Multiscale Plume Transport from the Collapse of the World Trade Center on September 11, 2001

The collapse of the world trade center (WTC) produced enhanced levels of airborne contaminants in New York City and nearby areas on September 11, 2001 through December, 2001. This catastrophic event revealed the vulnerability of the urban environment, and the inability of many existing air monitoring systems to operate efficiently in a crisis. The contaminants released circulated within the street canyons, but were also lifted above the urban canopy and transported over large distances, reflecting the fact that pollutant transport affects multiple scales, from single buildings through city blocks to mesoscales. In this study, ground-and space-based observations were combined with numerical weather forecast fields to initialize fine-scale numerical simulations. The effort is aimed at reconstructing pollutant dispersion from the WTC in New York City to surrounding areas, to provide means for eventually evaluating its effect on population and environment. Atmospheric dynamics were calculated with the multi-grid Regional Atmospheric Modeling System (RAMS), covering scales from 250 m to 300 km and contaminant transport was studied using the Hybrid Particle and Concentration Transport (HYPACT) model that accepts RAMS meteorological output. The RAMS/HYPACT results were tested against PM2.5 observations from the roofs of public schools in New York City (NYC), Landsat images, and Multi-angle Imaging SpectroRadiometer (MISR) retrievals. Calculations accurately reproduced locations and timing of PM2.5 peak aerosol concentrations, as well as plume directionality. By comparing calculated and observed concentrations, the effective magnitude of the aerosol source was estimated. The simulated pollutant distributions are being used to characterize levels of human exposure and associated environmental health impacts.     

Leaf volatiles and polyphenols in pear trees infested byPsylla pyricola. Evidence of simultaneously induced responses

Summary Feeding by the homopteranPsylla pyricola on leaves of pear trees induces the production of volatile compounds, such as (E,E)--farnesene and methyl-salicylate, as well as the production of polyphenols. The inference on induction is based on GC-MS and HPLC chromatograms from the same samples ofPsylla infested leaves, leaves from the same pear tree beforePsylla infestation and uninfested leaves from other pear trees.Psylla infestation greatly enhanced the production of volatiles ((E,E)--farnesene, methyl-salicylate and others) and triggered the production of new polyphenols, characterized by much longer retention times.However, the responses to infestation depend critically on leaf age (defined by leaf distance to apex). With respect to the leaf volatiles it appears that infested, old leaves produce fewer compounds and lower amounts of the volatiles than infested, young leaves. Moreover, there seem to be differences in pattern. Relative to (E,E)--farnesene, methyl-salicylate was found in much lower amounts in heavily infested, old leaves. With respect to polyphenols it was found that infested old leaves collected in August have polyphenols with the same retention times, but more or less equal amounts as uninfested young leaves collected in May. This shows thatPsylla infestation causes the induced response mostly in young leaves.The induced leaf volatiles may act as synomones to heteropteran bugs. As shown elsewhere,Anthocoris nemoralis responds significantly to (E,E)--farnesene and methyl-salicylate when offered in pure form against clean air in a Y-tube olfactometer. The effect of polyphenols on the performance ofP. pyricola is not yet known. Hence, a role in direct defence is still to be investigated.     

BDE-47对人胚肾细胞HEK293的毒理效应及作用机制

2,2’,4,4’-四溴联苯醚(BDE-47)是生物体中含量最高且毒性最强的PBDEs之一,有关BDE-47对肾细胞的毒性及其作用机制的研究仍有待补充。选取3个剂量组(低:10-6mol·L-1、中:10-5mol·L-1、高:10-4mol·L-1)及溶剂对照组,研究了BDE-47对人胚肾细胞(HEK293)的细胞凋亡率及活性氧(ROS)水平的影响;并从分子水平对细胞氧化损伤、凋亡相关蛋白(APE1及p53)及凋亡相关基因m RNA(p53、Bax、Caspase 3、Caspase 8)的表达量进行测定。实验结果显示:与对照组相比,中、高剂量组细胞凋亡率显著增加(P0.05);ROS水平在中剂量组显著上升(P0.01);随BDE-47浓度的变化,APE1蛋白表达量与细胞ROS水平存在一致性;p53、Bax、Caspase 8 m RNA表达量与BDE-47的浓度间存在剂量-效应关系。结果表明,BDE-47可诱导HEK293细胞凋亡及氧化应激,APE1可能是细胞ROS升高与细胞凋亡间重要的中介因子;BDE-47可以通过影响Caspase 8及线粒体途径中p53及Bax的表达诱导细胞凋亡。