沙尘暴细颗粒物的化学成分及其毒理学研究

沙尘暴已成为影响人类健康的主要危害因素之一,沙尘暴细颗粒物包括水溶性离子、有机物及不溶性物质,目前其对人体健康的影响引起人们的关注。流行病学研究表明,沙尘暴细颗粒物不仅可以引起呼吸系统疾病,对心血管、神经、免疫系统都会产生影响;毒理学研究也表明,沙尘暴细颗粒物对人和动物多种组织器官均有毒性作用,通过产生各种自由基引起器官组织发生氧化损伤和遗传损伤可能是沙尘暴细颗粒物毒作用的主要机制。     

大气颗粒物健康效应生物学机制研究进展

大量流行病学研究发现，大气颗粒物的污染水平与心肺系统疾病的超额发病、死亡存在密切关联，但其毒理学机制尚未阐明。本文对近年来大气颗粒物毒理学研究进行综述，包括大气颗粒物对呼吸系统、心血管系统及神经系统的毒性作用，并对氧化应激损伤、细胞钙稳态失衡及激活关键转录因子等分子毒理学机制进行了初步的阐述。     

大气超细颗粒物的分布特征及其对健康的影响

许多流行病学和毒理学研究表明大气颗粒物与人群死亡率和发病率明显相关。超细颗粒物是大气颗粒物的重要组成成分,与呼吸系统和心血管系统疾病密切相关。本文综述了超细颗粒物的分布特征及其组成成分,综合大气超细颗粒物与人群健康效应的流行病学及毒理学资料,以获取超细颗粒物健康效应的可能机制,并总结超细颗粒物的研究方向,为大气中超细颗粒物污染的健康危险度评价提供依据。     

可吸入颗粒物心血管毒性作用机制研究进展

空气可吸入颗粒物由于其粒径小、比表面积大、吸附性强、成分复杂等特点成为越来越受关注的空气污染物.近几年,颗粒物对肺外组织器官——心血管系统毒性机制的研究为人关注.该文主要从氧化应激、炎性损伤、血液系统损伤、自主神经系统失衡、心肌离子通道等方面对近20年大气颗粒物心血管毒性作用机制研究进行综述.     

大气颗粒物及其组分对肾脏影响的研究进展

大气颗粒物对人体的健康损害已成为研究热点,对心肺系统产生的直接不良影响已被熟知,随着研究的深入,学者们逐渐将重心转向其他靶器官,尤其是肾脏.但大气颗粒物及其组分对肾脏的影响和作用机制尚不明确,本文以全颗粒物及其组分为出发点,分别从流行病学及实验研究两方面探讨其与肾损伤间的关联,在此基础上从氧化应激与炎症损伤、细胞DNA...     

大气颗粒物相关心肺系统生物标志物的研究进展

大气污染造成的健康损害已成为当前公共卫生领域研究的热点。流行病学和临床医学的研究发现大气颗粒物与心肺系统疾病的发病和死亡显著相关。目前主要观点认为其导致心肺疾病的主要途径是通过系统炎症反应和氧化应激反应,但发病机制和致病通路尚不明确,部分学者针对大气颗粒物相关心肺系统生物标志物的研究发现其可能在致病机制中发挥重要作用。本文将系统汇总目前报道的流行病学和毒理学相关生物标志物的研究结果,为筛选特异性强、敏感性高且能实现快速检验的生物标志物用于评价个体暴露水平和健康损害效应,以及探索其致病机制提供可以借鉴的依据。     

大气污染物对呼吸系统炎性细胞因子表达的研究进展

大气污染物是由颗粒污染物与气态污染物组成.颗粒污染物是指悬浮在大气中固体与液体颗粒物的总称.国际上将可吸入颗粒物(PM10)分为3类,即粗颗粒物:其空气动力学直径在2.5～10 μm;细颗粒物:其空气动力学直径在0.1～2.5μm;极细颗粒物或超细颗粒物(PM0.1):其空气动力学直径<0.1μm.而我们常说的细颗粒物(PM2.5)是指空气动力学直径≤2.5μm的颗粒物,包括上述的细颗粒物和极细颗粒物.气态污染物主要包括含硫化合物、含氮化合物和碳氧化合物,其中主要是SO2、NO2、CO及O3等.国内外大量流行病学研究证明,大气污染物与许多健康效应直接或间接相关.可对人体多个系统造成危害,尤其是呼吸系统.     

沙尘天气的呼吸系统健康效应及机制研究进展

沙尘天气导致严重的大气颗粒物污染,造成人体以呼吸系统为主的多系统损害。该文综述了沙尘天气的呼吸系统健康效应及作用机制,主要包括急性刺激症状发生率、呼吸系统疾病医院就诊情况和肺功能急性损伤等急性健康效应研究;呼吸系统疾病患病率和沙漠尘肺等慢性健康效应研究;沙尘颗粒物的细胞毒性研究;沙尘天气对太阳辐射的影响。以期对今后沙尘天气呼吸系统健康效应及作用机制的更深入研究有所借鉴和帮助。     

地铁系统可吸入颗粒物污染现状及其对人群健康的影响

文章对地铁系统中可吸入颗粒物的污染现状、主要影响因素、来源和成分进行综述,分析地铁系统中可吸入颗粒物的暴露途径、健康损害机制及其对健康影响的最新进展,提出未来应进一步加强对可吸入颗粒物的来源及其元素组成的监测以及动物毒理学和人类流行病学方面研究,为法规标准制订和卫生管理提供参考。     

大气颗粒物化学成分与健康效应的关系及其机制的研究进展

随着大气颗粒物与人群健康效应关系研究的不断深入,不同来源的颗粒物对健康损害的差异引起了世界各国科学家的广泛重视,由此展开了大量流行病学研究和实验研究,以探讨颗粒物中不同成分对人体健康的影响程度和可能机制。本文对有关大气颗粒物化学成分的健康效应及其机制进行综述。     

The role of reactive oxygen species and oxidative stress in mediating particulate matter injury

Numerous reports link oxidative stress to particulate matter (PM)-induced adverse health effects. Increasing evidence is being collected that reactive oxygen species and oxidative stress are involved in PM-mediated injury. The physical characteristics and the chemical composition of PM play a key role in reactive oxygen species generation in vitro and in vivo. According to the hierarchical oxidative stress hypothesis, antioxidant phase II enzymes protect against PM-induced inflammation and cytotoxicity. This concept is useful in understanding PM-induced disease models, susceptibility, and biomaker development to access exposures outcomes and is useful for developing therapeutic intervention in PM-induced adverse health effects.     

Redox activity of airborne particulate matter at different sites in the Los Angeles Basin

Epidemiologic studies have shown associations between ambient particulate matter (PM) and adverse health outcomes including increased mortality, emergency room visits, and time lost from school and work. The mechanisms of PM-related health effects are still incompletely understood, but a hypothesis under investigation is that many of the adverse health effects may derive from oxidative stress, initiated by the formation of reactive oxygen species (ROS) within affected cells. While the adverse effects from PM have historically been associated with the airborne concentration of PM and more recently fine-particle PM, we considered it relevant to develop an assay to quantitatively measure the ability of PM to catalyze ROS generation as the initial step in the induction of oxidative stress. This ability of PM could then be related to different sources, chemical composition, and physical and spatial/temporal characteristics in the ambient environment. The measurement of ROS-forming ability in relation to sources and other factors will have potential relevance to control of redox-active PM. If oxidative stress represents a relevant mechanism of toxicity from PM, the measurement of redox activity represents a first step in the elucidation of the subsequent downstream processes. We have developed an assay for PM redox activity, utilizing the reduction of oxygen by dithiothreitol which serves as an electron source. We have found that PM will catalyze the reduction of oxygen and have examined the distribution and chemical characteristics of the redox activity of PM fractions collected in different sites in the Los Angeles Basin. Samples of concentrated coarse, fine, and ultrafine PM, obtained with aerosol concentrators, were studied with regard to their chemical properties and redox activity. Redox activity was highest in the ultrafine fraction, in agreement with results indicating ultrafines were the most potent toward inducing that heme oxygenase expression and depleting intracellular glutathione, which has relevance to induction of oxidative stress. Comparison of the redox activity with chemical composition showed a reasonable correlation of redox activity with elemental carbon (r(2)=0.79), organic carbon (r(2)=0.53), and with benzo[ghi]perylene (r(2)=0.82), consistent with species typically found in mobile emission sources.     

The fine fraction of airborne particulate: a pollutant of increasing environmental and health relevance. Methodologies for sampling and characterizing single particles

Among the atmospheric pollutants detectable in the environment, the inhalable airborne particulate (PM10) is regarded with increasing care. Indeed a number of epidemiological studies support the correlation between both acute and chronic adverse health effects and the PM10 pollution in the urban environment. According to recent results the health effects could be related to the physico-chemical characteristics of the particulate itself. With the aim of characterising the individual particles, PM10 samples collected by multi-stage cascade impactor are examined by scanning electron microscopy (SEM) and X-ray microanalysis with energy dispersion spectroscopy (EDS). The obtained data are analysed using multivariate statistical techniques (hierarchical clustering methods, principal factor analysis) to determine the components of the particulate. By these methods a series of studies was carried out by the Istituto Superiore di Sanità to investigate the PM10 pollution in several environmental situations.     

大气颗粒物对人体皮肤健康影响的研究进展

近年来我国大气污染问题日益严重,国内外大量研究表明,大气污染与许多健康效应直接或间接相关。已有流行病学研究证实,大气颗粒物污染与皮肤疾病的发病率密切相关。该文从氧化应激与炎症反应、芳香烃受体(Ah R)的活化、皮肤表面微生物的影响,就现有大气颗粒物对皮肤健康影响的流行病学及毒理学研究进行综述。     

Health effects of particles in ambient air

A summary of a critical review by a working group of the German commission on Air Pollution Prevention of VDI and DIN of the actual data on exposure and health effects (excluding cancer) of fine particulate air pollution is presented. EXPOSURE: Typical ambient particle concentrations for PM10 (PM2.5) in Germany are in the range of 10-45 (10-30) microg/m3 as annual mean and 50-200 (40-150) microg/m3 as maximum daily mean. The ratio of PM2.5/PM10 generally amounts between 0.7 and 0.9. HEALTH EFFECTS: During the past 10 years many new epidemiological and toxicological studies on health effects of particulate matter (PM) have been published. In summary, long-term exposure against PM for years or decades is associated with elevated total, cardiovascular, and infant mortality. With respect to morbidity, respiratory symptoms, lung growth, and function of the immune system are affected. Short-term studies show consistant associations of exposure to daily concentrations of PM with mortality and morbidity on the same day or the subsequent days. Patients with asthma, COPD, pneumonia, and other respiratory diseases as well as patients with cardio-vascular diseases and diabetes are especially affected. The strongest associations are found for PM2.5 followed by PM10, with no indication of a threshold value for the health effects. The data base for ultra fine particles is too small for final conclusions. The available toxicological data support the epidemiological findings and give hints as to the mechanisms of the effects. CONCLUSION: The working group concludes that a further reduction of the limit values proposed for 2005 will substantially reduce health risks due to particulate air pollution. Because of the strong correlation of PM10 with PM2.5 at most German sites there is no specific need for limit values of PM2.5 for Germany in addition to those of PM10.     

Potential mechanisms of adverse pulmonary and cardiovascular effects of particulate air pollution (PM10)

PM10 is the international convention for measuring environmental particulate air pollution. Increases in PM₁₀ have been linked to exacerbations of airways disease and deaths from respiratory and cardiovascular causes. PM₁₀ is a complex and variable mixture but toxicological data suggests that ultrafine particles, transition metals and endotoxins are the most likely components to mediate adverse health effects. Potential mechanisms for the local and systemic adverse effects of PM₁₀ are discussed.     

Cardiovascular health and particulate vehicular emissions: a critical evaluation of the evidence

A major public health goal is to determine linkages between specific pollution sources and adverse health outcomes. This paper provides an integrative evaluation of the database examining effects of vehicular emissions, such as black carbon (BC), carbonaceous gasses, and ultrafine PM, on cardiovascular (CV) morbidity and mortality. Less than a decade ago, few epidemiological studies had examined effects of traffic emissions specifically on these health endpoints. In 2002, the first of many studies emerged finding significantly higher risks of CV morbidity and mortality for people living in close proximity to major roadways, vs. those living further away. Abundant epidemiological studies now link exposure to vehicular emissions, characterized in many different ways, with CV health endpoints such as cardiopulmonary and ischemic heart disease and circulatory-disease-associated mortality; incidence of coronary artery disease; acute myocardial infarction; survival after heart failure; emergency CV hospital admissions; and markers of atherosclerosis. We identify numerous in vitro, in vivo, and human panel studies elucidating mechanisms which could explain many of these cardiovascular morbidity and mortality associations. These include: oxidative stress, inflammation, lipoperoxidation and atherosclerosis, change in heart rate variability (HRV), arrhythmias, ST-segment depression, and changes in vascular function (such as brachial arterial caliber and blood pressure). Panel studies with accurate exposure information, examining effects of ambient components of vehicular emissions on susceptible human subjects, appear to confirm these mechanisms. Together, this body of evidence supports biological mechanisms which can explain the various CV epidemiological findings. Based upon these studies, the research base suggests that vehicular emissions are a major environmental cause of cardiovascular mortality and morbidity in the United States. As a means to reduce the public health consequences of such emissions, it may be desirable to promulgate a black carbon (BC) PM_2.5 standard under the National Ambient Air Quality Standards, which would apply to both on and off-road diesels. Two specific critical research needs are identified. One is to continue research on health effects of vehicular emissions, gaseous as well as particulate. The second is to utilize identical or nearly identical research designs in studies using accurate exposure metrics to determine whether other major PM pollutant sources and types may also underlie the specific health effects found in this evaluation for vehicular emissions.     

Oxidative stress in toxicology: established mammalian and emerging piscine model systems.

Interest in the toxicological aspects of oxidative stress has grown in recent years, and research has become increasingly focused on the mechanistic aspects of oxidative damage and cellular responses in biological systems. Toxic consequences of oxidative stress at the subcellular level include lipid peroxidation and oxidative damage to DNA and proteins. These effects are often used as end points in the study of oxidative stress. Typically, mammalian species have been used as models to study oxidative stress and to elucidate the mechanisms underlying cellular damage and response, largely because of the interest in human health issues surrounding oxidative stress. However, it is becoming apparent that oxidative stress also affects aquatic organisms exposed to environmental pollutants. Research in fish has demonstrated that mammalian and piscine systems exhibit similar toxicological and adaptive responses to oxidative stress. This suggests that piscine models, in addition to traditional mammalian models, may be useful for further understanding the mechanisms underlying the oxidative stress response.