细颗粒物免疫毒性研究进展

大气中细颗粒物的暴露是多种健康问题的危险因素 ,而免疫系统是细颗粒物毒性作用的靶器官之一 ,细颗粒物对非特异性免疫系统和特异性免疫系统均有一定影响。免疫系统作用有两面性 ,既对颗粒物具有一定的清除能力 ,同时也是机体受损的重要原因。免疫毒性与颗粒物产生的其他生物效应有密切关系。免疫毒性的作用机制可能通过氧化、炎症刺激和神经性炎症反应等有关 ,但具体致病机制仍不清楚 ,有必要从整体上研究颗粒物的毒性及其作用机制。本文从不同角度和不同水平对细颗粒物的免疫毒性进行综述。     

PM2.5的污染特征及其生物效应研究进展

直经≤2．5μm细颗粒物(PM2．5)是一种重要的空气污染物,不仅含有大量的有机物,而且含有许多重金属。这些组分大多数是有毒的,其中有一些可以引起呼吸系统疾病,有一些具有遗传毒性甚至致癌。PM2．5与疾病发病率和死亡率的上升有关。PM2．5污染越来越严重,正受到人们的密切关注。现就PM2．5污染特征与生物效应指标的研究进展进行综述。     

大气细颗粒物不同组分的毒理学效应及其分子作用机制研究进展

大气细颗粒物(PM2.5)是指空气动力学直径小于或等于2.5 μm的颗粒物, 经由靶器官肺脏进入机体, 可诱发多种不良健康效应(如心血管疾病、糖尿病、呼吸系统疾病、神经退行性疾病和不良出生结局等)。PM2.5具有组成的复杂性(可溶性/非可溶性成分和生物成分等)、来源的多样性和二次转化等特性, 大量的流行病学和毒理学研究提示PM2.5的不同组成在诱发不良健康效应时所涉及的毒理学作用机制存在差异。另外, PM2.5作为载体, 还存在多组分间的混合暴露和联合效应。本文对近几年大气细颗粒物不同成分暴露所涉及的毒理学作用机制及不同组分间的联合效应进行了较为系统的阐述, 主要包含炎症反应、氧化应激、内质网应激、核因子κB(NF-κB)信号通路的激活等, 为PM2.5不同组分暴露所引发的不良健康效应的防治提供依据。     

可吸入颗粒物的心血管效应

可吸入颗粒物是诱导心血管疾病发生的重要环境危险因素。文章综述了粗颗粒物、细颗粒物、超细颗粒物等主要可吸入空气颗粒物的心血管效应,并从氧化应激、炎症反应、自主神经功能紊乱及心血管功能失调等方面简单介绍了可吸入颗粒物诱导心血管效应的主要分子机制。     

丹参酮IIA磺酸钠对环境细颗粒物所致大鼠肺部炎性损伤的影响

[背景]吸入环境细颗粒物(PM2.5)易造成机体肺部炎性损伤,寻找有效的干预物质十分必要.[目的]研究丹参酮ⅡA磺酸钠(TanⅡA)对PM2.5所致大鼠肺部炎性损伤的影响.[方法]健康SD雄性大鼠,随机分为4组,每组6只,分别为对照组、模型组、TanⅡA组,地塞米松阳性对照组.采用气管滴注细颗粒物建立大鼠肺部炎症模型....     

粉笔尘对教室颗粒物浓度影响分析

<正>空气中悬浮的颗粒污染物会对人体健康产生重要影响[1]。粒径大于50μm的颗粒物受重力作用会沉降到地面,小于10μm的颗粒物(PM10)可随着呼吸进入人体肺部。PM10引起的流行病研究表明,多种有机化合物如苯、二噁英、多环芳烃以及一些含有高毒性成分的金属如铅、镉会附着在颗粒物表面而进入人体,容易引起呼吸道感染、心脏病、支气管炎、哮喘、肺炎、肺气肿等多种疾病[2-4]。细小颗粒物对人体     

车用柴油机排放细颗粒物和超细颗粒物特征与人体健康效应

机动车排放大量细颗粒物和超细颗粒物引起的环境污染问题日益严重,这些很小的粒子相比大颗粒对人体健康潜在影响可能更大。该文主要阐述柴油发动机排放细颗粒物和超细颗粒物的特征,包括物理化学成分和粒度分布;综述柴油机排放颗粒物对人体的健康效应。     

大气PM2.5对心血管疾病影响的研究进展

PM2.5是指空气动力学直径≤2.5μm的颗粒物,又称为细颗粒物,是评估大气污染与疾病负担的重要指标。PM2.5可以深入肺部,沉积在肺泡区域,通过触发氧化应激和炎症反应等机制,加快血管和心脏功能受损,危害人体健康。长期和短期暴露于PM2.5浓度的环境中,心血管疾病的风险将持续增加,而心血管疾病(Cardiovascular disease,CVD)是全球伤残率和死亡率上升的重要原因,因此我们应高度重视大气污染,积极采取有效手段,控制降低PM2.5浓度。     

室内生物源性污染物对健康影响的研究进展

室内空气质量与人体健康密切相关。随着空调普及导致室内空气循环减少以及家庭宠物的流行等,为室内微生物的生存和繁殖提供了条件。空气中的微生物及其产生的毒素、致敏原经常附着于飞沫及颗粒物上,降落地面或长时间漂浮空气中形成微生物气溶胶。长期暴露于生物源性污染物可能对人体造成健康危害,以呼吸系统病变(如慢性阻塞性肺部疾患,炎症等)和变态反应(如变应性鼻炎,肺炎及哮喘等)为主。本文对近十年来有关空气生物源性污染物的研究进展进行综述。     

PM_(2.5)对慢性阻塞性肺疾病发生发展影响及药物治疗研究进展

慢性阻塞性肺疾病(慢阻肺)是一种以气流受限为特征可以预防和治疗的疾病,与肺部对有害气体的异常炎症及免疫反应有关。目前环境问题受到广泛关注,细颗粒物(PM_(2.5))作为危害严重的环境污染物,其对健康的影响不容忽视。研究表明PM_(2.5)在慢阻肺发生发展的过程中起到重要作用。PM_(2.5)主要通过氧化应激、炎症反应和免疫功能失衡影响慢阻肺的进展。本文从慢阻肺危险因素入手,综述PM_(2.5)对慢阻肺疾病发生发展影响的可能机制,分析不同药物对PM_(2.5)影响下慢阻肺进展的干预,为慢阻肺的预防与治疗提供新的思路。     

Combustion of diesel fuel from a toxicological perspective

Epidemiological data and results of toxicity studies in experimental animals indicate the possible health risk of diesel exhaust exposure. Acute effects of this exposure include odor, eye irritations, lung function decrements, cardiovascular symptoms, and some non-specific effects. Most of these effects are reported among persons highly exposed to diesel exhaust. Lung function decrements are reported as chronic effects. Another chronic effect that has been studied extensively among occupationally exposed persons in lung cancer. In addition to lung cancer, but at a less frequent rate, an enhanced incidence of bladder cancer is reported. The carcinogenic action of diesel exhaust exposure is ascribed to effects of the soot particles, particle-associated organics, and/or gas phase compounds. Direct effects of the particle load may include retardation of lung clearance, inflammation, and increased cell proliferation. These effects were all demonstrated in rodents. The particles may also prolong the residence time of particulate organics or induce the generation of reactive oxygen species. These compounds are known to react with macromolecules, causing lipid peroxidation, DNA damage, and/or activation of other genotoxic substances such as polycyclic aromatic hydrocarbons (PAHs). However, these results have not yet been confirmed in mammals in vivo. A direct interaction of particles with lung tissue is also suggested as a cause of cancer but a mechanism for this interaction has not yet been proposed. Organics associated with the particles are known to contain genotoxic properties attributable to PAHs and their derivatives. A number of these compounds are also identified as carcinogens in animal studies. However, it is not clear whether parent PAHs, their nitro-, oxy-, alkylated, or heterocyclic derivatives, or possibly other compounds are principally responsible for inducing tumors in the lungs of animals after diesel exhaust exposure. Furthermore, the mechanism of the bioavailability of these organics is not completely understood. The effects of gas phase constituents on the carcinogenic properties of the particles and/or particle-associated organics either have not been investigated or the findings have been inconclusive.     

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。     

Fine particles, a major threat to children

BACKGROUND: There is a growing body of evidence for serious health consequences of exposure to ambient air pollution. The general question of who is susceptible is one of the most important gaps in current knowledge regarding particulate matter (PM)-related health effects. Who is susceptible depends on the specific health endpoint being evaluated and the level and length of exposure. Here, we restrict the review on the impact of fine particle exposure on children's health to the following outcomes: infant death, lung function, respiratory symptoms and reproductive outcomes. METHODS: This is a strategic review of children's susceptibility to ambient fine particles and characteristics of infant and children which underlie their increased susceptibility to PM. RESULTS: Ambient fine PM is associated with intra-uterine growth retardation, infant mortality; it is associated with impaired lung function and increased respiratory symptoms, particularly in asthmatics. Concerning infant mortality, exposure to PM is strongly and consistently associated with postneonatal respiratory mortality and less consistently with sudden infant death syndrome. Although most of the studies reported adverse effects for this health outcome, the evidence is weaker than for infant death. Exposure to fine PM has been associated with impaired lung function and lung function growth. Most of the studies reported increased prevalence of symptom with increased exposure to fine PM. CONCLUSION: Fine PM is a major threat to children, because of their higher exposure to PM compared to adults, the immature state of the lung in childhood and also of the immune function at birth. The first months of life might be a period of particular sensitivity. Although the mechanisms of air pollution effects have not yet been completely understood, pregnant women, infants and children need specific protection against exposure to fine particles.     

Fine environmental particulate engenders alterations in human lung epithelial A549 cells

Particulate matter (PM), a component of urban air pollution that derives primarily from the combustion of fossil fuels, is responsible for a number of health effects in humans. Recent studies have demonstrated that the fine particles (PM(2.5)) present in high numbers in PM samples can be more harmful than larger particles, since they are more efficiently retained in the peripheral lung. In the present study, we have investigated the biological effects of PM(2.5) on human lung epithelial cell line A549. Morphological analysis performed by immunofluorescence and electron microscopy showed that fine particles interact with the cell surface, where they induce evident alterations and, subsequently, are internalized in the cytoplasm. Cytoskeletal components, in particular microfilaments and microtubules, cause modifications upon challenge with PM(2.5). Of interest, an early cell response to the fine particulate is an increase of reactive oxygen species content, which can account for the observed cytoskeletal changes and the production of proinflammatory cytokines in A549 cells. In particular, exposure to PM(2.5) promoted a dose- and time-dependent release of TNF-alpha and IL-6 in the cell medium.     

Health effects of nanoparticles and nanomaterials (I) recent oveview of health effects of nanoparticles

Recently, the impact of nanoparticles and nanomaterials on health and environmental effects has become a big issue. There are two types of nanoparticles to be considered in hygiene science; environmental nanopartcles emitted from automobiles and manufactured nanoparticles such as fullerenes, carbon nanobutbes, and ultrafine metals/metal oxides. These very fine particles are potentially health threatening, because they are supposed to be highly permeable in the lung and skin tissues and small enough to evade phagocytosis by reticuloendothelial system. The dose metrics are critical to evaluate toxicity of nanoparticles, because the surface-based rather than weight-based concentration has been reported to correlate well with effects and endopoints of nanoparticles. Research on environmental nanoparticles should be done as a part of research for fine particles or particulate materials less than 2.5 microm (PM2.5). Variety of materials, such as carbon, metals, and metal oxides, are included in manufactured nanoparticles. Moreover, some of manomaterials are generated in the shape of fiber and sheet. Thus, we should focus more on nano-specific biological interactions and tissue permeability to investigate health effects of manufactured nanoparticles. In this report trend in health effects of nanoparticles is overviewed.     

颗粒物中粗细粒子的毒性比较

颗粒物是影响人体健康的重要污染物之一.人们通常认为越细小的颗粒物对人体危害越大,但是也有一些学者指出细粒子的毒性并不一定大于粗粒子.该文通过初步分析粗、细粒子的毒性,探讨了影响颗粒物对人体危害效应的一些因素,例如其表面形态特征以及吸附组分等,希望能有助于人们正确评价颗粒物的毒性.     

Pulmonary effects of inhaled ultrafine particles

INTRODUCTION AND OBJECTIVES: Recent epidemiological studies have shown an association between increased particulate urban air pollution and adverse health effects on susceptible parts of the population, in particular the elderly with pre-existing respiratory and cardiovascular diseases. Urban particles consist of three modes: ultrafine particles, accumulation mode particles (which together form the fine particle mode) and coarse mode particles. Ultrafine particles (those of < 0.1 micron diameter) contribute very little to the overall mass, but are very high in number, which in episodic events can reach several hundred thousand/cm3 in the urban air. The hypothesis that ultrafine particles are causally involved in adverse responses seen in sensitive humans is based on several studies summarized in this brief review. METHODS AND RESULTS: Studies on rodents demonstrate that ultrafine particles administered to the lung cause a greater inflammatory response than do larger particles, per given mass. Surface properties (surface chemistry) appear to play an important role in ultrafine particle toxicity. Contributing to the effects of ultrafine particles is their very high size-specific deposition when inhaled as singlet ultrafine particles rather than as aggregated particles. It appears also that ultrafine particles, after deposition in the lung, largely escape alveolar macrophage surveillance and gain access to the pulmonary interstitium. Inhaled low doses of carbonaceous ultrafine particles can cause mild pulmonary inflammation in rodents after exposure for 6 h. Old age and a compromised/sensitized respiratory tract in rodents can increase their susceptibility to the inflammatory effects of ultrafine particles significantly, and it appears that the aged organism is at a higher risk of oxidative stress induced lung injury from these particles, compared with the young organism. Results also show that ultrafine particle effects can be significantly enhanced by a gaseous co-pollutant such as ozone. CONCLUSIONS: The studies performed so far support the ultrafine particle hypothesis. Additional studies are necessary to evaluate mechanistic pathways of responses.     

Inflammation and airborne particles

Inflammation provides a potential mechanistic link between inhalation of particles and the diverse health effects found in epidemiologic studies. Considerable uncertainty remains as to the importance of the inflammation in mediating these effects and where that inflammation is occurring: lung, vascular endothelium, or distant organs, including the heart. This article briefly reviews the role of inflammation in pulmonary and cardiovascular disease and explores the evidence that the health effects of PM exposure are mediated, at least in part, by inflammation.     

Effect of lunar dust on humans: -lunar dust: regolith-

We reviewed the effect of lunar dust (regolith) on humans by the combination of the hazard/exposure of regolith and microgravity of the moon. With regard to the physicochemical properties of lunar dust, the hazard-related factors are its components, fibrous materials and nanoparticles. Animal exposure studies have been performed using a simulant of lunar dust, and it was speculated that the harmful effects of the simulant lies between those of crystalline silica and titanium dioxide. Fibrous materials may not have a low solubility judging from their components. The nanoparticles in lunar dust may have harmful potentials from the view of the components. As for exposure to regolith, there is a possibility that particles larger than ones in earth (1 gravity) are respirable. In microgravity, 1) the deposition of particles of less than 1 μm in diameter in the human lung did not decrease, 2) the functions of macrophages including phagocytosis were suppressed, 3) pulmonary inflammation was changed. These data on hazard/exposure and microgravity suggest that fine and ultrafine particles in regolith may have potential hazards and risks for humans.     

Biological effects of PM10 relevant to human health

Recent epidemiological studies have shown a consistent association between ambient levels of inhalable particles (PM10) and exacerbation of respiratory diseases as well as cardiovascular morbidity and adult mortality in high risk groups. The particles responsible of the observed health effects are unknown; it seems that different particles could be related to different effects, depending on the deposition pattern in the airways and on the chemical reactivity. Larger particles could be more related to upper airway and tracheobronchial effects while the smaller carbonaceous particles seem to be preferentially involved in inflammation and cardiopulmonary injury. It has been proposed that the possible biological mechanisms of action of PM could be related to its radical activity and the induction of oxidative stress and lung inflammation followed by systemic low grade inflammation and pro-coagulant state.