Particulate matter (PM2.5) exposure season-dependently induces neuronal apoptosis and synaptic injuries

Epidemiological studies have shown that particulate matter 2.5 (PM_2.5) not only increases the incidence of cardiopulmonary illnesses but also relates to the development of neurodegenerative diseases. Considering that PM_2.5 is highly heterogeneous with regional disparity and seasonal variation, we investigated whether PM_2.5 exposure induced neuronal apoptosis and synaptic injuries in a season-dependent manner. The results indicated that PM_2.5 altered the expression of apoptosis-related proteins (mainly bax and bcl-2), activated caspase-3 and caused neuronal apoptosis. Additionally, PM_2.5 decreased the levels of synaptic structural protein postsynaptic density (PSD-95) and synaptic functional protein N-methyl-D-aspartate (NMDA) receptor subunit (NR2B) expression. These effects occurred in a season-dependent manner, and PM_2.5 collected from the winter showed the strongest changes. Furthermore, the effect was coupled with the inhibition of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and phosphorylated cAMP-response element binding protein (p-CREB). Based on the findings, we analyzed the correlations between the chemical composition of PM_2.5 samples and the biological effects, and confirmed that winter PM_2.5 played a major role in causing neuronal apoptosis and synaptic injuries among different season samples.     

Endocannabinoid 2-arachidonoylglycerol protects inflammatory insults from sulfur dioxide inhalation via cannabinoid receptors in the brain

Sulfur dioxide(SO_2) pollution in the atmospheric environment causes brain inflammatory insult and inflammatory-related microvasculature dysfunction.However,there are currently no effective medications targeting the harmful outcomes from chemical inhalation.Endocannabinoids(eCBs) are involved in neuronal protection against inflammation-induced neuronal injury.The 2-arachidonoylglycerol(2-AG),the most abundant eCBs and a full agonist for cannabinoid receptors(CB1 and CB2),is also capable of suppressing proinflammatory stimuli and improving microvasculature dysfunction.Here,we indicated that endogenous 2-AG protected against neuroinflammation in response to SO_2 inhalation by inhibiting the activation of microglia and astrocytes and attenuating the overexpression of inflammatory cytokines,including tumor necrosis factor alpha(TNF-a),interleukin(IL)-1β,and inducible nitric oxide synthase(iNOS).In addition,endogenous 2-AG prevented cerebral vasculature dysfunction following SO_2 inhalation by inhibiting endothelin 1(ET-1),vascular cell adhesion molecule-1(VCAM-1) and intercellular adhesion molecule 1(ICAM-1) expression,elevating endothelial nitric oxide synthase(eNOS) level,and restoring the imbalance between thromboxane A2(TXA2) and prostaglandin 12(PGI2).In addition,the action of endogenous 2-AG on the suppression of inflammatory insult and inflammatory-related microvasculature dysfunction appeared to be mainly mediated by CB1 and CB2 receptors.Our results provided a mechanistic basis for the development of new therapeutic approaches for protecting brain injuries from SO_2 inhalation.     

Abnormal energy metabolism and tau phosphorylation in the brains of middle-aged mice in response to atmospheric PM2.5 exposure

In light of the accelerated aging of the global population and the deterioration of the atmosphere pollution, we sought to clarify the potential mechanisms by which fine particulate matter (PM_2.5) can cause cognitive impairment and neurodegeneration through the alteration of mitochondrial structure and function. The results indicate that PM_2.5 inhalation reduces ATP production by disrupting the aerobic tricarboxylic acid cycle and oxidative phosphorylation, thereby causing the hypophosphorylation of tau in the cortices of middle-aged mice. Furthermore, excessive reactive oxygen species generation was involved in the impairment. Interestingly, these alterations were partially reversed after exposure to PM_2.5 ended. These findings clarify the mechanism involved in mitochondrial abnormality-related neuropathological dysfunction in response to atmospheric PM_2.5 inhalation and provide an optimistic sight for alleviating the adverse health outcomes in polluted areas.     

规划环境影响评价的发展机遇与挑战

《环境影响评价法》的出台，为我国规划环境影响评价提供了新的发展机遇，同时也对传统项目环境影响评价和规划环境影响评价的发展提出了严峻的挑战。为促进《环境影响、平价法》的实施，笔者认为充分认识项目环境影响评价的局限性，加强规划环境影响评价的理论创新研究和实践，是当前应着手准备解决的问题。本文在分析传统环境影响评价局限性的基础上，研究了规划环境影响评价的发展机遇和挑战，以期能对国内规划环境影响评价工作的开展提供一些参考。     

绿色包装材料的进展

较为详尽地论述和介绍了绿色包装及绿色材料的内涵，从可降解包装材料、包装纸、可食性包装材料、天然生物包装材料和陶瓷包装材料等几个方面来探讨绿色包装材料的发展趋势。绿色包装材料是绿色包装的重要组成部分，包装问题与环境密不可分，采用绿色包装材料是2l世纪包装工业的发展方向和必然抉择。     

战略环境评价的实践进展和问题讨论

首先考察了战略环境评价（SEA）的起源及概念发展，述平了国内外SEA的最新实践进展，并从实践经验角度讨论了影响SEA进一步发展的评价方法、管理模式及评价内容等重要问题。提出了我国目前如何开展SEA研究的工作建议。     

用大型底栖动物再次对珠江广州河段污染的评价

本文利用1982年和1983年的资料,对用大型底栖动物作珠江广州河段污染评价及其建立的生物污染指数公式作进一步分析.用Morisita指数公式计算了三大类动物的分布,结果皆呈负二项分布.计算了各采样点底栖动物的Shannon-Weiver等六种多样性指数,未发现有明显的规律性.生物污染指数效果较好。两岸存在差异.     

上海嘉定区农民新村污水收集处理调查

在对上海嘉定区农民新村污水纳管,污水处理及污水最终排放去向作全面调查的基础上,分析了农民新村污水排放现状.存在的主要问题和发展趋势,并从排水管网基础建设、污水就地处理技术应用、环保部门执法监督和农民环境意识提高等方面,剖析了问题的根源,阐述了解决问题的思路,并得出相应的对策和建议。