne allergen content of PM2.5. The heavy metals and water-soluble ions in PM2.5 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.

In vitro assessments of bioaccessibility and bioavailability of PM2.5 trace metals in respiratory and digestive systems and their oxidative potential.

Air pollution is a serious environmental issue. As a key aerosol component, PM2.5 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 PM2.5 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 PM2.5 showed diverse bioaccessibility in different human organs. The PM2.5 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.

In-vitro human lung cell injuries induced by urban PM2.5 during a severe air pollution episode: Variations associated with particle components.

Environmental air pollutants pose significant threats to public health, especially the toxicity and diseases caused by the atmospheric fine particulate matters (PM2.5). Since the health risks vary with both the concentrations and compositions of PM2.5 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 PM2.5 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 PM2.5 varied with the transition of haze event. Although the concentration of PM2.5 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 PM2.5 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.

The cytotoxicity and genotoxicity of PM2.5 during a snowfall event in different functional areas of a megacity.

Atmospheric fine particulate matter (PM2.5) can harm human health, but the chemical composition and toxicity of PM2.5 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 PM2.5 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 PM2.5, 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 PM2.5 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 PM2.5 during snowfall, As, Co, Cr, Sr, V, water-soluble Na+ and Ca2+ showed positive correlations with toxicity indicators. Therefore, snowfall will clean air by deposition, but also make the PM2.5 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.

Seasonally varied cytotoxicity of organic components in PM2.5 from urban and industrial areas of a Chinese megacity.

The atmospheric fine particulate matters (PM2.5) 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 PM2.5, 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 PM2.5 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 PM2.5, 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 PM2.5 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.