[Effects of ursolic acid on oxidative stress and inflammatory factors in a rat model of AR after PM2.5 exposure].

Objective: To investigate the effects of ursolic acid (UA) on oxidative stress and inflammatory factors in a rat model of AR after PM2.5 exposure. Methods: Sixty healthy female SD rats were randomly divided into five groups: normal control group (NC group), PM2.5 unexposed AR group (AR group), PM2.5 exposed AR group (ARE group), UA intervention AR group (AR+UA group), and UA intervention PM2.5 exposed AR group (ARE+UA group), with 12 rats in each group. AR model was performed by a basal sensitization with intraperitoneal injection of ovalbumin (OVA) and followed by nasal instillation. PM2.5 exposure was carried out by inhalation exposure system at a concentration of 200 µg/m3 for 3 h/d for 30 days. UA intervention group was given UA intragastric administration at 20 mg/(kg·d). AR symptoms including sneezing, nasal scratching and nasal secretion of rats in each group were observed. The activities of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in nasal mucosa were tested. The pathological changes of nasal mucosa were observed by HE staining. The levels of OVA-sIgE, IL-6 and IL-17 in serum were measured by enzyme-linked immunosorbent assay (ELISA). Protein microarray was used to measure the expression of multiple inflammation cell factors in nasal mucosa. Statistical analysis was performed with SPSS 20.0. Results: After UA intervention, the frequency of nasal sneezing, scratching and nasal secretion in ARE+UA group were lower than those of ARE group (P<0.05). Pathological examination of nasal mucosa showed that ARE+UA group had less inflammatory granulocyte infiltration and less pathological damage to the epithelial layer than ARE group. The activities of SOD in nasal mucosa of ARE+UA group were higher than those of ARE group ((50.10±3.09) U/mg vs (20.13±1.30) U/mg, F value was 597.54, P<0.01). The contents of MDA in nasal mucosa of ARE+UA group were lower than those of ARE group ((57.78±12.36) nmol/g vs (124.12±9.40) nmol/g, F value was 115.51, P<0.01). The expression levels of OVA-sIgE, IL-6 and IL-17 proteins were lower in the ARE+UA group than those in ARE group ((11.61±0.27) ng/ml vs (20.30±0.67) ng/ml, (47.59±15.49) pg/ml vs (98.83±10.98) pg/ml, (623.30±8.75) pg/ml vs (913.32±9.06) pg/ml, F value was 283.42, 80.45, 683.73, respectively, all P<0.01). After UA intervention, protein microarray analysis showed that the expression of IL-4, IL-6, IL-13, chemokine CXCL7, IL-1α, IL-1ß, MMP-8 and MCP-1 in ARE+UA group was decreased compared with ARE group while IFN-γ and IL-10 increased (all P<0.01). Conclusion: UA can reduce the aggravated AR symptoms and pathological damage of nasal mucosa, inhibit oxidative stress and release of inflammatory factors after PM2.5 exposure, and thus plays a protective role in the pathological damage of AR induced by PM2.5 exposure.

Effects of rosmarinic acid on the inflammatory response in allergic rhinitis rat models after PM2.5 exposure.

BACKGROUND: Studies have shown the promising prospects of rosmarinic acid (RosA) for the prevention and treatment of allergic diseases. OBJECTIVE: The aim of this study was to investigate the effects of RosA on inflammatory reaction in rat models of allergic rhinitis (AR) after PM2.5 exposure. METHODS: Allergic rhinitis rat models were established by ovalbumin sensitization, and PM2.5 was applied at a concentration of 1000 µg/m3 , 3 h a day for 30 consecutive days. RosA was administered via intraperitoneal injection (20 mg/kg/d) for seven consecutive days. Allergic nasal symptoms were recorded. The expressions of interleukin (IL)-4, IL-13, interferon (INF)-γ, and OVA-sIgE were determined by ELISA. Histopathological changes in nasal mucosa were observed by HE staining. mRNA expressions of T-bet and GATA-3 in nasal mucosa were detected by RT-PCR. NF-κBp65 in cell nuclei and IκBα in cytoplasm were analyzed by Western blot. RESULTS: PM2.5 exposure worsened allergic nasal symptoms in AR rats, while RosA ameliorated these symptoms. Histopathologically, AR rats exhibited disorganized nasal mucosal epithelium, cell exfoliation, eosinophilic infiltration of lamina propria, gland swelling, and submucosal vascular congestion, which were aggravated by PM2.5 exposure and alleviated by RosA. RosA decreased the expressions of IL-4, IL-13, and increased the level of IFN-γ in PM2.5-exposed AR rats. After RosA intervention, the expressions of GATA-3 mRNA and NF-κBp65 in PM2.5-exposed AR rats were significantly reduced, while those of T-bet mRNA and IκBα were markedly increased. CONCLUSION: Rosmarinic acid may alleviate symptoms of AR rat models exposed to PM2.5 through the modulation of the NF-κB pathway and Th1/Th2 balance.

Toxicological Effects of Artificial Fine Particulate Matter in Rats through Induction of Oxidative Stress and Inflammation.

Airborne fine particulate matter with an aerodynamic diameter equal to or smaller than 2.5 µm (abbreviated as PM2.5) increases the risk of nasal lesions, but the underlying molecular mechanism has not been fully elucidated. In the atmosphere, the composition of PM2.5 collected varies in physical and chemical properties, which affects its damage to human health. Thus, we constructed artificial PM2.5 particles based on actual PM2.5 and investigated the in vivo effects of artificial PM2.5 exposure on the oxidative stress, inflammatory response, and nasal mucosa morphology of rats. The results showed that artificial PM2.5 is comparable in composition ratio, size, and morphology to actual PM2.5. This in vivo study indicated that artificial PM2.5 exposure reduces total superoxide dismutase and glutathione peroxidase activities, elevates malondialdehyde content in the nasal mucosa, and induces increased levels of pro-inflammatory mediators, including interleukin-1, interleukin-6 and tumor necrosis factor-α. Our data shows that artificial PM2.5 particles could be used for experimental study of PM2.5 toxicology, ensuring that the physical and chemical properties of experimental PM2.5 are relatively constant and allowing for repeatability of this research. Oxidative damage and inflammatory response may be the toxic mechanisms that cause nasal lesions after exposure to artificial PM2.5.

miR-338-3p inhibits autophagy in a rat model of allergic rhinitis after PM2.5 exposure through AKT/mTOR signaling by targeting UBE2Q1.

Exposure to fine particulate matter (PM2.5) increases the incidence of allergic rhinitis (AR). microRNA (miRNA) can regulate cell proliferation, invasion and apoptosis. However, the mechanism of miR-338-3p in mediating PM2.5-induced autophagy in AR animal models remains unknown. To explore the mechanism of miR-338-3p in PM2.5-induced autophagy in AR, the human nasal epithelium cells and AR model exposed to PM2.5 were deployed. The results showed that miR-338-3p was down-regulated in both nasal mucosa of PM2.5-exacerbated AR rat models and PM2.5-treated RPMI-2650 cells. Forced expression of miR-338-3p could inhibit autophagy in vitro. miR-338-3p specifically bound to UBE2Q1 3'-untranslated region (3' UTR) and negatively regulated its expression. Overexpression of UBE2Q1 attenuated the inhibitory effects of miR-338-3p on PM2.5-induced autophagy of RPMI-2650 cells through AKT/mTOR pathway. Moreover, our in vivo study found that after administration of agomiR-338-3p in AR rats model, the expression of autophagy-related proteins decreased and nasal symptoms alleviated. In conclusion, this study revealed that miR-338-3p acts as an autophagy suppressor in PM2.5-exacerbated AR by directly targeting UBE2Q1 and affecting AKT/mTOR pathway.

Ursolic Acid Alleviates Mucus Secretion and Tissue Remodeling in Rat Model of Allergic Rhinitis After PM2.5 Exposure.

BACKGROUND: According to recent epidemiologic studies, exposure to fine particulate matter (particulate matter 2.5 ≤ µm [PM2.5]) in the air increases the incidence and severity of allergic rhinitis (AR). Ursolic acid (UA) has activities in immune regulation and anti-inflammatory. However, the role of UA intervention on PM2.5-exposed AR remains unknown. In this study, we investigated the effects of UA on tissue remodeling and mucus hypersecretion in a rat model of AR after PM2.5 exposure. METHODS: AR was induced in rats with ovalbumin (OVA) and they were exposed to ambient PM2.5(200 µg/m3) via a PM2.5 inhalation exposure system for 30 days(ARE group). Ursolic acid intervention was administrated in the AR model after PM2.5 exposure (UA group). Hyperplasia of goblet cells was detected by periodic acid-Schiff (PAS) staining and collagen deposition in the nasal mucosa was detected by Masson trichrome (MT) staining.MUC5AC expression was measured by immunohistochemistry. RESULTS: UA group showed reduced goblet cell hyperplasia and collagen deposition in the nasal mucosa which exacerbated after PM2.5 exposure, as reflected by PAS and MT staining when compared with the ARE group. Immunohistochemical results showed that the expression of MUC5AC in the UA group was lower than that in the ARE group. CONCLUSION: Analysis of our data indicated that UA could attenuate nasal remodeling and mucus hypersecretion in aggravation of AR after PM2.5 exposure, which may be the pathophysiologic mechanisms for the prevention of AR exacerbated by exposure to PM2.5.

Effects of N-acetylcysteine on oxidative stress and inflammation reactions in a rat model of allergic rhinitis after PM2.5 exposure.

Particulate matter 2.5 (PM2.5) exposure can increase the prevalence of allergic rhinitis (AR), the mechanism underlying which may include oxidative stress and inflammatory response. As a ROS quenching agent, N-acetylcysteine (NAC) can attenuate the accumulation of inflammatory cells and hyper-responsiveness in animal asthma models. To explore the effect of NAC on the oxidative stress and inflammatory reactions in AR rats exposed to PM2.5, we analyzed the components of PM2.5 and examined the nasal symptoms, redox level in nasal mucosa, Th1/Th2-related serum cytokines, nasal mucosal histopathology and ultrastructure in AR rat models with NAC intervention after PM2.5 exposure. The results showed that the high concentrations of metal cations and PAHs in PM2.5 could aggravate Th2-dominant allergic inflammation in AR model and cause redox imbalance, accompanied by nasal epithelial cell stripping and eosinophil infiltration, while NAC intervention could alleviate the clinical symptoms of AR model after PM2.5 exposure, correct the redox imbalance, reduce the Th2 cytokines, reduce eosinophil infiltration, and promote the moderate regeneration of epithelial cells. The mechanism of NAC reversing PM2.5-mediated action may be related to its anti-oxidant and anti-inflammatory effects, which may provide some new insights for the prevention of AR exacerbated by exposure to PM2.5.

Effects of Ursolic Acid on the Expression of Th1-Th2-related Cytokines in a Rat Model of Allergic Rhinitis After PM2.5 Exposure.

BACKGROUND: Allergic rhinitis (AR) is a global health problem and closely related to environmental factors. Ursolic acid (UA) has potential in the treatment of allergic inflammation. The effects of UA intervention on PM2.5-induced AR remain uncertain. OBJECTIVE: To assess the effects of UA on nasal symptoms and the expression of T-helper (Th)1-Th2-related cytokines in a rat model of AR after fine particulate matter (particulate matter ≤ 2.5 µm [PM2.5]) exposure. METHODS: A total of 40 healthy female Sprague-Dawley rats were randomly divided into 4 groups: normal control group (NC group), ovalbumin (OVA)- induced AR model (AR group), PM2.5-exposed AR group exposed to 200 g/m3 PM2.5 for 30 days via inhalation (ARE group), and a group with UA intervention to the AR model after PM2.5 exposure (UA group). UA intervention was adopted after PM2.5 exposure in the UA group. Nasal symptoms and levels of Th1-Th2 cytokines in the serum were detected in each individual rat. The pathological changes and expression of Eotaxin in the nasal mucosa of each individual rat were examined by histology. RESULTS: PM2.5 significantly increased the number of sneezes and nasal rubs in the rats with AR, and UA alleviated these symptoms. UA decreased interleukin (IL)-4, IL-5, IL-13, Eotaxin-1, and OVA Immunoglobulin E (IgE) protein levels. In the AR group, hematoxylin and eosin staining showed disordered arrangement of the nasal mucosa epithelium, cell shedding, eosinophilic infiltration, swelling of the glands, and submucosal vascular congestion. UA group showed reduced eosinophilic infiltration and orderly arrangement of the mucosal epithelium when compared with the ARE group. Immunohistochemical results showed that the expression of Eotaxin in the UA group was lower than that in the ARE group. CONCLUSION: UA could relieve nasal symptoms caused by PM2.5 exposure, the possible mechanism of which is to inhibit the expression of Th2 cytokines, eosinophilic infiltration, and specific IgE production.

Effect of PM2.5 on MicroRNA Expression and Function in Nasal Mucosa of Rats With Allergic Rhinitis.

BACKGROUND: Particulate matter 2.5 (PM2.5) refers to particulate matter with aerodynamic equivalent diameter less than or equal to 2.5 µm, which is an important component of air pollution. PM2.5 aggravates allergic rhinitis (AR) and promotes AR nasal mucosa inflammation. Therefore, the influence of PM2.5 inhalation exposure on microRNA (miRNA) expression profiles and function in the nasal mucosa of AR rats was investigated. METHODS: Female Sprague Dawley rats were distributed randomly to 2 groups: AR model PM2.5 exposure group (ARE group) and AR model PM2.5-unexposed control group (ARC group). The rats of ARE group were made to inhale PM2.5 at a concentration of 200 µg/m3, 3 h/day, for 30 days. miRNA expression profiles of the nasal mucosa from both groups were determined using an miRNA gene chip and were verified by quantitative real-time PCR (qRT-PCR). Gene function enrichment analysis was performed using bioinformatics analysis. RESULTS: The ARE group revealed 20 significantly differentially expressed miRNAs, including 4 upregulated and 16 downregulated miRNAs (fold change > 1.5 or < 0.66, P < .05). Of these, 9 selected miRNAs were verified by qRT-PCR, and the results of 8 miRNAs were in accordance with the miRNA gene chip results, with highly positive correlation (r = .8583, P = .0031). Numerous target genes of differentially expressed miRNAs were functionally enriched in high-affinity immunoglobulin E receptor signaling, ErbB signaling, mucin O-glycans biosynthesis, transforming growth factor ß signaling, mitogen-activated protein kinase signal transduction, phosphatidylinositol signaling, mucopolysaccharide biosynthesis, mammalian target of rapamycin signaling, T cell receptor signaling, Wnt signaling, chemokine signal transduction, and natural killer cell-mediated cytotoxicity pathways. CONCLUSIONS: PM2.5 causes significant changes in miRNA expression in the nasal mucosa of AR rats. miRNA plays an important role in regulating PM2.5 effects in AR rat biological behavior and mucosal inflammation. This study provides a theoretical basis for the prevention and treatment of AR from the effects of environmental pollution on the gene regulation mechanism.

Effects of PM2.5 on mucus secretion and tissue remodeling in a rabbit model of chronic rhinosinusitis.

BACKGROUND: According to epidemiologic studies, fine particulate matter (particulate matter ≤2.5 µm, PM2.5) is closely associated with increases in the incidence and severity of chronic rhinosinusitis (CRS). However, the role of PM2.5 in the pathophysiology of CRS remains largely unknown. In this study, we investigated the effects of PM2.5 on nasal cilia, tissue remodeling, and mucus hypersecretion in a rabbit model of CRS. METHODS: CRS rabbits were exposed to ambient PM2.5 via a PM2.5 inhalation exposure system. The degree of ciliary damage was evaluated using scanning electron microscopy (SEM). Histopathologic changes were determined using periodic acid-Schiff (PAS) staining of goblet cells and Masson trichrome (MT) staining for collagen in the nasal mucosa. MUC5AC expression was assessed by immunohistochemistry. RESULTS: PM2.5 exposure substantially aggravated ciliary disruption in rabbits with CRS. PM2.5 also significantly increased goblet cell hyperplasia and collagen deposition, as reflected by PAS and MT staining. The nasal mucosa of CRS rabbits displayed markedly elevated MUC5AC expression after PM2.5 exposure. CONCLUSION: Increases in ciliary disruption, nasal remodeling, and mucus hypersecretion may be the pathophysiologic mechanisms underlying the PM2.5-induced aggravation of CRS.

First long-term detection of paleo-oceanic signature of dust aerosol at the southern marginal area of the Taklimakan Desert.

We firstly conducted a long-term in-situ field measurement at a marginal area (Hotan) of the southern Taklimakan Desert covering all four seasons. Detailed chemical characterization of dust aerosol over Hotan showed several unconventional features, including (1) ubiquity of high Na+ and Cl- abundances in the Taklimakan dust aerosol and its Cl-/Na+ ratio close to seawater; (2) high Ca content in the Taklimakan dust (7.4~8.0%) which was about two times of that in the natural crust; (3) high abundance of soluble sulfate concentrations and strong correlations between sulfate and Na+ and Cl- as well as typical mineral tracers such as Al and Ca. Our results collectively indicated that the dust aerosol from the Taklimakan Desert was characterized of evident paelo-oceanic signature as the Taklimakan Desert was found as an ocean in the ancient times from the perspective of paleogeology. It was estimated that primary sources dominated the total abundances of sulfate during the dust seasons while previous climate modeling works had seldom considered the cooling effects of sulfate from the Taklimakan Desert.

Nasal epithelial barrier disruption by particulate matter ≤2.5 µm via tight junction protein degradation.

Upper airway diseases including sinonasal disorders may be caused by exposure to fine particulate matter (≤2.5 µm; PM2.5), as proven by epidemiological studies. PM2.5 is a complex entity whose chemical constituents and physicochemical properties are not confined to a single, independent "particle" but which in this study means a distinctive environmental "toxin." The mechanism whereby PM2.5 induces nasal epithelial barrier dysfunction leading to sinonasal pathology remains unknown. In the present study, human nasal epithelial cells were exposed to non-cytotoxic doses of PM2.5 to examine how PM2.5 affects the nasal epithelial barrier. Tight junction (TJ) integrity and function were assessed by transepithelial electric resistance and paracellular permeability. The expression levels of TJ proteins such as zona occludens-1, occludin and claudin-1 were assessed by immunofluorescence staining and western blot. PM2.5 exposure induced epithelial barrier dysfunction as reflected by increased paracellular permeability and decreased transepithelial electric resistance. TJ proteins zona occludens-1, occludin and claudin-1 were found to be downregulated. Pretreatment with N-acetyl-l-cysteine alleviated PM2.5-mediated reactive oxygen species generation in RPMI 2650 cells, further preventing barrier dysfunction and attenuating the degradation of TJ proteins. These results suggest that PM2.5 induces nasal epithelial barrier disruption via oxidative stress, and N-acetyl-l-cysteine counteracts this PM2.5-mediated effect. Thus, nasal epithelial barrier disruption caused by PM2.5, which leads to sinonasal disease, may be prevented or treated through the inhibition of reactive oxygen species.

Insights into the characteristics and sources of primary and secondary organic carbon: High time resolution observation in urban Shanghai.

There is growing evidence suggesting that organic aerosols play an important role in the evolution of severe haze episodes. However, long-term investigations of the different characteristics of carbonaceous aerosols during haze and non-haze days are insufficient. In this work, hourly measurements of organic carbon (OC) and elemental carbon (EC) in PM2.5 were conducted in Shanghai, a megacity in Eastern China, over the course of a year from July 2013 to June 2014. Both OC and EC exhibited a bimodal diel pattern and were highly dependent on the wind speed and direction. The concentration-weighted trajectory (CWT) analysis illustrated that primary OC (POC) and EC were largely associated with regional and long-range transport. Secondary OC (SOC) formation was the strongest during the harvest season owing to significant biomass burning emissions from the adjacent Yangtze River Delta and farther agricultural regions. Compared to OC (6.7 µg m-3) and EC (2.0 µg m-3) in the non-haze days, higher levels of both OC (15.6 µg m-3) and EC (7.7 µg m-3) were observed in the haze days as expected, but with lower OC/EC ratios in the haze days (2.4) than in non-haze days (4.6). The proportion of POC and EC in PM2.5 remained relatively constant as a function of PM2.5 mass loadings, while that of SOC significantly decreased on the highly polluted days. It is concluded that the haze pollution in urban Shanghai was influenced more by the primary emissions (POC and EC), while the role of SOC in triggering haze was limited.

[Airborne fine particle decreases the cell viability and induces inflammation in human bronchial epithelial cells].

OBJECTIVE: To investigate the effects of airborne fine particle on cell viability and inflammation in human bronchial epithelial cells.
 Methods: Atmospheric PM2.5 samples were collected by PM2.5 sampler. PM2.5 morphology was observed by scanning electron microscope (SEM). Human bronchial epithelial cells (BEAS-2B) were treated with PM2.5 at different concentrations (0, 50, 100, 200, 400, 800 µg/mL) for 12, 24 or 48 hours, and the cell activity were evaluated by cell counting kit-8 (CCK-8). The mRNA expression levels of (granulocyte-macrophage colony stimulating factor，GM-CSF) and TNF-α were detected by quantitative real-time PCR (qRT-PCR). Western blot was used to detect the protein expressions of GM-CSF and TNF-α.
 Results: According to SEM, the shape of PM2.5 varied, and the diameter was different and mostly equal to or less than 2.5 µm. CCK-8 assay showed that different concentrations of PM2.5 exposure for 12 hours, 24 hours and 48 hours resulted in loss of cell viability of BEAS-2B cells (P<0.05). Different concentrations of PM2.5 increased the mRNA and protein expression of GM-CSF and TNF-α, and the higher concentration of PM2.5 induced higher expression, which have statistical significant difference between the groups (P<0.05).
 Conclusion: Atmospheric PM2.5 can cause inflammatory response in human bronchial epithelial cells. They can reduce cell viability, which may be related to the PM2.5 trigger and aggravation of bronchopulmonary inflammatory diseases.

Signal Transductions of BEAS-2B Cells in Response to Carcinogenic PM2.5 Exposure Based on a Microfluidic System.

PM2.5 (particulate matter less than 2.5 µm in diameter) is considered as a harmful carcinogen. Determining the precise relationship between the chemical constituents of PM2.5 in the air and cancer progression could aid the treatment of environment related disease and establishing risk reduction strategies. Herein, we used transcriptomics (RNA-seq) and an integrated microfluidic system to identify the global gene expression and differential target proteins expression induced by ambient fine particles collected from the heavy haze in China. The results clearly indicated that cancer related pathways exhibited the strongest dysregulation. The ambient fine particles could be uptaken into the cells by pinocytosis, mainly promoting the PI3K-Akt pathway, FGF/FGFR/MAPK/VEGF signaling, and the JAK-STAT pathway, leading to evading apoptosis, sustained angiogenesis, and cell proliferation, which are the most important hallmarks of cancer. And fine particles also have been demonstrated to create intracellular reactive oxygen species (ROS) and mitochondrial ROS, change intracellular free Ca2+, and induce apoptosis, which are all key players in mediating cancer progression. It was observed by transmission electron microscopy (TEM) that the particles from the haze could enter the mitochondria, resulting in disturbance of the mitochondrial membrane and disruption of the mitochondria, and these particles can even enter inside the nucleus. It was also found in our study of organics (OC, PAHs) and metals (Zn, As, V) that compounds of fine particles were more closely associated with the exacerbation of cancer and secondary aerosols generated by traffic had the largest impact on cancer related signal transductions.

T-helper type 1-T-helper type 2 shift and nasal remodeling after fine particulate matter exposure in a rat model of allergic rhinitis.

BACKGROUND: Exposure to fine particulate matter (particulate matter ≤2.5 µm [PM2.5]) increases the risk of allergic rhinitis (AR), but the underlying mechanisms remains unclear. Thus, we investigated the roles of T-helper (Th)1-Th2 cytokines and nasal remodeling after ambient PM2.5 exposure in a rat model of AR. METHODS: Female Sprague-Dawley rats were randomized into six groups: a negative control group, a group of healthy rats exposed to 3000 µg/m3 PM2.5, an ovalbumin (OVA) induced AR model, and three PM2.5-exacerbated AR groups exposed to three different concentrations (200, 1000, and 3000 µg/m3) of PM2.5 for 30 days via inhalation. Nasal symptoms, levels of Th1-Th2 cytokines, the degree of eosinophilia in nasal lavage fluid (NLF), and the messenger RNA (mRNA) expressions of transcription factors GATA-3 and T-bet in the nasal mucosa were measured in each individual rat. Hyperplasia of globet cells and collagen deposition were examined by histology. RESULTS: PM2.5 significantly increased the number of sneezes and nasal rubs in rats with AR. PM2.5 also significantly decreased interferon gamma and increased interleukin (IL) 4 and IL-13 expressions as well as the number of eosinophils in NLF. The mRNA expression of GATA-3 in the nasal mucosa of rats with AR was upregulated by PM2.5, whereas T-bet was significantly downregulated. Statistically significant differences in OVA-specific serum immunoglobulin E, goblet cell hyperplasia, collagen deposition, and transforming growth factor beta 1 levels were observed between the PM2.5-exacerbated AR groups and the AR model group. CONCLUSION: Analysis of our data indicated that an increase in the immune response with Th2 polarization and the development of nasal remodeling may be the immunotoxic mechanisms behind the exacerbation of AR after exposure to PM2.5.

PM2.5-Induced Oxidative Stress and Mitochondrial Damage in the Nasal Mucosa of Rats.

Exposure to PM2.5 (particulate matter ≤2.5 µm) increases the risk of nasal lesions, but the underlying mechanisms, especially the mechanisms leading to mitochondrial damage, are still unclear. Thus, we investigated the in vivo effects of PM2.5 exposure on the inflammatory response, oxidative stress, the enzyme activities of Na⁺K⁺-ATPase and Ca2+-ATPase, and the morphology and function of mitochondria in the nasal mucosa of rats. Exposure to PM2.5 occurred through inhalation of a PM2.5 solution aerosol. The results show that the PM2.5 exposure induced increased levels of malondialdehyde (MDA) and levels of proinflammatory mediators, including interleukin 6 (IL-6), IL-8, and tumor necrosis factor-α (TNF-α). These changes were accompanied by decreases in the activities of total superoxide dismutase (T-SOD), Na⁺K⁺-ATPase, and Ca2+-ATPase in rat nasal mucosa. PM2.5 significantly affected the expression of specific mitochondrial fission/fusion genes (OPA1, Mfn1, Fis1, and Drp1) in nasal mucosa. These changes were accompanied by abnormal alterations of mitochondrial structures, including mitochondrial swelling, cristae disorder, and even fission resulting from higher doses of PM2.5. Our data shows that oxidative damage, inflammatory response, and mitochondrial dysfunction may be the toxic mechanisms that cause nasal lesions after exposure to PM2.5.

Effectiveness of SO2 emission control policy on power plants in the Yangtze River Delta, China-post-assessment of the 11th Five-Year Plan.

Facing the air pollution problems in China, emission control strategies have been implemented within the framework of national Five-Year Plan (FYP). According to the lack of post-assessment studies in the literature, this study assessed the effectiveness of the SO2 emission control policies on power plants after the 11th FYP (2006-2010) by modeling emission control scenarios. The idealized emission control policy (the PS90 scenario with assumption of 90% SO2 emission reduction from power plants) could reduce the SO2 and SO42- concentrations by about 51 and 14%, respectively, over the Yangtze River Delta region. While the actual emission control condition (the P2010 scenario based on the actual emissions from power plants in 2010) demonstrated that the actual reduction benefits were 30% of SO2 and 9% of SO42-. On the city scale, the P2010 scenario imposed positive benefits on Shanghai, Nanjing, Nantong, and Hangzhou with SO2 reductions of about 55, 12, 30, and 21%, respectively, while an 11% increase of SO2 concentration was found in Ningbo. The number of days exceeding China's National Ambient Air Quality Standard of Class I daily SO2 concentration was estimated to be 75, 52, 7, 77, and 40 days for Shanghai, Nanjing, Nantong, Ningbo, and Hangzhou under the real SO2 control condition (P2010). The numbers could be decreased by 16, 11, 2, 21, and 11% if the control effect reaches the level of the PS90 scenario. This study serves as a scientific basis to design capable enforcement of emission control strategies in China in the future national plans.

Quantitative analysis of aliphatic amines in urban aerosols based on online derivatization and high performance liquid chromatography.

A method combining online derivatization with high performance liquid chromatography/fluorescence detection was developed for the determination of seven aliphatic amines (ethanolamine, methylamine, ethylamine, propylamine, butylamine, pentylamine and hexylamine) in urban aerosols. The collected amines were online derivatized with o-phthalaldehyde to form highly fluorescent sulfonatoisoindole derivatives. The derivatives were completely separated in 13 min through gradient elution and detected by fluorescence detection at an excitation wavelength of 334 nm and an emission wavelength of 443 nm. Under the optimized conditions, the relative standard derivations (RSDs) of all detected amines were 0.02-2.03% and 1.04-1.52% for the retention time and peak area, respectively. Excellent linearity was achieved for each analyte, ranging from 5 µg L(-1) to 1000 µg L(-1) (R(2) > 0.99). The detection limits for all analytes were below 1.1 µg L(-1). The proposed method was used to analyze aliphatic amines in 35 samples of urban PM2.5 collected in Shanghai and was found to be suitable for the determination of particulate aliphatic amines at ng m(-3) levels in ambient air. Based on our measurements, ethanolamine and methylamine were the most abundant species on average in Shanghai during dry and wet seasons. The highest concentration was 15.3 ng m(-3) for ethanolamine and 13.2 ng m(-3) for methylamine.

Airborne Fine Particulate Matter Induces Oxidative Stress and Inflammation in Human Nasal Epithelial Cells.

Airborne fine particulate matter with an aerodynamic diameter equal to or smaller than 2.5 µm is abbreviated as PM2.5, which is one of the main components in air pollution. Exposure to PM2.5 is associated with increased risk of many human diseases, including chronic and allergic rhinitis, but the underlying molecular mechanism for its toxicity has not been fully elucidated. We have hypothesized that PM2.5 may cause oxidative stress and enhance inflammatory responses in nasal epithelial cells. Accordingly, we used human RPMI 2650 cells, derived from squamous cell carcinoma of the nasal septum, as a model of nasal epithelial cells, and exposed them to PM2.5 that was collected at Fudan University (31.3°N, 121.5°E) in Shanghai, China. PM2.5 exposure decreased the viability of RPMI 2650 cells, suggesting that PM2.5 may impair the barrier function of nasal epithelial cells. Moreover, PM2.5 increased the levels of intracellular reactive oxygen species (ROS) and the nuclear translocation of NF-E2-related factor-2 (Nrf2). Importantly, PM2.5 also decreased the activities of superoxide dismutase, catalase and glutathione peroxidase. Pretreatment with N-Acetyl-L-cysteine (an anti-oxidant) reduced the degree of the PM2.5-induced oxidative stress in RPMI 2650 cells. In addition, PM2.5 increased the production of granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-α, interleukin-13 and eotaxin (C-C motif chemokine ligand 11), each of which initiates and/or augments local inflammation. These results suggest that PM2.5 may induce oxidative stress and inflammatory responses in human nasal epithelial cells, thereby leading to nasal inflammatory diseases. The present study provides insights into cellular injury induced by PM2.5.

Human Excreta as a Stable and Important Source of Atmospheric Ammonia in the Megacity of Shanghai.

Although human excreta as a NH3 source has been recognized globally, this source has never been quantitatively determined in cities, hampering efforts to fully assess the causes of urban air pollution. In the present study, the exhausts of 15 ceiling ducts from collecting septic tanks in 13 buildings with 6 function types were selected to quantify NH3 emission rates in the megacity of Shanghai. As a comparison, the ambient NH3 concentrations across Shanghai were also measured at 13 atmospheric monitoring sites. The concentrations of NH3 in the ceiling ducts (2809(-2661)(+5803) µg m(-3)) outweigh those of the open air (~10 µg m(-3)) by 2-3 orders of magnitude, and there is no significant difference between different seasons. δ15N values of NH3 emitted from two ceiling ducts are also seasonally consistent, suggesting that human excreta may be a stable source of NH3 in urban areas. The NH3 concentration levels were variable and dependent on the different building types and the level of human activity. NH3 emission rates of the six residential buildings (RBNH3) were in agreement with each other. Taking occupation time into account, we confined the range of the average NH3 emission factor for human excreta to be 2-4 times (with the best estimate of 3 times) of the averaged RBNH3 of 66.0±58.9 g NH3 capita(-1) yr(-1). With this emission factor, the population of ~21 million people living in the urban areas of Shanghai annually emitted approximately 1386 Mg NH3, which corresponds to over 11.4% of the total NH3 emissions in the Shanghai urban areas. The spatial distribution of NH3 emissions from human excreta based on population data was calculated for the city of Shanghai at a high-resolution (100×100 m). Our results demonstrate that human excreta should be included in official ammonia emission inventories.