Irisin attenuates fine particulate matter induced acute lung injury by regulating Nod2/NF-κB signaling pathway.

Air pollution consisting of fine particulate matter (PM2.5) can induce or aggravate pulmonary inflammatory injury. Irisin has been shown to inhibit inflammation and help to protect against acute kidney, lung or brain injury. However, the role of irisin in lung inflammation after exposure to PM2.5 remains unclear. The aim of this study was to investigate the effect and molecular mechanism of irisin supplementation on in vitro and in vivo models of PM2.5-induced acute lung injury（ALI). C57BL/6 mice and alveolar macrophage cell line (MH-S) were treated with PM2.5. Histopathological examination and FNDC5/ irisin immunofluorescence staining was performed on lung tissue sections. MH-S cell viability was determined by CCK-8 assay. The levels of Nod2, NF-κB p65 and NLRP3 were detected by qRT-PCR and western blotting. The levels of cytokines (IL-1ß, IL-18 and TNF-α) were detected by ELISA. PM2.5 exposure induced increased secretion of pro-inflammatory factors and activation of Nod2, NF-κB p65 and NLRP3 as well as endogenous levels of irisin. In vivo and in vitro inflammation was alleviated by irisin supplementation. Irisin significantly decreased IL-1ß, IL-18, and TNF-α production at both mRNA and protein level. Expression levels of Nod2, NF-κB p65, and NLRP3 were all significantly affected by irisin. In vivo the degree of pulmonary injury and inflammatory infiltration was weakened after irisin administration. In vitro, irisin could inhibit the activation of the NLRP3 inflammasome for a sustained period of 24 h, and its inhibitory ability was gradually enhanced. In conclusion, our findings indicate that irisin can modulate the inflammatory injury of lung tissue caused by PM2.5 through the Nod2/NF-κB signaling pathway, suggesting that irisin can be a candidate for the therapeutic or preventive intervention in acute lung inflammation.

Irisin attenuates acute lung injury by suppressing the pyroptosis of alveolar macrophages.

Irisin is a hormone­like myokine that regulates cell signaling pathways and exerts anti­inflammatory effects. However, the specific molecular mechanisms involved in this process are currently unknown. The present study explored the role and mechanisms underlying the functions of irisin in alleviating acute lung injury (ALI). The present study used MH­S, an established murine alveolar macrophage­derived cell line, and a mouse model of lipopolysaccharide (LPS)­induced­ALI to examine the efficacy of irisin against ALI in vitro and in vivo, respectively. Fibronectin type III repeat­containing protein/irisin was expressed in the inflamed lung tissue, but not in normal lung tissue. Exogenous irisin reduced alveolar inflammatory cell infiltration and pro­inflammatory factor secretion in mice following LPS stimulation. It also inhibited the polarization of M1­type macrophages and promoted the repolarization of M2­type macrophages, thus reducing the LPS­induced production and secretion of interleukin (IL)­1ß, IL­18 and tumor necrosis factor­α. In addition, irisin reduced the release of the molecular chaperone heat shock protein 90 (HSP90), inhibited the formation of nucleotide­binding and oligomerization domain­like receptor protein 3 (NLRP3) inflammasome complexes, and decreased the expression of caspase­1 and the cleavage of gasdermin D (GSDMD), leading to reduced pyroptosis and the accompanying inflammation. On the whole, the findings of the present study demonstrate that irisin attenuates ALI by inhibiting the HSP90/NLRP3/caspase­1/GSDMD signaling pathway, reversing macrophage polarization and reducing the pyroptosis of macrophages. These findings provide a theoretical basis for understanding the role of irisin in the treatment of ALI and acute respiratory distress syndrome.

Irisin Ameliorates PM2.5-Induced Acute Lung Injury by Regulation of Autophagy Through AMPK/mTOR Pathway.

Background: PM2.5 exposure is one of the major inducements of various respiratory diseases and related mortality. Meanwhile, irisin, a metabolism and thermogenesis-related hormone, is found to be protective against acute lung injury induced by LPS, which indicates its therapeutic function in lung injury. However, the function and underlying mechanism of irisin in PM2.5-induced acute lung injury (ALI) are still unclear. This study is aimed to discover the potential mechanisms of irisin in PM2.5-induced acute lung injury. Methods: Atg5 deficient mice and cells were established to clarify the relationship between irisin and autophagy in PM2.5-induced ALI. We also used Ad-mCherry-GFP-LC3B as a monitor of autophagy flux to claim the effects of irisin on autophagy. Western blotting and qPCR were used to reveal the molecular mechanism. Results: As a result, PM2.5 exposure induced lung injury whereas mitigated by irisin. Moreover, PM2.5 hampered autophagy flux, characterized by accumulation of p62, and autophagosomes, as well as blocked autolysosomes. Irisin improved the disturbed autophagy flux, which was abrogated by deficiency of Atg5. Additionally, we demonstrated that irisin activated AMPK and inhibited mTOR, which indicated the enhanced autophagy. Moreover, blockage of AMPK by compound C terminated irisin's induction of autophagy in cultured MH-S cells. Conclusion: Our findings reveal that irisin performs protective effects against PM2.5-induced ALI by activating autophagy through AMPK/mTOR signaling pathway.

Activation of the Chemokine Receptor CCR1 and Preferential Recruitment of Gαi Suppress RSV Replication: Implications for Developing Novel Respiratory Syncytial Virus Treatment Strategies.

Respiratory syncytial virus (RSV) is a major pathogen that can cause acute respiratory infectious diseases of the upper and lower respiratory tract, especially in children, elderly individuals, and immunocompromised people. Generally, following viral infection, respiratory epithelial cells secrete cytokines and chemokines to recruit immune cells and initiate innate and/or adaptive immune responses. However, whether chemokines affect viral replication in nonimmune cells is rarely clear. In this study, we detected that chemokine CCL5 was highly expressed, while expression of its receptor, CCR1, was downregulated in respiratory epithelial cells after RSV infection. When we overexpressed CCR1 on respiratory epithelial cells in vivo or in vitro, viral load was significantly suppressed, which can be restored by the neutralizing antibody for CCR1. Interestingly, the antiviral effect of CCR1 was not related to type I interferon (IFN-I), apoptosis induction, or viral adhesion or entry inhibition. In contrast, it was related to the preferential recruitment and activation of the adaptor Gαi, which promoted inositol 1,4,5-triphosphate receptor type 3 (ITPR3) expression, leading to inhibited STAT3 phosphorylation; explicitly, phosphorylated STAT3 (p-STAT3) was verified to be among the important factors regulating the activity of HSP90, which has been previously reported to be a chaperone of RSV RNA polymerase. In summary, we are the first to reveal that CCR1 on the surface of nonimmune cells regulates RSV replication through a previously unknown mechanism that does not involve IFN-I induction. IMPORTANCE Our results revealed a novel mechanism by which RSV escapes innate immunity. That is, although it induces high CCL5 expression, RSV might attenuate the binding of CCL5 by downregulating the expression of CCR1 in respiratory epithelial cells to weaken the inhibitory effect of CCR1 on HSP90 activity and thereby facilitate RSV replication in nonimmune cells. This study provides a new target for the development of co-antiviral inhibitors against other components of the host and co-molecular chaperone/HSP90 and provides a scientific basis for the search for effective broad-spectrum antiviral drugs.

PM2.5 activated NLRP3 inflammasome and IL-1ß release in MH-S cells by facilitating autophagy via activating Wnt5a.

Particulate matter 2.5 (PM2.5)-induced pulmonary inflammation is an important issue worldwide. NLRP3 inflammasome activation has been found to be involved in pulmonary inflammation development. However, whether PM2.5 induces pulmonary inflammation by activating the NLRP3 inflammasome has not yet been fully elucidated. This study researched whether PM2.5 induces the NLRP3 inflammasomes activation to trigger pulmonary inflammation.Mice and MH-S cells were exposed to PM2.5, BOX5, and Rapamycin. Hematoxylin and eosin staining was performed on the lung tissues of mice. M1 macrophage marker CD80 expression in the lung tissues of mice and LC3B expression in MH-S cells was detected by immunofluorescence. IL-1ß level in the lavage fluid and MH-S cells were detected by enzyme-linked immunosorbent assay. Protein expression was detected by Western blot. Autophagy assay in MH-S cells was performed by LC3B-GFP punctae experiment.PM2.5 exposure induced the lung injury of mice and increased NLRP3, P62, Wnt5a, LC3BII/I, and CD80 expression and IL-1ß release in the lung tissues. PM2.5 treatment increased NLRP3, pro-caspase-1, cleaved caspase-1, Pro-IL-1ß, Pro-IL-18, P62, LC3BII/I, and Wnt5a expression, IL-1ß release, and LC3B-GFP punctae in MH-S cells. However, BOX5 treatment counteracted this effect of PM2.5 on lung tissues of mice and MH-S cells. Rapamycin reversed the effect of BOX5 on PM2.5-induced lung tissues of mice and MH-S cells.PM2.5 activated the NLRP3 inflammasome and IL-1ß release in MH-S cells by facilitating the autophagy via activating Wnt5a. The findings of this study provided a new clue for the treatment of pulmonary inflammation caused by PM2.5.

Idiopathic mesenteric phlebosclerosis associated with long-term oral intake of geniposide.

BACKGROUND: Idiopathic mesenteric phlebosclerosis (IMP) is a rare disease, and its etiology and risk factors remain uncertain. AIM: To investigate the possible influence of Chinese herbal liquid containing geniposide on IMP. METHODS: The detailed formula of herbal liquid prescriptions of all patients was studied, and the herbal ingredients were compared to identify the toxic agent as a possible etiological factor. Abdominal computed tomography (CT) and colonoscopy images were reviewed to determine the extent and severity of mesenteric phlebosclerosis and the presence of findings regarding colitis. The disease CT score was determined by the distribution of mesenteric vein calcification and colon wall thickening on CT images. The drinking index of medicinal liquor was calculated from the daily quantity and drinking years of Chinese medicinal liquor. Subsequently, Spearman's correlation analysis was conducted to evaluate the correlation between the drinking index and the CT disease score. RESULTS: The mean age of the 8 enrolled patients was 75.7 years and male predominance was found (all 8 patients were men). The patients had histories of 5-40 years of oral Chinese herbal liquids containing geniposide and exhibited typical imaging characteristics (e.g., threadlike calcifications along the colonic and mesenteric vessels or associated with a thickened colonic wall in CT images). Calcifications were confined to the right-side mesenteric vein in 6 of the 8 patients (75%) and involved the left-side mesenteric vein of 2 cases (25%) and the calcifications extended to the mesorectum in 1 of them. The thickening of colon wall mainly occurred in the right colon and the transverse colon. The median disease CT score was 4.88 (n = 7) and the median drinking index was 5680 (n = 7). After Spearman's correlation analysis, the median CT score of the disease showed a significant positive correlation with the median drinking index (r = 0.842, P < 0.05). CONCLUSION: Long-term oral intake of Chinese herbal liquid containing geniposide may play a role in the pathogenesis of IMP.

Thermolysis of scrap tire and rubber in sub/super-critical water.

The rapid growth of waste tires has become a serious environmental issue. Energy and material recovery is regarded as a promising use for waste tires. Thermolysis of scrap tire (ST), natural rubber (NR), and styrene-butadiene rubber (SBR) was carried out in subcritical and supercritical water using a temperature-pressure independent adjustable batch tubular reactor. As a result, oil yields increased as temperature and pressure increased, and they reached maximum values as the state of water was near the critical point. However, further increases in water temperature and pressure reduced the oil yields. The maximum oil yield of 21.21% was obtained at 420 °C and 18 MPa with a reaction time of 40 min. The relative molecular weights of the chemicals in the oil products were in the range of 70-140 g/mole. The oil produced from ST, NR, and SBR contained similar chemical compounds, but the oil yield of SR was between those of NR and SBR. The oil yield from thermolysis of subcritical or supercritical water should be further improved. The main gaseous products, including CH4, C2H2, C2H4, C2H6, and C3H8, increased with reaction time, temperature, and pressure, whereas the solid residues, including carbon black and impurities, decreased. These results provide useful information to develop a sub/super-critical water thermolysis process for energy and material regeneration from waste tires.

Role of CCL20/CCR6 and the ERK signaling pathway in lung adenocarcinoma.

Previous studies have revealed that carcinoma-associated fibroblasts communicate microenvironment-derived signals through chemokine/chemokine receptor interaction, resulting in carcinogenesis. C-C motif chemokine ligand 20 (CCL20)/C-C motif chemokine receptor 6 (CCR6) interactions are involved in the pathogenesis of colonic malignancies. The present study aimed to characterize the roles of CCL20/CCR6 and the extracellular signal-regulated kinase (ERK) signaling pathway in lung adenocarcinoma growth. Lung adenocarcinoma samples obtained at surgery were assessed for the expression, tissue localization and production of CCL20/CCR6. In addition, colony formation, ERK signaling and chemokine production were measured to assess the responsiveness of the A549 cell line to CCL20 stimulation. CCL20 and CCR6 were found to be highly expressed in the majority of samples in the recurrence group (76 and 66%, respectively). The staining indexes of CCL20 and CCR6 in the recurrence group were 149.3 and 134.4, respectively, which were significantly higher than those in the non-recurrence group (57.2 and 58.0, respectively); the protein and mRNA expression levels determined by western blot and reverse transcription-quantitative polymerase chain reaction were also found to be high in the recurrence group For A549 cells, the colony-forming capacity was increased by CCL20 stimulation, and this effect was dependent in part on ERK phosphorylation. Collectively, the findings suggest that CCR6 and CCL20 may serve a role in lung adenocarcinoma, leading to proliferation and migration via autocrine or paracrine mechanisms. The disruption of CCL20/CCR6 interactions may be a promising strategy for the treatment of cancer.

In vitro modeling of COPD inflammation and limitation of p38 inhibitor - SB203580.

BACKGROUND: Systemic inflammation and steroid resistance are the hallmarks of COPD. We examined the impact of p38 inhibitor (SB203580) in in vitro assays of systemic inflammation using pulmonary cells and patients' sera. OBJECTIVE AND METHODS: Data from 66 COPD patients and 15 age-/sex-matched healthy controls were compared. Interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), and CCL5 were measured in serum samples and culture media from peripheral blood mononuclear cells. The impact of sera on IL-10 and CCL5 expression in alveolar macrophage cell line (MH-S) was examined. The in vitro effects of SB203580 on lipopolysaccharide-induced inflammation were investigated. RESULTS: Peripheral blood mononuclear cells from Global initiative for chronic Obstructive Lung Disease (GOLD) D patients produced more CCL5 and TNF-α, and less IL-10 compared to GOLD A-C patients. SB203580 treatment suppressed CCL5 and TNF-α and stimulated IL-10 production; however, the effect of SB203580 on IL-10 was lower in the COPD group. Culture of MH-S cells with COPD serum showed a significant increase in CCL5 and a significant decrease in IL-10 compared to healthy serum. This effect was not suppressed with SB203580 treatment. CONCLUSION: COPD serum has a potent proinflammatory effect on pulmonary cells. Inhibition of p38 phoshorylation had a limited effect in restoring impaired lymphocyte function and suppressing inflammation induced by COPD serum, implying important p38-independent inflammatory mechanisms in COPD.

Pyrolysis and gasification of typical components in wastes with macro-TGA.

The pyrolysis and gasification of typical components of solid waste, cellulose, hemicellulose, lignin, pectin, starch, polyethylene (PE), polystyrene (PS), polyvinyl chloride (PVC) and poly(ethylene terephthalate) (PET) were performed and compared in a macro thermogravimetric analyzer (macro-TGA). Three model biomasses, poplar stem, orange peel and Chinese cabbage, were applied to pyrolysis and gasification simulation by their components based on TG curves. Compared to those from TGA, peaks temperature of the differential thermogravimetric (DTG) curves of each samples pyrolysis on macro-TGA delayed 30-55°C due to heat transferring effect. CO2 promoted the thermal decomposition of hemicellulose, lignin, starch, pectin and model biomasses significantly by Boudouard reaction, and enhanced slightly the decomposition of PET. The activation energy (AE) of biomass components pyrolysis on macro-TGA was 167-197 kJ/mol, while that of plastic samples was 185-235 kJ/mol. The activation energy of 351-377 kJ/mol was corresponding to the Boudouard reaction in CO2 gasification. All overlap ratios in pseudo-components simulation were higher than 0.98 to indicate that pseudo-components model could be applied to both pyrolysis and CO2 gasification, and the mass fractions of components derived from pyrolysis and gasification were slightly different but not brought in obvious difference in simulating curves when they were applied across.

Thermogravimetric characteristics of typical municipal solid waste fractions during co-pyrolysis.

The interactions of nine typical municipal solid waste (MSW) fractions during pyrolysis were investigated using the thermogravimetric analyzer (TGA). To compare the mixture results with the calculation results of superposition of single fractions quantitatively, TG overlap ratio was introduced. There were strong interactions between orange peel and rice (overlap ratio 0.9736), and rice and poplar wood (overlap ratio 0.9774). The interactions of mixture experiments postponed the peak and lowered the peak value. Intense interactions between PVC and rice, poplar wood, tissue paper, wool, terylene, and rubber powder during co-pyrolysis were observed, and the pyrolysis at low temperature was usually promoted. The residue yield was increased when PVC was blended with rice, poplar wood, tissue paper, or rubber powder; while the residue yield was decreased when PVC was blended with wool.

Additive Suppression of LPS-Induced IL-10 and TNF-α by Pre-treatment of Dexamethasone and SB203580 in a Murine Alveolar Macrophage Cell Line (MH-S).

P38 inhibitors are potent anti-inflammatory agents with distinctive mechanism of action from corticosteroid; the potential combined use of both anti-inflammatory agents could be an effective treatment for inflammatory lung disease; however, the impact of such combination on the homeostasis of immune response was poorly understood. To investigate the combined effect of dexamethasone (DEX) and/or SB203580 on tumor necrosis factor (TNF)-α (pro-inflammatory) and interleukin (IL)-10 (anti-inflammatory) secretion in mouse alveolar macrophage cell line. Secreted TNF-α and IL-10 were measured by ELISA. Phosphorylated STAT3 were investigated using Western blotting and immunocytochemistry. Pre-treatment of DEX or SB203580 inhibited lipopolysaccharide (LPS)-stimulated IL-10, TNF-α secretion, and STAT3 phosphorylation. Combined use of both agents showed stronger inhibitory effect. Combining DEX and SB203580 showed strong inhibition on the LPS-induced IL-10 secretion and STAT3 phosphorylation, which might reflect a very important drawback from the combined use of both anti-inflammatory agents.

Polycyclic aromatic hydrocarbons (PAH) formation from the pyrolysis of different municipal solid waste fractions.

The formation of 2-4 ring polycyclic aromatic hydrocarbons (PAH) from the pyrolysis of nine different municipal solid waste fractions (xylan, cellulose, lignin, pectin, starch, polyethylene (PE), polystyrene (PS), polyvinyl chloride (PVC), and polyethylene terephthalate (PET)) were investigated in a fixed bed furnace at 800 °C. The mass distribution of pyrolysis was also reported. The results showed that PS generated the most total PAH, followed by PVC, PET, and lignin. More PAH were detected from the pyrolysis of plastics than the pyrolysis of biomass. In the biomass group, lignin generated more PAH than others. Naphthalene was the most abundant PAH, and the amount of 1-methynaphthalene and 2-methynaphthalene was also notable. Phenanthrene and fluorene were the most abundant 3-ring PAH, while benzo[a]anthracene and chrysene were notable in the tar of PS, PVC, and PET. 2-ring PAH dominated all tar samples, and varied from 40 wt.% to 70 wt.%. For PS, PET and lignin, PAH may be generated directly from the aromatic structure of the feedstock.

A review of dioxin-related substances during municipal solid waste incineration.

Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs) are among the most toxic chemicals and the main restriction on municipal solid waste incineration. To exert more effective control over the formation of dioxin homologues during municipal solid waste incineration, it is significant to investigate dioxin-related compounds. Despite the numerous studies about PCDD/Fs, a unified understanding regarding many problems has yet to be reached because the homologues of PCDD/Fs are excessive, the measurement of PCDD/Fs is difficult, and the formation mechanisms of PCDD/Fs are complicated. Firstly, this paper briefly introduces the different formation mechanisms of PCDD/Fs, including high temperature homogeneous reaction PCDD/Fs formation and low temperature heterogeneous reaction PCDD/Fs formation. Then the sources of PCDD/Fs including precursors (chlorophenols and polycyclic aromatic hydrocarbons) and residual carbon are summarized. In particular, this paper analyzes the substances that influence PCDD/Fs formation and their impact mechanisms, including different categories of chlorine (Cl2, HCl and chloride in fly ash), O2, copper, sulfur, water, and nitrogen compounds (ammonia and urea). Due to the high cost and complexity of PCDD/Fs measurement, PCDD/Fs indicators, especially chlorobenzenes and polycyclic aromatic hydrocarbons, are summarized, to find an effective surrogate for quick, convenient and real-time monitoring of PCDD/Fs. Finally, according to the results of the current study, recommendations for further research and industrial applications prospects are proposed.

Role of p38 MAPK and STAT3 in lipopolysaccharide-stimulated mouse alveolar macrophages.

Excessive production of inflammatory mediators is an important feature of inflammatory lung disease. In macrophages, mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription-3 (STAT3) are crucial mediators for the production of proinflammatory cytokines. In the present study, the role of MAPK and STAT3 on tumor necrosis factor (TNF)-α and interleukin (IL)-10 production was investigated in mouse alveolar macrophages. The levels of TNF-α and IL-10 in lipopolysaccharide (LPS; 100 ng/ml)-stimulated MH-S cell lines were measured by an enzyme-linked immunosorbent assay, with or without p38 inhibitor (SB203580; 5, 10 or 15 µM) intervention. Phosphorylated STAT3 (p-STAT3) expression was examined by western blot analysis and immunocytochemistry following LPS stimulation for 15 or 30 min. Antibodies against STAT3 were used to verify comparable sample loading. Cells stimulated with LPS showed significantly increased levels of p-STAT3 protein (P<0.05) when compared with the baseline levels. TNF-α and IL-10 protein levels also increased following LPS stimulation (P<0.05). By contrast, treatment with the p38 inhibitor, SB203580, decreased the levels of p-STAT3, TNF-α and IL-10 (P<0.05) following LPS stimulation. SB203580 was shown to inhibit LPS-stimulated TNF-α expression (P<0.05) in a concentration-dependent manner, reaching significance at a concentration of 10 µM. However, the inhibition of IL-10 expression was not concentration-dependent. Therefore, LPS-stimulated overproduction of TNF-α and IL-10 is mediated at least partially by the MAPK pathway. Inhibition of p38 prevented LPS-induced STAT3 phosphorylation, indicating an interaction between the STAT3 and MAPK signaling pathways.

High serum macrophage inflammatory protein-3α is associated with the early recurrence or metastasis of non-small cell lung cancer following primary pulmonary resection.

The present study sought to characterize the role of macrophage inflammatory protein-3α (MIP-3α) in non-small cell lung cancer (NSCLC) patients with early recurrence or metastasis after primary pulmonary resection. Follow-up examinations were conducted for 203 NSCLC patients with primary pulmonary resection for two years post-operatively, and data was also collected for 20 healthy subjects. Serum MIP-3α levels were determined prior to surgery and at post-operative days (PODs) 30, 90 and 180, and the relevant clinical and operative variables were collected. Serum MIP-3α was measured using a commercially available enzyme-linked immunosorbent assay. There were no significant differences in age, gender and histological type among all groups (P>0.05). Serum MIP-3α levels on POD 180 were significantly higher in the recurrence group than in the non-recurrence group and healthy subjects (P=0.001). There was no significant difference in the serum MIP-3α level at PODs 90 and 180 in the patients with or without adjuvant chemotherapy (P>0.05). The recurrence rate in the high serum MIP-3α level group was 41.67%, much higher than the 23.53% observed in the low level group (P=0.006). The patients with high serum levels of MIP-3α had a significantly shorter overall recurrence-free time compared with those with low levels (P=0.004). Multivariate Cox's regression analyses showed that only serum MIP-3α level was significant, with a hazard ratio of 1.061, a 95% confidence interval of 1.044-1.078 and a P-value of 0.001. The serum MIP-3α level in the patients with liver and bone metastases were remarkably higher than those with recurrence at other sites. The high post-operative serum MIP-3α levels were associated with an increased risk of post-operative early recurrence or metastasis in the lung cancer patients, specifically in those with bone or liver metastases.

Classification and comparison of municipal solid waste based on thermochemical characteristics.

UNLABELLED: Municipal solid waste (MSW) has been normally sorted into six categories, namely, food residue, wood waste, paper textiles, plastics, and rubber In each category, materials could be classified further into subgroups. Based on proximate and ultimate analysis and heating value, statistical methods such as analysis of variance (ANOVA) and cluster analysis were applied to analyze the characteristics of MSW in every subgroup and to try to distinguish their relative properties. The chemical characteristics analysis of MSW showed that polyethylene (PE), polypropylene (PP), and polystyrene (PS) had the highest volatile matter content, with almost no ash and fixed carbon, while polyethylene terephthalate (PET) had high carbon content but low hydrogen content. Bones and vegetables had the highest ash content, while nutshells and rubber had the highest fixed carbon content. Paper and starch food had the highest oxygen content, and wool and bones had the highest nitrogen and sulfur content. Polyvinyl chloride (PVC) had the highest chlorine content at about 55%. PE, PP and PS had the highest heating value, followed by chemical products such as rubber and chemical fiber. Conversely, paper, vegetables and bones had the lowest heating value. The results of cluster analysis of MSW components showed that fruit peel, weeds, wood, bamboo, leaves and nutshells could be classified as the lignocellulose category; starch food, cotton, toilet paper, printing paper and cardboard could be classified as the glucose monomer category; wood and chemical fiber could be classified as the high nitrogen and sulfur category; and PE, PP, and PS could be cluster as the polyolefin category. IMPLICATIONS: The yield of municipal solid waste (MSW) is constantly increasing and waste to energy (WTE) has been used extensively all over the world. During the processes of incineration, pyrolysis, or gasification, the impact of physical and chemical properties of MSW is of great significance. However, the traditional classification of MSW is too general to provide more detailed information in many investigations. It is necessary to perform the investigation of characteristics of combustible MSW to distinguish different categories of MSW and find out their subclassification.

Thermodynamic analysis on heavy metals partitioning impacted by moisture during the MSW incineration.

A thermodynamic calculation was carried out to predict the behavior and speciation of heavy metals (HMs), Pb, Zn, Cu, and Cd, during municipal solid waste (MSW) incineration with the different moisture levels. The calculation was based on the minimization of the total Gibbs free energy of the multi-components and multi-phases closed system reaching chemical equilibrium. The calculation also indicated the reaction directions and tendencies of HMs components. The impacts of chlorine additives (No PVC, 1%PVC, and 5%PVC) and moisture on the behavior of HMs were investigated at different temperature levels in the system (750 °C, 950 °C, and 1150 °C). Furthermore, because the incineration temperature falls down with the increase in moisture in waste, the co-influence of moisture and temperature in combusting MSW on the HMs was also studied with the given chlorine (as 1%PVC+0.5%NaCl). The results showed that in the non-chlorine system, the impact of the moisture on Pb, Zn, and Cu was not significant, and the ratio of compound transformation was less than 10%, except the Cd compounds at 950 °C and 1150 °C. In the system with low chlorine (as 1%PVC) at constant temperature, the chlorides of HMs (Cd, Pb, Zn, and Cu) transferred to oxides, and when the content of chlorine rose up (as 5%PVC), the ratio of the chlorides of HMs (Cd, Pb, Zn, and Cu) transferring to oxides fell down noticeably. When the moisture varied together with the temperature, the Zn and Cu compounds transferred from chlorides to oxides with increase in moisture as well as decrease in temperature. At the temperature of 700-1000 °C, the impact of temperature on Pb and Cd was little and the moisture was the main factor; while at the temperature of 1000-1200 °C, the impact of increase in moisture and decrease in temperature on Pb and Cd was almost equal and reversed.

Investigation of heavy metal partitioning influenced by flue gas moisture and chlorine content during waste incineration.

The impact of moisture on the partitioning of the heavy metals including Pb, Zn, Cu and Cd in municipal solid waste (MSW) was studied in a laboratory tubular furnace. A thermodynamic investigation using CHEMKIN software was performed to compare the experimental results. Simulated waste, representative of typical MSW with and without chlorine compounds, was burned at the background temperature of 700 and 950 degrees C, respectively. In the absence of chlorine, the moisture content has no evident effect on the volatility of Pb, Zn and Cu at either 700 or 950 degrees C, however, as flue gas moisture increasing the Cd distribution in the bottom ash increased at 700 degrees C and reduced at 950 degrees C, respectively. In the presence of chlorine, the flue gas moisture reduced the volatility of Pb, Zn and Cu due to the transformation of the more volatile metal chlorides into less volatile metal oxides, and the reduction became significant as chlorine content increase. For Cd, the chlorine promotes its volatility through the formation of more volatile CdCl2. As a result, the increased moisture content increases the Pb, Zn, Cu and Cd concentrations in the bottom ash, which limits the utilization of the bottom ash as a construction material. Therefore, in order to accumulate heavy metals into the fly ash, MSW should be dried before incineration.

[Effects of adsorbents on partitioning of Cd and Pb in MSW incineration].

An incineration experiment using simulated municipal solid waste (MSW) in the tubular furnace was performed to study the effects of SiO2, Al2o3 and CaO on the partitioning of Cd and Pb under different operating conditions which included adsorbents percentage, furnace temperature and residence time. The results indicated that the increasing of SiO2, AL2O3, CaO concentration were favorable for Cd to partition in the bottom ash. And for Pb, SiO2 and Al2O3 had the same effects. However, the condition with CaO showed an opposite tendency of increasing Pb distribution in fly ash. While all of these adsorbents increasing, the effects were also enhanced. When the temperature of the tubular furnace was 850 degrees C, the adsorption efficiencies of these adsorbents for Cd were in the sequence of CaO > Al, O3 > SiO2, and for Pb, Al2O3 > SiO2 > CaO. In addition,with increasing of tubular furnace temperature and residence time, there would be more Cd and Pb compounds moving to the fly ash.