Yongjie Wei

Source profiles of particulate organic matters emitted from cereal straw burnings

Cereal straw is one of the most abundant biomass burned in China but its contribution to fine particulates is not adequately understood. In this study, three main kinds of cereal straws were collected from five grain producing areas in China. Fine particulate matters (PM2.5) from the cereal straws subjected to control burnings, both under smoldering and flaming status, were sampled by using a custom made dilution chamber and sampling system in the laboratory. Element carbon (EC) and organic carbon (OC) was analyzed. 141 compounds of organic matters were measured by gas chromatography-mass spectrum (GC-MS). Source profiles of particulate organic matters emitted from cereal straw burnings were obtained. The results indicated that organic matters contribute a large fraction in fine particulate matters. Levoglucosan had the highest contributions with averagely 4.5% in mass of fine particulates and can be considered as the tracer of biomass burnings. Methyloxylated phenols from lignin degradation also had high concentrations in PM2.5, and contained approximately equal amounts of guaiacyl and syringyl compounds. beta-Sitostrol also made up relatively a large fraction of PM2.5 compared with the other sterols (0.18%-0.63% of the total fine particle mass). Normal alkanes, PAHs, fatty acids, as well as normal alkanols had relatively lower concentrations compared with the compounds mentioned above. Carbon preference index (CPI) of normal alkanes and alkanoic acids showed characteristics of biogenic fuel burnings. Burning status significantly influenced the formations of EC and PAHs. The differences between the emission profiles of straw and wood combustions were displayed by the fingerprint compounds, which may be used to identify the contributions between wood and straw burnings in source apportionment researches.

Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing

Epidemiologic evidence suggests that air pollution is a risk factor for childhood obesity. Limited experimental data have shown that early‐life exposure to ambient particles either increases susceptibility to diet‐induced weight gain in adulthood or increases insulin resistance, adiposity, and inflammation. However, no data have directly supported a link between air pollution and non‐diet‐induced weight increases. In a rodent model, we found that breathing Beijings highly polluted air resulted in weight gain and cardiorespiratory and metabolic dysfunction. Compared to those exposed to filtered air, pregnant rats exposed to unfiltered Beijing air were significantly heavier at the end of pregnancy. At 8 wk old, the offspring prenatally and postnatally exposed to unfiltered air were significantly heavier than those exposed to filtered air. In both rat dams and their offspring, after continuous exposure to unfiltered air we observed pronounced histologic evidence for both perivascular and peribronchial inflammation in the lungs, increased tissue and systemic oxidative stress, dyslipidemia, and an enhanced proinflammatory status of epididymal fat. Results suggest that TLR2/4‐dependent inflammatory activation and lipid oxidation in the lung can spill over systemically, leading to metabolic dysfunction and weight gain.—Wei, Y., Zhang, J., Li, Z., Gow, A., Chung, K. F., Hu, M., Sun, Z., Zeng, L., Zhu, T., Jia, G., Li, X., Duarte, M., Tang, X. Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing. FASEB J. 30, 2115–2122 (2016). www.fasebj.org

Harmonizing Molecular Marker Analyses of Organic Aerosols

Analysis of molecular markers in aerosol samples using GC-MS has become widely used in air pollution studies. There is considerable variability in the analytical details of molecular marker analyses across different research and regulatory groups. These discrepancies result in the use of different methods for the interpretation of source and ambient measurements used in source apportionment and atmospheric particulate studies. As a demonstration of the utility of harmonizing laboratorial methods, inter-laboratory comparison experiments were conducted in which two laboratories used similar methods, including extraction, derivatization, instrumental analyses, and quantification algorithms. Duplicate samples, including ambient and source aerosol samples, were analyzed. Results showed that when using the same analytical methods, good agreement was achieved between laboratories. The results of the molecular marker analyses at both laboratories were suitable for use in source apportionment. Non-and moderately polar compounds, including hopanes and steranes showed the best agreements of the compounds analyzed by both labs with a relative deviation of 7.7%. Although consistent results for all key molecular markers were obtained, the sensitivity of different compounds and compound groups to analytical parameters were examined to assess analytical accuracies. Quantification was most sensitive to internal standard reference due to varying recoveries for different internal standards.

Transcriptome Profiling of the Lungs Reveals Molecular Clock Genes Expression Changes after Chronic Exposure to Ambient Air Particles

The symptoms of asthma, breathlessness, insomnia, etc. all have relevance to pulmonary rhythmic disturbances. Epidemiology and toxicology studies have demonstrated that exposure to ambient air particles can result in pulmonary dysfunction. However, there are no data directly supporting a link between air pollution and circadian rhythm disorder. In the present study, we found that breathing highly polluted air resulted in changes of the molecular clock genes expression in lung by transcriptome profiling analyses in a rodent model. Compared to those exposed to filtered air, in both pregnant and offspring rats in the unfiltered group, key clock genes (Per1, Per2, Per3, Rev-erbα and Dbp) expression level decreased and Bmal1 expression level increased. In both rat dams and their offspring, after continuous exposure to unfiltered air, we observed significant histologic evidence for both perivascular and peribronchial inflammation, increased tissue and systemic oxidative stress in the lungs. Our results suggest that chronic exposure to particulate matter can induce alterations of clock genes expression, which could be another important pathway for explaining the feedbacks of ambient particle exposure in addition to oxidative stress and inflammation.

Exposure to Ambient Air Particles Increases the Risk of Mental Disorder: Findings from a Natural Experiment in Beijing

Epidemiology studies indicated that air pollution has been associated with adverse neurological effects in human. Moreover, the secretion of glucocorticoid (GC) affects the mood regulation, and the negative feedback of hippocampal glucocorticoid receptors (GR) inhibits the GC secretion. Meanwhile, the over secretion of GC can interfere the immune system and induce neurotoxicity. In the present study, the human test showed that the secretion of the cortisol in plasma was elevated after exposure in heavy air pollution. In the mouse model, we found that breathing the highly polluted air resulted in the negative responses of the mood-related behavioral tests and morphology of hippocampus, as well as the over secretion of GC in plasma, down regulation of GR, and up-regulation of cytokine and chemokine in the hippocampus. When considering the interrelated trends between the hippocampal GR, inflammatory factors, and plasmatic GC, we speculated that PM2.5 exposure could lead to the increased secretion of GC in plasma by decreasing the expression of GR in hippocampus, which activated the inflammation response, and finally induced neurotoxicity, suggesting that PM2.5 exposure negatively affects mood regulation. When combined with the results of the human test, it indicated that exposure to ambient air particles increased the risk of mental disorder.