Identification and contribution of potential sources to atmospheric lead pollution in a typical megacity: Insights from isotope analysis and the Bayesian mixing model.

Atmospheric particulate matter (PM) enriched with lead (Pb) has severe irreversible effects on human health. Therefore, identifying the contribution of Pb emission sources is essential for protecting the health of residents. Using the Pb isotopic tracer method, this study explored the seasonal characteristics and primary anthropogenic Pb sources for atmospheric PM in Tianjin in 2019. We calculated the contribution of Pb sources using the end-member and MixSIAR models. The results showed that Pb loaded in PM10 was more abundant in January than in July, and was strongly influenced by meteorological conditions and anthropogenic emissions. The primary Pb sources of the aerosol samples originated from coal combustion and vehicle and steel plant emissions, mainly originating from local Pb emission sources in Tianjin. The PM10-bond Pb in January was influenced by regional transportation and local sources. The MixSIAS model calculated the contribution of coal combustion as approximately 50 %. Compared with that in January, the contribution of coal combustion decreased by 9.6 % in July. Our results indicate that some of the benefits of phased-out leaded gasoline have been short-lived, whereas other industrial activities releasing Pb have increased. Furthermore, the results emphasise the practicability of the Pb isotope tracer source approach for identifying and distinguishing between different anthropogenic Pb inputs. Based on this study, scientific and effective air pollution prevention and control programs can be formulated to provide decision support for the guidance and control of air pollutant emissions.

Interleukin-17 is involved in neuropathic pain and spinal synapse plasticity on mice.

Neuropathic pain seriously affects people's life, but its mechanism is not clear. Interleukin-17 (IL-17) is a proinflammation cytokine and involved in pain regulation. Our previous study found that IL-17 markedly enhanced the excitatory activity of spinal dorsal neurons in mice spinal slices. The present study attempts to explore if IL-17 contributes to neuropathic pain and spinal synapse plasticity. A model of spared nerve injury (SNI) was established in C57BL/6 J mice and IL-17a mutant mice. The pain-like behaviors was tested by von Frey test and dynamic mechanical stimuli, and the expression of IL-17 and its receptor, IL-17RA, was detected by immunohistochemical staining. C-fiber evoked field potentials were recorded in vivo. In the spinal dorsal horn, IL-17 predominantly expressed in the superficial spinal astrocytes and IL-17RA expressed mostly in neurons and slightly in astrocytes. The SNI-induced static and dynamic allodynia was significantly prevented by pretreatment of neutralizing IL-17 antibody (intrathecal injection, 2 µg/10 µL) and attenuated in IL-17a mutant mice. Post-treatment of IL-17 neutralizing antibody also partially relieved the established mechanical allodynia. Moreover, spinal long-term potentiation (LTP) of C-fiber evoked field potentials, a substrate for central sensitization, was suppressed by IL-17 neutralizing antibody. Intrathecal injection of IL-17 recombinant protein (0.2 µg/10 µL) mimicked the mechanical allodynia and facilitated the spinal LTP. These data implied that IL-17 in the spinal cord played a crucial role in neuropathic pain and central sensitization.

Source tracing of potentially toxic elements in soils around a typical coking plant in an industrial area in northern China.

Coking plants are a substantial source of potentially toxic elements (PTEs) in soil. In this study, we examined the concentration of PTEs, the soil physicochemical properties, and the Pb isotopes in the soil inside and around a coking plant in an industrial city in northern China. We analyzed the spatial distribution of PTEs and the pollution risk areas by Igeo index, the enrichment factor (EF), and the Nemerow index, and we quantitatively identified the contribution of PTE pollution sources in the soil on a small- and medium-scale (plant and work section). Our results indicated that the Hg concentration inside the plant and the Cd concentration in the agricultural land around the plant were both relatively high. A comprehensive analysis of the soil in the study area was performed using the positive matrix factorization model and Pb isotope (206/207Pb, 208/206Pb) tracing method, based on the MixSIAR model, this analysis indicated that burning coal was the main source of Pb both inside (46.8%) and outside (26.3%) the coking plant. The pollution emission sources with significant influence on the soil outside the coking plant were diesel vehicles (12.5%), gas tanks (12.4%), and coke ovens (11.5%), while the sources inside the plant were quenching sections (11.1%), atmospheric deposition (11.0%), coke oven sections (9.6%), and diesel vehicles (6.1%). The results of PTE pollution risk zoning and Pb isotope tracing indicated that pollution is more serious in the western part of the plant, which is the area where coking and gas production takes place, and the most serious pollution outside the plant is mainly distributed to the southeast. This study provides theoretical and practical data indicating the contribution of industrial enterprises to soil pollution, and will help identify pollution responsibility and the management of pollution sources.

Adsorption of Polycyclic Aromatic Hydrocarbons from aqueous solution by Organic Montmorillonite Sodium Alginate Nanocomposites.

The adsorption method is generally considered a promising technique to remove inorganic and organic contaminants in an economically and environmentally friendly superior manner. In this study, organic montmorillonite sodium alginate composites were prepared, in which, montmorillonite and cationic surfactant (cetyltrimethylammonium bromide, CTAB) in different added amounts were coagulated with sodium alginate using CaCl2 as the crosslinking agent. The morphological properties of the composites were characterized thoroughly and employed in three typical target pollutants of polycyclic aromatic hydrocarbons (PAHs) (acenaphthene, fluorene, and phenanthrene) by batch adsorption experiments from aqueous solution. The composites provide an efficient alternative for PAHs removals. The composites could be stably separated and regenerated with methyl alcohol. Furthermore, the adsorption kinetic and isotherm data were well described by the Elovich kinetic and the Freundlich isotherm model, respectively. According to these, the adsorption process occurred via multilayer adsorption on the composite's energetically heterogeneous surface. Moreover, pore diffusion and hydrophobicity played a dominant role in the adsorption mechanism. Overall, our study offers a developed adsorbent that has the advantage of being recyclable, low cost, biodegradable and biocompatible for effectively removing PAHs from aqueous solution.

Involvement of Interleukin-10 in Analgesia of Electroacupuncture on Incision Pain.

OBJECTIVE: Postincision pain often occurs after surgery and is an emergency to be treated in clinic. Electroacupuncture (EA) is a Chinese traditional treatment widely used to cure acute or chronic pain, but its mechanism is not clear. Interleukin-10 (IL-10) is a powerful anti-inflammatory cytokine that shows neuroprotective effects in inflammation and injury in the CNS. The present study attempts to reveal that IL-10 is crucial for EA analgesia on postincision pain. METHODS: A model of incision pain was established in C57BL/6J mice. The pain threshold was detected by behavioral test, and the expression of IL-10 and its receptor was detected by an immunohistochemical method. C-fiber-evoked field potentials were recorded by in vivo analysis. RESULTS: The mechanical allodynia induced by paw incision was significantly inhibited by pretreatment of EA in mice. Intrathecal injection of IL-10 neutralizing antibody (2 µg/10 µL) but not intraplantar injection (10 µg/10 µL) reversed the analgesia of EA. The upregulations of IL-10 mRNA and protein were induced by EA at 6 h and 1 d after incision, respectively. Spinal long-term potentiation (LTP), a substrate for central sensitization, was also suppressed by EA with IL-10. IL-10 recombinant protein (1 µg/10 µL, i.t.) mimicked the analgesia of EA on mechanical allodynia and inhibition on the spinal LTP. Posttreatment of EA after incision also transitorily relieved the mechanical allodynia, which can be blocked by spinal IL-10 antibody. IL-10 and its receptor, IL-10RA, are predominantly expressed in the superficial spinal astrocytes. CONCLUSIONS: These results suggested that pretreatment of EA effectively prevented postincision pain and IL-10 in spinal astrocytes was critical for the analgesia of EA and central sensitization.

Downregulation of microRNA-9 reduces inflammatory response and fibroblast proliferation in mice with idiopathic pulmonary fibrosis through the ANO1-mediated TGF-ß-Smad3 pathway.

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with increasing occurrence, high death rates and unfavorable treatment regimens. In the current study, we identified the expression of microRNA-9 (miR-9) and anoctamin-1 (ANO1) in IPF mouse models induced by bleomycin, and their effects on inflammation and fibroblast proliferation through the transforming growth factor-ß (TGF-ß)-Smad3 pathway. To verify the targeting relationship between miR-9 and ANO1, we used bioinformatics prediction and conducted a dual-luciferase reporter gene assay. The underlying regulatory mechanisms of miR-9 and the target gene ANO1 were investigated mainly with the treatment of miR-9 mimic, miR-9 inhibitor, or siRNA against ANO1 in fibroblasts isolated from IPF mice. Enzyme-linked immunosorbent assay was performed to investigate the effect of miR-9 or ANO1 on inflammatory factors. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry were used to detect fibroblast proliferation and apoptosis. Reverse transcription quantitative polymerase chain reaction and western blot analysis were applied to measure the expression of the TGF-ß-Smad3 pathway-related genes. The determination of luciferase activity suggested that miR-9 targets ANO1. Upregulation of miR-9 or silencing of ANO1 intensified inflammation in IPF, promoted proliferation and inhibited apoptotic ability of lung fibroblasts. MiR-9 negatively modulated ANO1, and thus activated the TGF-ß-Smad3 pathway. These findings suggest that miR-9 can indirectly activate the TGF-ß-Smad3 pathway by inhibiting the expression of ANO1, thereby aggravating inflammation, promotes proliferation and suppressing apoptosis of lung fibroblasts in mice models of IPF.

Apigenin inhibits allergen-induced airway inflammation and switches immune response in a murine model of asthma.

Many flavonoids were demonstrated to possess the antiallergic effect. Here we detected whether apigenin, a flavonoid, can attenuate allergen-induced airway inflammation and what is the possible mechanism in a murine model of asthma. Apigenin decreased the degree of the inflammatory cell infiltration, airway hyperresponsiveness, and total immunoglobulin E levels compared with the ovalbumin group. In addition, apigenin triggered the switching of the immune response to allergens toward a T-helper type 1 (Th1) profile. Our data clearly demonstrated that apigenin exhibits an anti-inflammatory activity in a murine asthma model, and can switch the immune response to allergens toward the Th1 profile.

Targeted NF-kappaB inhibition of asthmatic serum-mediated human monocyte-derived dendritic cell differentiation in a transendothelial trafficking model.

Transendothelial trafficking model mimics in vivo differentiation of monocytes into dendritic cells (DC). The serum from patients with systemic lupus erythematosus promotes the differentiation of monocytes into mature DC. We have shown that selective inhibition of NF-kappaB by adenoviral gene transfer of a novel mutated IkappaBalpha (AdIkappaBalphaM) in DC contributes to T cell tolerance. Here we demonstrated for the first time that asthmatic serum facilitated human monocyte-derived DC (MDDC) maturation associated with increased NF-kappaB activation in this model. Furthermore, selective blockade of NF-kappaB by AdIkappaBalphaM in MDDC led to increased apoptosis, and decreased levels of CD80, CD83, CD86, and IL-12 p70 but not IL-10 in asthmatic serum-stimulated MDDC, accompanied by reduced proliferation of T cells. These results suggest that AdIkappaBalphaM-transferred MDDC are at a more immature stage which is beneficial to augment the immune tolerance in asthma.