云南罗平医院PM调查的分析与对策

文章以云南罗平医院为研究对象,调查了65名一般员工和21名科主任级中层领导,使用PM量表对该医院的高层及中层领导行为进行评估,对情景因素与领导行为的内在联系进行探讨,并提出改进对策。目的是了解员工需求,促进人力资源合理配置,从而提高医院的管理水平。     

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。     

Ability of rosetting or non-rosetting individual control and inflammatory macrophages to kill Escherichia coli X43 intracellularly

An autoradiographic method combined with a rosette technique was used to assess the bactericidal activity of individual control and inflammatory peritoneal macrophages (PM phi) in the presence or absence of expression of Fc receptor for IgG (FcR). There was a lack of FcR reactivity in a certain percentage of both categories of PM phi exposed to E. coli X43, a bacterium which is readily phagocytosed in the presence of specific antibody. Both rosetting and non-rosetting PM phi were capable of phagocytosing E. coli X43, but inflammatory PM phi showed a marked reduction in their capacity to ingest these bacteria compared with control PM phi. Once ingested the E. coli X43 were killed equally well by non-rosetting and rosetting control and inflammatory PM phi.     

武汉市颗粒物污染对呼吸系统健康影响及经济损失分析

目的评估颗粒物(particulate matter,PM)污染对呼吸系统疾病(respiratory disease,RD)住院人数的影响,估计降低PM水平可避免的经济损失,为评估空气污染治理的成本-效益提供依据。方法收集武汉市2015—2019年两家三甲医院RD住院患者资料、同期武汉市PM浓度和气象数据。采用广义相加模型(generalized additive model,GAM)估计PM对RD住院人数的影响,采用疾病成本法(cost of illness approach,COI)估算PM浓度降低带来的可避免经济损失。结果PM污染造成RD住院人数增加,PM_(2.5)和PM_(10)浓度每上升10μg/m^(3),分别导致RD住院人数上升1.71%和0.71%。其中男性和0~14岁人群受影响较大,PM_(2.5)浓度每上升10μg/m^(3),男性和0~14岁住院人数分别上升1.97%和2.65%;PM_(10)浓度每上升10μg/m^(3),男性和0~14岁住院人数分别上升0.87%和0.88%。2015—2019年PM污染造成武汉市6.33万人住院和12.14亿元经济损失。若PM浓度降低至同期世界卫生组织建议值,武汉市每年可避免1.94亿元经济损失和1.01万人住院。结论PM暴露可导致沉重的疾病负担和经济损失,采取有效的措施控制PM浓度,将带来较大的经济效益。     

广州市大气PM2.5中多环芳烃的现状及分布情况

目的 了解广州市大气PM_2.5中多环芳烃在不同时间、不同地区内的分布特征。 方法 于2018年在广州市越秀区(市区),从化区(农村)和番禺区(市郊)采集PM_2.5有效样品252份,用高效液相色谱法测定样品中16种多环芳烃的浓度,以分析不同地区、不同时间及季节间的分布特征和变化趋势。结果 广州市大气PM_2.5中16种多环芳烃均有检出,但质量浓度处于较低水平,年均值为(4.907±3.642)ng/m³。PM_2.5及多环芳烃的质量浓度呈现明显的季节性波动,表现为冬春季较高,夏秋季较低,不同季节差异有统计学意义(F=3.624～72.439,均P<0.05)。市区为(54.321±35.106)μg/m³,农村地区为(46.298±25.933)μg/m³,市郊PM_2.5的质量浓度为(51.821±30.033)μg/m³,差异无统计学意义(F=1.513,P>0.05),多环芳烃中萘、苯并[a]芘、二苯并[a,h]蒽、茚并[1,2,3-cd]芘的污染水平在不同地区之间差异有统计学意义(F=4.428～6.422,P<0.05),农村高于市区和市郊。结论 广州市大气PM_2.5中多环芳烃污染水平较低,呈现明显的季节性波动和城乡差别。     

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。     

冶炼厂烟尘PM_(2.5)复合污染探讨

目的　通过本研究确定 ,现有除尘设备是否还存在PM2 5复合污染。方法　通过化学、电子显微镜及电子能谱、GC MS等仪器对上述样品多种污染成分及粒径进行定性、定量测定。结果　上述复合污染成分 :水 2 2 % ,有机物 34 75 % ,无机物 4 3 75 %。无机物以Cu、C、Pb、Al为主 ,它们的粒径≤ 1 1μm ,有机污染物14 0多种 ,以酚类及PAHs为主 ,无机物中除铅、砷等重金属 ,还有砷酸、磷酸。结论　在现有除尘设备条件下的冶炼厂烟尘污染为多种重金属、酸性氧化物及几十种有机污染物 (酚类及PAHs)的复合污染 ,它们的粒径分布大多≤ 1 1μm。     

沙尘暴细颗粒物致大鼠肺泡巨噬细胞DNA损伤

[目的]探讨沙尘暴和正常天气细颗粒物(PM2.5)及其水提取物和有机提取物对大鼠肺泡巨噬细胞的细胞毒性和DNA的损伤作用。[方法]沙尘暴和正常天气PM2.5于2004年3月采集自甘肃省武威市和内蒙古自治区包头市。细胞毒性用四甲基偶氮唑盐(MTT)分析法观察,细胞DNA损伤用单细胞凝胶电泳(SCGE)技术检测。[结果]沙尘暴和正常天气PM2.5及其水提取物和有机提取物均对大鼠肺泡巨噬细胞产生一定的细胞毒性,且随剂量的增大而增强;然而,沙尘暴与正常天气之间除了包头沙尘暴PM2.5有机提取物之外,余差异均无显著性。正常天气PM2.5和沙尘暴PM2.5水提取物和有机提取物均可引起细胞DNA损伤,且随剂量增加而损伤增大;正常天气PM2.5比沙尘暴PM2.5水提取物和有机提取物对细胞DNA损伤作用更大。不论正常天气PM2.5还是沙尘暴PM2.5,其有机提取物对DNA的损伤作用均比水提取物作用更强,表明PM2.5中引起DNA损伤的主要化学物是有机化合物种类。武威与包头两城市工业水平不同,大气污染程度不同,但两地沙尘暴PM2.5及其水提取物和有机提取物对细胞DNA的损伤作用,在两地之间并无明显差异。[结论]正常天气PM2.5和沙尘暴PM2.5及其水提取物和有机提取物均可引起DNA损伤,且正常天气PM2.5的损伤作用更强;然而不同地方沙尘暴PM2.5毒性作用未见差异,推测其所含遗传毒性化学物可能类似。     

Assessment of intracellular cytokines and regulatory cells in patients with autoimmune diseases and primary immunodeficiencies — Novel tool for diagnostics and patient follow-up

Serum and intracytoplasmic cytokines are mandatory in host defense against microbes, but also play a pivotal role in the pathogenesis of autoimmune diseases by initiating and perpetuating various cellular and humoral autoimmune processes.     

PM2.5‐induced lung inflammation in mice: Differences of inflammatory response in macrophages and type II alveolar cells

Particulate matter 2.5 (<PM2.5 μm) leads to chronic obstructive pulmonary disease. In this study, biomarkers related to inflammation and oxidative stress in vitro and in vivo experiments were investigated to clarify the PM2.5‐induced lung inflammation mechanisms. In an in vitro study using RAW264.7 cells, PM2.5 caused phosphorylation of nuclear factor‐κB, p38 mitogen‐activated protein kinase and extracellular response kinases, an increase of proinflammatory gene and protein expressions (e.g. monocyte chemotactic protein‐1, tumor necrosis factor‐α). These biomarkers were substantially attenuated by polymyxin B (PMB). PM2.5 induced heme oxygenase‐1 (HO‐1) gene, which was attenuated by N‐ acetylcysteine (NAC). However, the suppressive effects of NAC on inflammatory biomarkers were very weak. In bone marrow‐derived macrophages (BMDMs) of wild‐type BALB/c mice, the effects of PMB and NAC on PM2.5‐induced inflammatory responses were similar to RAW264.7 cells. In BMDMs of MyD88^−/− mice, PM2.5‐induced proinflammatory mediators were substantially more attenuated. PM2.5 caused an increase of proinflammatory gene expressions (interleukin‐6, cyclooxygenase 2) and HO‐1 gene in MLE‐12 cells (mouse alveolar cell line). These biomarkers were substantially attenuated by NAC, but not by PMB. When BALB/c mice were exposed intratracheally to 0.2 mg PM2.5, PM2.5 caused severe lung inflammation, an increase of neutrophils along with proinflammatory mediators in bronchoalveolar lavage fluid. The inflammation was attenuated by NAC, particularly by NAC + PMB, but not by PMB alone. These results indicate that macrophages may act sensitively to lipopolysaccharide (LPS) present in PM2.5 and release proinflammatory mediators via the LPS/MyD88 pathway. However, type II alveolar cells may react sensitively to oxidative stress induced by PM2.5 and cause inflammatory response. Therefore, overall, PM2.5 may cause predominantly oxidative stress‐dependent inflammation rather than LPS/MyD88‐dependent inflammation in type II alveolar cell‐rich lungs. Copyright © 2017 John Wiley & Sons, Ltd.