Congrui Deng

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.

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.

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.

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.

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.

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.

Determination of atmospheric alkylamines by ion chromatography using 18-crown-6 as mobile phase additive

An improved ion chromatographic method including two elution procedures was proposed for the quantitative determination of atmospheric alkylamines in field atmospheric samples involving high levels of inorganic cations by using 18-crown-6 as mobile phase additive. When 18-crown-6 was added to the mobile phase, the retention times increased significantly for Na+, NH4+, K+ and primary alkylamines but decreased for secondary and tertiary alkylamines due to the complexation with certain cations and interaction with both stationary and mobile phases of 18-crown-6. As a result, the separation of the cations was greatly promoted, which reduced the interference of peak distortion of overloaded inorganic cations on the quantitation of adjacent alkylamines. By using the presented method, five inorganic cations (Na+, NH4+, K+, Mg2+, Ca2+) and six alkylamines (dimethylamine (DMAH+), trimethylamine + diethylamine (TMAH+ + DEAH+), propylamine (MPAH+), triethylamine (TEAH+), ethanolamine (MEOAH+) and triethanolamine (TEOAH+)) were effectively separated and determined, and the relative standard derivations (RSDs) of objective cations were all less than 1% for retention time and 3.1% for peak area (n = 9), respectively. The linearity was excellent for each cation (R2 > 0.993) except for NH4+ and TEOAH+ showing a non-linear response (R2 > 0.998 for theoretical non-linear fitting), and the detection limit of these cations were 0.03-1.19 ng. The proposed method was successfully used in the determination of both alkylamines and inorganic cations in ambient particulate matters and gaseous alkylamines in ceiling duct exhaust. The annual average concentrations of DMAH+, TMAH+ + DEAH+ and TEAH+ were 15.56, 4.35 and 16.00 ng m-3 in PM2.5 over Shanghai in 2013. The concentrations of gaseous DMA and TMA + DEA in ceiling duct exhaust reached a maximum of 940.0 and 112.7 μg m-3, and were positively correlated with the human activity intensity, suggesting that human excreta emissions was a potential important source of atmospheric alkylamines in urban area of Shanghai.

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

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.

Impact of mixed anthropogenic and natural emissions on air quality and eco-environment—the major water-soluble components in aerosols from northwest to offshore isle

Based on more than 300 atmospheric TSP and PM2.5 samples collected at five sites over China in 2007 and 2008, characteristics, sources, and interactions of the major water-soluble species were investigated for a better understanding of their role in urban air quality and offshore eco-environment. From the dust source regions in Northwestern China to an offshore isle over the East China Sea, concentration levels and fine/coarse particle distributions of five representative water-soluble components were well elucidated, reflecting the distinct differences of geo-history, location, and present economic situation among the target areas. NO3−/SO42− mass ratios reflected significant divergence of motorization among the studied regions. Specifically, a case study during the World Car-Free Day proved that traffic restriction measures could indeed help mitigate the aerosol species formed from vehicle emissions. Investigation on the molar concentration stoichiometry and mass percentage variations of particulate NO3−, SO42−, and NH4+ revealed that NH3 was a driving factor in the formation of major secondary water-soluble ions in atmospheric fine particles over urban areas. Based on the prevailing wind analysis, observation over an offshore isle clearly indicated the influence of the relative strength of anthropogenic sources and ocean-related natural sources on the formation and size distribution of MSA (methanesulfonic acid), a major water-soluble organic component in aerosol. Annual dry deposition flux of particulate NO3− and NH4+ over the East China Sea was estimated based on the strength of an improved calculation formula. Reductive nitrogen was found to be the major form of the deposited atmospheric inorganic nitrogen, accounting for ~ 69% of the total nitrogen depositions.