大气细颗粒物免疫毒性研究进展

机体暴露于大气细颗粒物(PM2.5)可引起多种健康损害,PM2.5引起免疫系统的破坏与机体各种疾病密切相关.该文从固有免疫系统、适应性免疫系统、细胞因子和免疫毒性作用机制4个方面阐述了PM2.5对免疫系统不同水平的损伤以及可能的作用机制,指出了PM2.5免疫毒性的复杂性,为更深入研究PM2.5的免疫毒性提供科学依据.     

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。     

空气细颗粒物(PM2.5)生物效应指标研究进展

本文阐述了细颗粒物生物效应指标的研究进展。细颗粒物是一种重要的空气污染物 ,它的形态和组成相当复杂 ,不仅含有大量的有机物如B(a)p ,而且含有许多重金属如Pb、Cd、Cr等。这些组分大多数是有毒的 ,其中一些可以引起肺部炎症和哮喘 ,另一些具有遗传毒性的物质可能是潜在的致癌物。细颗粒物可经过呼吸进入肺部 ,并且沉积在肺组织 ,因此它严重危害人类健康。流行病学研究已经显示细颗粒物与疾病发病率和死亡率的上升有关 ,尤其是心脏和肺部疾病。目前认为细颗粒物可能通过氧化、炎症刺激及对遗传物质的作用对机体造成损伤 ,但细颗粒物的致病机制仍不很清楚 ,因此有必要进一步探索其生物效应     

空气细颗粒物遗传毒性研究进展

细颗粒物已成为城市空气中的主要污染物之一。长期接触细颗粒物可使细胞遗传物质发生损害。利用体内外多种试验方法检测到细颗粒物的遗传毒性主要发生在细胞染色体、DNA、基因等不同水平的遗传物质。本文综述了空气中细颗粒物遗传毒性的研究进展 ,初步探讨了细颗粒物遗传毒性的可能作用机制。     

092 空气细颗粒物遗传毒性研究进展

细颗粒物已成为城市空气中的主要污染物之一.长期接触细颗粒物可使细胞遗传物质发生损害.利用体内外多种试验方法检测到细颗粒物的遗传毒性主要发生在细胞染色体、DNA、基因等不同水平的遗传物质.本文综述了空气中细颗粒物遗传毒性的研究进展,初步探讨了细颗粒物遗传毒性的可能作用机制.     

动物免疫毒性的生物学检测

多年来,许多毒理学家已经注意到免疫系统是在急性或亚急性接触环境化学物质,治疗甲药、滥用药物或物理因素产生毒性反应的靶器官,并研究化学品对免疫系统的毒性作用。由于很多化学物质对人免疫系统具有抑制作用,同样对动物也能产生类似的结果,而且产生免疫抑制作用的机制也很相似。因此从实验动物所获得的免疫毒性研究资料,对于人群接触     

空气细颗粒物对心血管系统的影响研究进展

通过对大气环境中重要污染物细颗粒物(PM_2.5)毒理学作用及其机制方面文献综述,从来源、组成、化学成分对PM_2.5进行概述,并对PM_2.5环境质量标准限值进行分析得出对健康威胁的结论。分述PM_2.5对健康所造成的影响,以心血管系统为例,对相关蛋白表达的影响及细胞毒性进行述评。研究PM_2.5对健康带来的负面效应:血管功能障碍、氧化应激和炎症反应等。完善大气颗粒物(PM_2.5)对健康污染的健康风险评价,为深入研究细颗粒物对心血管系统毒性机制等前沿问题提供科学依据,并阐述其在预防和控制心血管疾病方面发挥重要作用。     

ＰＭ２．５组分的细胞毒性效应研究进展

摘要：ＰＭ２．５污染已成为大气污染研究领域的热点与前沿。由于ＰＭ２．５组分复杂多样,产生的细胞效应也不 尽相同。本研究通过分析最新的ＰＭ２．５组分细胞毒性效应国内外研究成果,包括氧化损伤、致突变性和致 癌性、免疫毒性和炎症反应、细胞周期及活力变化等,指出了不同组分与细胞毒性效应之间存在的关系。 为进一步评估细胞毒性与特定化学物质之间的关系,以及二者相关作用机制的研究提供了理论参考。 关键词：ＰＭ２．５;细颗粒物;细胞毒性效应;氧化损伤;免疫毒性;致突变性 中图分类号：Ｒ１２２,Ｘ５１３　　文献标识码：Ａ　　文章编号：１００９ ６６３９ （２０１８）０４ ０３１３ ０３     

环境细颗粒物亚慢性染毒对大鼠炎症损伤及免疫功能的影响研究

目的建立细颗粒物的亚慢性暴露动物模型,探讨PM2.5对大鼠炎症损伤及免疫功能的影响。方法应用气管滴注建立细颗粒物的亚慢性暴露动物模型;光镜下观察各脏器病理学变化;采用相应的试剂盒测定肺泡灌洗液中的总蛋白和唾液酸水平;ELISA方法检测细胞因子IL-6和TNF-α水平,采用RT-PCR方法检测肺组织中这两种细胞因子的表达水平;收集肺泡巨噬细胞,采用孔雀绿比色法检测巨噬细胞的吞噬功能;取脾脏,采用MTT方法检测淋巴细胞的增殖功能。结果在染毒后的大鼠肺内均观察到异物性肉芽肿形成;在肝脏血窦内观察到有单核吞噬细胞聚集形成肉芽肿的趋势;在肺门淋巴结和肝脏、肾脏血管内观察到明显的吞噬PM2.5的巨噬细胞和游离的PM2.5。总蛋白和唾液酸水平随着暴露时间和剂量升高而增加。在观察的前3个月,染毒组TNF-α表达水平逐渐升高,而在6个月时,TNF-α水平明显降低;IL-6表达水平随着染毒剂量的增加而升高,并呈现明显的剂量-效应关系,染毒3个月后最高,而在6个月后表达水平回落。肺泡巨噬细胞的吞噬功能随着剂量的增加而下降。淋巴细胞增殖功能没有出现显著性变化。结论细颗粒物的亚慢性暴露可以引起机体的持续炎症损伤;细颗粒物对免疫系统的损伤随着剂量和暴露时间的增加而增加,细颗粒物引起的细胞因子网络紊乱会加重免疫系统的损伤;细颗粒物引起巨噬细胞吞噬功能下降,是肺部慢性疾病的致病机制之一。     

大气细颗粒物对A549细胞炎性因子分泌影响

目的探讨大气沙尘与非沙尘天气细颗粒物（PM25）对人肺腺癌上皮细胞炎性因子分泌的影响。方法沙尘与非沙尘细颗粒物采自甘肃省武威市;实验细胞为人肺腺癌上皮A549细胞（A549细胞）。分别用25,50,100,200μg/ml沙尘与非沙尘细颗粒物对A549细胞进行染毒,染毒24 h后,细胞计数法测定细胞毒性。收集细胞上清,用放射免疫法测定细胞因子白介素-8（IL-8）和肿瘤坏死因子-α（TNF-α）的浓度。结果（1）沙尘细颗粒物对A549细胞作用24 h后,在细胞毒性上表现出低浓度促进细胞增殖,高浓度抑制增殖现象;非沙尘颗粒物随染毒剂量增加,细胞存活率明显降低,抑制细胞增殖。（2）沙尘、非沙尘细颗粒物对A549细胞作用24 h后,均可促进A549细胞分泌炎性因子IL-8。（3）沙尘、非沙尘颗粒物对A549细胞作用24 h后,对TNF-α分泌的影响不明显。结论沙尘与非沙尘细颗粒物均有早期炎症效应。     

Seasonal and regional short-term effects of fine particles on hospital admissions in 202 US counties, 1999-2005

The authors investigated whether short-term effects of fine particulate matter with an aerodynamic diameter < or =2.5 microm (PM(2.5)) on risk of cardiovascular and respiratory hospitalizations among the elderly varied by region and season in 202 US counties for 1999-2005. They fit 3 types of time-series models to provide evidence for 1) consistent particulate matter effects across the year, 2) different particulate matter effects by season, and 3) smoothly varying particulate matter effects throughout the year. The authors found statistically significant evidence of seasonal and regional variation in estimates of particulate matter effect. Respiratory disease effect estimates were highest in winter, with a 1.05% (95% posterior interval: 0.29, 1.82) increase in hospitalizations per 10-microg/m(3) increase in same-day PM(2.5). Cardiovascular diseases estimates were also highest in winter, with a 1.49% (95% confidence interval: 1.09, 1.89) increase in hospitalizations per 10-microg/m(3) increase in same-day PM(2.5), with associations also observed in other seasons. The strongest evidence of a relation between PM(2.5) and hospitalizations was in the Northeast for both respiratory and cardiovascular diseases. Heterogeneity of PM(2.5) effects on hospitalizations may reflect seasonal and regional differences in emissions and in particles' chemical constituents. Results can help guide development of hypotheses and further epidemiologic studies on potential heterogeneity in the toxicity of constituents of the particulate matter mixture.     

Heart rate variability and particulate exposure in vehicle maintenance workers: a pilot study

The association between occupational exposure to PM(2.5) and heart rate variability was investigated in a repeated measures, longitudinal study of vehicle maintenance workers occupationally exposed to automobile emissions. Five subjects were monitored for occupational exposure to fine particulate matter (PM(2.5)) on 6 workdays using an aerosol photometer, validated with side-by-side sampling with a gravimetric method. End-of-day heart rate variability statistics were derived using short-term electrocardiogram recordings for each participant. Workplace carbon monoxide and outdoor, ambient fine particulate matter were also monitored. Regression statistics were used to investigate associations between same-day PM(2.5) levels and heart rate variability statistics using mixed-effects multiple regression of pooled data. No statistically significant associations were observed between occupational PM(2.5) and measures of heart rate variability. A statistically significant increase in total spectral power was associated with ambient PM(2.5) (p < 0.05). The data suggest a threshold below which no degradation in cardiac autonomic control of healthy workers occurs when challenged by occupational PM(2.5) exposure. This study was limited in population, exposure level, and type of particulate exposures. Additional studies are recommended on broader occupational populations.     

Atmospheric pollutants study of particles and metallic elements during high wind speed (wind speed >6 m/s) near Taiwan Strait around central Taiwan

The purpose of this study was to characterize metallic elements associated with atmospheric particulate matter in total suspended particulate (TSP), fine particles (particle matter with an aerodynamic diameter of <2.5 microm, PM2.5) and coarse particles (particle matter with an aerodynamic diameter of 2.5-10 microm, PM2.5-10), at high wind speed (wind speed >6 m/s) at Taichung Harbor (TH) and Wuci traffic (WT) in central Taiwan from March to December 2004. The correlation coefficient (R2) between TSP, coarse, fine particulate concentrations versus wind speed at the TH and WT sampling site during high wind speed (>6 m/s) are shown in this study. In addition, the correlation coefficients between TSP, coarse and fine particles of metallic species versus high wind speed were also observed. The results indicated that the correlation coefficient order was TSP> coarse>fine for particles at both sampling sites during high wind speed (>6 m/s) near central Taiwan. In addition, the concentrations of Fe, Zn, Mn, Cu, Pb, Cr, Mg for TSP, coarse and fine particulates were also analysed in this study.     

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.     

The influence of ambient coarse particulate matter on asthma hospitalization in children: case-crossover and time-series analyses

In this study, we used both case-crossover and time-series analyses to assess the associations between size-fractionated particulate matter and asthma hospitalization among children 6-12 years old living in Toronto between 1981 and 1993. Specifically, we used exposures averaged over periods varying from 1 to 7 days to assess the effects of particulate matter on asthma hospitalization. We calculated estimates of the relative risk of asthma hospitalization adjusted for daily weather conditions (maximum and minimum temperatures, and average relative humidity) for an incremental exposure corresponding to the interquartile range in particulate matter. Both bidirectional case-crossover and time-series analyses revealed that coarse particulate matter (PM10-2.5) averaged over 5-6 days was significantly associated with asthma hospitalization in both males and females. The magnitude of this effect appeared to increase with increasing number of days of exposure averaging for most models, with the relative risk estimates stabilizing at about 6 days. Using a bidirectional case-crossover analysis, the estimated relative risks were 1.14 [95% confidence interval (CI), 1.02, 1.28] for males and 1.18 (95% CI, 1.02, 1.36) for females, for an increment of 8.4 microg/m(3) in 6-day averages of PM10-2.5. The corresponding relative risk estimates were 1.10 and 1.18, respectively, when we used time-series analysis. The effect of PM10-2.5 remained positive after adjustment for the effects of the gaseous pollutants carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3). We did not find significant effects of fine particulate matter (PM2.5) or of thoracic particulate matter (PM10) on asthma hospitalizations using either of these two analytic approaches. For the most part, relative risk estimates from the unidirectional case-crossover analysis were more pronounced compared with both bidirectional case-crossover and time-series analyses.     

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.     

Comparison of fine particle measurements from a direct-reading instrument and a gravimetric sampling method

Particulate air pollution, specifically the fine particle fraction (PM2.5), has been associated with increased cardiopulmonary morbidity and mortality in general population studies. Occupational exposure to fine particulate matter can exceed ambient levels by a large factor. Due to increased interest in the health effects of particulate matter, many particle sampling methods have been developed In this study, two such measurement methods were used simultaneously and compared. PM2.5 was sampled using a filter-based gravimetric sampling method and a direct-reading instrument, the TSI Inc. model 8520 DUSTTRAK aerosol monitor. Both sampling methods were used to determine the PM2.5 exposure in a group of boilermakers exposed to welding fumes and residual fuel oil ash. The geometric mean PM2.5 concentration was 0.30 mg/m3 (GSD 3.25) and 0.31 mg/m3 (GSD 2.90)from the DUSTTRAK and gravimetric method, respectively. The Spearman rank correlation coefficient for the gravimetric and DUSTTRAK PM2.5 concentrations was 0.68. Linear regression models indicated that log, DUSTTRAK PM2.5 concentrations significantly predicted loge gravimetric PM2.5 concentrations (p < 0.01). The association between log(e) DUSTTRAK and log, gravimetric PM2.5 concentrations was found to be modified by surrogate measures for seasonal variation and type of aerosol. PM2.5 measurements from the DUSTTRAK are well correlated and highly predictive of measurements from the gravimetric sampling method for the aerosols in these work environments. However, results from this study suggest that aerosol particle characteristics may affect the relationship between the gravimetric and DUSTTRAK PM2.5 measurements. Recalibration of the DUSTTRAK for the specific aerosol, as recommended by the manufacturer, may be necessary to produce valid measures of airborne particulate matter.     

镇江市大气颗粒物（PM10和PM2.5）对居民每日死亡率影响的时间序列分析

目的评价镇江市大气颗粒物(PM10和PM2.5)短期暴露对居民每日死亡率的影响。方法采用基于广义相加模型的时间序列分析方法评估大气颗粒物对镇江市居民死亡率的影响。结果 PM10和PM2.5对人群死亡影响存在滞后效应和累积滞后效应,对女性和≥65岁人群的影响更为显著。PM10和PM2.5分别在累积滞后1 d和2 d时效应最大,PM10和PM2.5每升高10μg/m3,居民死亡率分别增加0.52%(95%CI:0.10%～0.94%)和0.79%(95%CI:0.14%～1.43%)。结论镇江市大气颗粒物与居民的超额死亡风险显著相关。     

A Bayesian hierarchical approach for relating PM(2.5) exposure to cardiovascular mortality in North Carolina

Considerable attention has been given to the relationship between levels of fine particulate matter (particulate matter < or = 2.5 microm in aerodynamic diameter; PM(2.5) in the atmosphere and health effects in human populations. Since the U.S. Environmental Protection Agency began widespread monitoring of PM(2.5) levels in 1999, the epidemiologic community has performed numerous observational studies modeling mortality and morbidity responses to PM(2.5) levels using Poisson generalized additive models (GAMs). Although these models are useful for relating ambient PM(2.5) levels to mortality, they cannot directly measure the strength of the effect of exposure to PM(2.5) on mortality. In order to assess this effect, we propose a three-stage Bayesian hierarchical model as an alternative to the classical Poisson GAM. Fitting our model to data collected in seven North Carolina counties from 1999 through 2001, we found that an increase in PM(2.5) exposure is linked to increased risk of cardiovascular mortality in the same day and next 2 days. Specifically, a 10- microg/m3 increase in average PM(2.5) exposure is associated with a 2.5% increase in the relative risk of current-day cardiovascular mortality, a 4.0% increase in the relative risk of cardiovascular mortality the next day, and an 11.4% increase in the relative risk of cardiovascular mortality 2 days later. Because of the small sample size of our study, only the third effect was found to have > 95% posterior probability of being > 0. In addition, we compared the results obtained from our model to those obtained by applying frequentist (or classical, repeated sampling-based) and Bayesian versions of the classical Poisson GAM to our study population.     

Particulate air pollution and short-term mortality due to specific causes among the elderly in Madrid (Spain): seasonal differences

A time-series study was conducted to ascertain the short-term effects of different-sized airborne particulate matter (PM) on daily respiratory and cardiovascular cause-specific mortality in winter and summer, among subjects aged over 75 years in Madrid. Poisson regression was used to analyse the time-series, in which the dependent variable was daily mortality due to different specific respiratory and circulatory causes, and the principal independent variables were daily mean PM10, PM2.5 and PM10-2.5 concentrations; other variables: other air pollutants (chemicals, biotic and acoustic), influenza, trend, seasonality and autocorrelation of the series. The results indicated an association between coarser PM fractions (PM10 and PM10-2.5) and respiratory-specific mortality on the one hand, and between PM2.5 and cardiovascular-specific mortality on the other. While the risk of mortality due to exposure to particulate matter was greater in summer than in winter, this difference was statistically significant solely for total organic-cause mortality.