PM2.5呼吸系统毒性的研究进展

<正>大气颗粒污染物(PM)已经成为人类关注的重要公共问题之一。近年来,随着空气污染的逐渐加重,人类呼吸系统疾病如哮喘、慢性阻塞性肺疾病(COPD)、肺癌等发病率在全国范围内呈上升趋势。PM2.5是大气颗粒污染物的主要组分,可以携带细菌和有毒化学物质进入下呼吸道并不易排出。本文就PM2.5的一般理化性质、PM2.5与呼吸系统疾病的流行病学研究及PM2.5对呼吸系统损伤的相关机制进行综述。     

PM2.5致呼吸系统损伤的机制及药物防治进展

正近年来,随着工业化和城市化进程的加快,大气污染问题日益凸显,其对人类健康的危害已成为广泛共识。PM2.5作为大气污染物中重要的组成部分,直接与呼吸系统接触,可深入包括肺泡在内的各级支气管树,损害呼吸系统功能,引发或加重呼吸系统疾病[1-2]。了解PM2.5对呼吸系统损伤的机制及药物防治,对医学工作者更好地预防和诊疗与PM2.5有关的呼吸系统疾病具有重要意义。一、PM2.5简介1. PM2.5的定义及来源:大气颗粒物(particulate matter,PM)是指空气中分散的固体、液体悬浮物或固液颗粒混合物,PM2.5是指空气动力学当量直径≤2.5μm的大气悬浮颗     

山柰酚改善细颗粒物PM2.5诱导的老龄大鼠肺损伤的作用和机制研究

目的 细颗粒物(PM2.5)被认为与多种呼吸系统问题有关，在老年人群中尤为显著。本研究旨在探索山柰酚是否可以治疗PM2.5诱导的老龄大鼠肺损伤，并探讨其潜在的作用机制。方法 30只雄性Wistar大鼠(16个月龄)被随机分为5组：对照组、PM2.5暴露组和PM2.5暴露+山柰酚低剂量、中剂量和高剂量组。PM2.5暴露持续时间2周后，检测各组大鼠的肺功能、肺形态、炎症程度以及Toll样受体4(TLR4)/核因子-κB(NF-κB)信号通路相关蛋白的表达水平。结果 与对照组相比，PM2.5暴露导致老龄大鼠发生显著的肺损伤，表现为明显的肺功能受损和组织病理学改变，支气管肺泡灌洗液(BALF)中的炎性因子TNF-α和IL-6浓度增加，血液中炎性细胞比例改变，肺组织中TLR4的表达和核转录因子-κB(NF-κB)磷酸化水平增加。山柰酚的治疗则呈剂量依赖性地改善了PM2.5所致肺功能损伤和组织病理学改变，抑制炎性因子分泌和炎症细胞比例失衡，抑制了TLR4/NF-κB信号通路的激活。结论 山柰酚能够对PM2.5暴露引起的老龄大鼠肺损伤产生保护作用，抑制炎症反应和结构损伤，其作用机制可能与抑制TLR4...     

北京市PM2.5污染特性及对老年呼吸系统疾病的影响

目的探讨北京市大气中PM2.5的污染特性及其对老年呼吸系统疾病的影响。方法 2012年2月至2014年2月在北京市人口相对密集的城区设点,对大气中细颗粒污染物PM2.5的浓度、平均气温、最低气温、最高气温等气象资料进行收集,分析PM2.5的污染水平。收集该院呼吸科门诊老年患者就诊率,分析北京市PM2.5污染特性与老年呼吸系统疾病的相关性。结果 1~4月及11、12月(采暖期)PM2.5平均浓度较高,与5~10月(非采暖期)相比差异有统计学意义(P0.05);冬季采暖期PM2.5浓度与日照时长、降水量、最低气温、最高气温、平均温度均呈负相关(r=-0.488、-0.512、-0.565、-0.565、-0.629);PM2.5日均浓度与呼吸系统就诊率呈正相关(r=0.788)。结论北京市采暖期PM2.5日均浓度增大,老年患者呼吸系统疾病发病率升高,二者呈正相关。     

PM2.5暴露对呼吸系统黏液纤毛清除系统的影响

气道黏液纤毛清除系统是呼吸道重要的防御机制之一,在抵御外来微生物和有害刺激入侵中起重要作用.PM25暴露可破坏呼吸系统的防御功能,引起黏液纤毛清除系统损伤,黏液分泌增加及清除功能障碍,导致气道黏液阻塞,参与多种呼吸系统疾病的发生发展.本文就PM2.5暴露对气道黏液纤毛清除系统的影响作一综述.     

吉林市采暖期与非采暖期室外PM2.5浓度状况及对社区老年人呼吸系统疾病的影响

目的了解吉林市采暖期与非采暖期细颗粒物(PM2.5)污染水平与老年人呼吸系统健康的关系。方法 2013年采暖期,选择每年连续居住6个月以上(包含整个冬季)共900名老年人观察呼吸系统疾病情况。结果 2013年吉林市采暖期PM2.5浓度明显高于非采暖期,龙潭区(工业区)>昌邑区(生活区)>丰满区(旅游区)差异有统计学意义(P<0.05);2013年吉林市3个区老年人呼吸系统疾病以呼吸道感染、支气管炎、慢性阻塞性肺病(COPD)为主,采暖期社区老年人呼吸系统疾病患病明显高于非采暖期,龙潭区>昌邑区>丰满区,差异有统计学意义(P<0.05)。结论吉林市采暖期PM2.5污染严重,PM2.5污染水平与老年人呼吸系统健康有直接的关系,应通过多项措施改善空气质量,降低老年人呼吸系统疾病的发生。     

褪黑素对大气细颗粒物（PM 2.5）暴露大鼠肺部炎症反应和氧化应激的影响及其机制研究

目的：探讨褪黑素对大气细颗粒物(PM 2.5)暴露大鼠肺部炎症反应和氧化应激的影响及其机制。方法将48只清洁级 SD 大鼠随机(随机数字法)分成4组：空白对照组、NS 对照组、PM 2.5组及褪黑素(melatonin,MT)组,每组各12只。通过气管向肺内注入 PM 2.5悬液构建大鼠肺组织PM 2.5染毒模型,并通过灌胃溶液,采用肺组织 HE 染色、酶联免疫吸附试验(enzyme linked immunosorbent assay,ELISA)及蛋白印迹等方法分别检测肺组织病理改变,如 TNF-α、IL-6、IL-1、MPO、SOD、MDA 以及 NF-κB p65蛋白表达。结果①与空白对照组及 NS 对照组比较,PM 2.5组大鼠肺组织出现明显损伤改变,MT 组大鼠肺组织损伤较 PM 2.5组明显减轻;②PM 2.5组大鼠肺组织 TNF-α、IL-6、IL-1表达明显增加(P <0.05),MT 组较 PM 2.5组 TNF-α、IL-6、IL-1表达明显下降(P <0.05);③PM 2.5组大鼠肺组织 SOD 表达较空白对照组及 NS 对照组明显下降(P <0.05),而 MPO 及 MDA 表达明显增加(P <0.05),而与 PM 2.5组比较,MT 组大鼠肺组织 SOD 表达增加,MPO 及 MDA 表达下降(P <0.05);④PM 2.5组 p65蛋白表达明显上调(P <0.05),而MT 组较 PM 2.5组 p65蛋白表达明显下降(P <0.05)。结论 PM 2.5能通过介导肺组织炎性反应及氧化应激导致肺组织损伤,且与活化 NF-κB 相关,MT 能显著抑制 PM 2.5所致 NF-κB 活化,减轻炎性反应及氧化应激,改善PM 2.5暴露大鼠肺损伤。     

PM2.5对循环和呼吸系统的影响、相关机制及研究进展

PM2.5严重影响人体健康。本文对PM2.5的来源和其各主要成分所造成的循环、呼吸系统的毒性作用和分子机制等进行概述，为后续的深入研究提供理论参考。     

PM2.5对心血管疾病影响的研究进展

PM2.5指环境空气中空气动力学直径≤2.5 μm的颗粒物(particulate matter，PM)。众多研究从不同方面将PM2.5中气体或金属成分与冠心病（Coronary heart disease ，CHD）、高血压（High blood pressure，HBP）、心力衰竭（Heart failure，HF）、心律失常等心血管疾病联系起来。潜在机制为：氧化应激、炎症反应、出凝血系统异常、自主神经系统紊乱、血管内皮细胞损伤、动脉粥样硬化或表观遗传学改变等。本文将从流行病学、作用机制、表观遗传学和预防策略这几个方面综述PM2.5对心血管疾病影响的研究进展。     

番茄红素解除PM2.5暴露内皮细胞的氧化损伤

目的探讨番茄红素对PM2.5暴露内皮细胞氧化损伤的分子机制。方法利用CCK-8明确番茄红素减轻PM2.5暴露内皮细胞损伤的最适宜浓度;检测细胞丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性,评估番茄红素解除PM2.5对内皮细胞氧化损伤的作用;Western印迹检测细胞内缺氧诱导因子(HIF)-1α表达;q-PCR、ELISA检测细胞白介素(IL)-6表达水平。结果解除因PM2.5暴露造成氧化损伤的最佳番茄红素浓度为80μg/ml;番茄红素作用使PM2.5暴露内皮细胞氧化应激指标SOD活性升高48.04%,MDA含量下降38.89%,IL-6、HIF-1α恢复到正常细胞水平。结论番茄红素具有解除PM2.5暴露内皮细胞氧化损伤的作用。     

The impact of PM2.5 on the human respiratory system

Recently, many researchers paid more attentions to the association between air pollution and respiratory system disease. In the past few years, levels of smog have increased throughout China resulting in the deterioration of air quality, raising worldwide concerns. PM2.5 (particles less than 2.5 micrometers in diameter) can penetrate deeply into the lung, irritate and corrode the alveolar wall, and consequently impair lung function. Hence it is important to investigate the impact of PM2.5 on the respiratory system and then to help China combat the current air pollution problems. In this review, we will discuss PM2.5 damage on human respiratory system from epidemiological, experimental and mechanism studies. At last, we recommend to the population to limit exposure to air pollution and call to the authorities to create an index of pollution related to health.     

Approaches to prevent the patients with chronic airway diseases from exacerbation in the haze weather

Haze weather is becoming one of the biggest problems in many big cities in China. It triggers both public anxiety and official concerns. Particulate matter (PM) plays the most important role in causing the adverse health effects. Chemical composition of PM2.5 includes primary particles and secondary particles. The toxicological mechanisms of PM2.5 to the human body include the oxidative stress, inflammation and carcinogenesis. Short or long-term exposure to PM (especially PM2.5) can cause a series of symptoms including respiratory symptoms such as cough, wheezing and dyspnea as well as other symptoms. There are positive associations between PM2.5 and mortality due to a number of causes. PM2.5 is considered to contribute to the onset of asthma, the exacerbation of chronic obstructive pulmonary disease (COPD) in haze weather. Some approaches including outdoor health care, indoor health care and preventive medications can prevent the patients with chronic airway diseases from exacerbations.     

PM2．5与肺癌

流行病学研究显示,PM2．5对呼吸、心血管、生殖系统疾病的发病和死亡有着重要影响。近期国际癌症研究机构把大气污染确认定为致癌物,其重要组成部分大气细颗粒物（PM2．5）对人群健康致癌性研究日益受到关注,综述介绍有关国内外对大气中细颗粒物PM2．5与肺癌的研究状况。     

Epidemiological evidence of effects of coarse airborne particles on health.

Studies on health effects of airborne particulate matter (PM) have traditionally focused on particles <10 microm in diameter (PM10) or particles <2.5 microm in diameter (PM2.5). The coarse fraction of PM10, particles >2.5 microm, has only been studied recently. These particles have different sources and composition compared with PM2.5. This paper is based on a systematic review of studies that have analysed fine and coarse PM jointly and examines the epidemiological evidence for effects of coarse particles on health. Time series studies relating ambient PM to mortality have in some places provided evidence of an independent effect of coarse PM on daily mortality, but in most urban areas, the evidence is stronger for fine particles. The few long-term studies of effects of coarse PM on survival do not provide any evidence of association. In studies of chronic obstructive pulmonary disease, asthma and respiratory admissions, coarse PM has a stronger or as strong short-term effect as fine PM, suggesting that coarse PM may lead to adverse responses in the lungs triggering processes leading to hospital admissions. There is also support for an association between coarse PM and cardiovascular admissions. It is concluded that special consideration should be given to studying and regulating coarse particles separately from fine particles.     

石家庄市空气污染与儿科呼吸系统疾病住院率的相关性研究

目的 研究石家庄市空气污染与儿科呼吸系统疾病(哮喘发作、喘息性支气管炎、肺炎)住院率的相关性.方法 连续记录河北省石家庄市2016年1月至2017年1月空气质量检测数据,并收集同期河北省儿童医院哮喘发作、喘息性支气管炎及肺炎住院率,结合同期环境监测资料,进行直线相关回归分析,分析大气污染物对儿科呼吸系统疾病住院率的影响.结果 喘息性支气管炎住院率与大气中SO2和NO2月平均浓度呈中度正相关(r=0.598、0.626,均P<0.05),喘息性支气管炎住院率与PM10、CO、PM2.5和O3均无直线相关关系;肺炎住院率与SO2、NO2、PM10、CO和PM2.5月平均浓度均呈高度正相关(r=0.867、0.811、0.825、0.931和0.860,均P<0.05),与O3月平均浓度无直线相关关系.污染物浓度每增加10单位,喘息性支气管炎住院率增加0.1%,肺炎住院率增加2.4%.结论 石家庄市大气污染物PM10、PM2.5、NO2、SO2和CO污染对儿童呼吸系统造成一定的损伤,并导致相应疾病住院率的增加.     

Modulating effects of maternal fish consumption on the occurrence of respiratory symptoms in early infancy attributed to prenatal exposure to fine particles

The purpose of the study was to test the hypothesis whether infants with higher prenatal exposure to fine particles (PM(2.5)) are at greater risk of developing respiratory symptoms and whether fish consumption in pregnancy may modulate the effect. The study was carried out in a cohort of 465 newborns in Krakow (Poland) who have been followed over the first 2 years of life and for whom data on the occurrence of respiratory symptoms and measurements of personal air monitoring in the second trimester of pregnancy were available. The incidence risk ratio (IRR) of respiratory symptoms due to prenatal PM(2.5) exposure were adjusted for potential confounders (gender of child, breastfeeding, parity, maternal atopy, maternal education as a proxy for the socio-economic status, exposure to postnatal environmental tobacco smoke (ETS), and moulds in households) in the generalized estimating equations (GEE) statistical models. The adjusted risk of coughing was associated significantly with PM(2.5) level (IRR = 2.51; 95% CI: 1.77-3.58), moulds in the household, parity, maternal atopy and postnatal ETS, but was lower in girls, and in infants whose mothers consumed more fish in pregnancy (IRR = 0.85; 95% CI: 0.79-0.91). The risk of wheezing was also correlated significantly with the prenatal exposure to PM(2.5) (IRR = 1.36; 95% CI: 1.29-1.43) but also with the presence of moulds in homes, parity, maternal atopy and postnatal ETS. The occurrence of wheezing was associated inversely with the gender of child, gestational age, and fish consumption in pregnancy (IRR = 0.97; 95% CI: 0.95-0.99). Similarly, the risk of difficult (puffy) breathing increased with prenatal exposure to PM(2.5) (IRR = 1.18; 95% CI: 1.12-1.25) moulds, maternal atopy, and parity. The symptom occurrence was lower in girls and associated inversely with the gestational age, and fish consumption in pregnancy (IRR = 0.94; 95% CI: 0.92-0.97). The results of the study support the hypothesis that fish consumption in pregnancy may mitigate the harmful effect of prenatal or perinatal exposure to components of PM(2.5) resulting in an increased burden of respiratory infections among infants.     

机动车尾气污染物对咳嗽的影响

机动车排放尾气对室外大气污染的贡献率逐年增加,其与呼吸系统疾病的关系已有大量的研究报道,例如机动车来源的PM25、NO2、CO、SO2等浓度的升高可增加呼吸系统疾病的病死率,并引起慢性气道疾病患病率的增加.此外,越来越多的流行病学研究表明,机动车尾气污染与儿童、青少年呼吸系统症状,例如咳嗽、咳痰、喘息的发生密切相关.本文主要综述机动车污染物(PM2.5、CO、NOx以及SO2)对咳嗽症状的流行病学研究,并总结潜在的致病机制.     

Fine particulate air pollution, resuspended road dust and respiratory health among symptomatic children.

The short-term association of particulate air pollution with peak expiratory flow rate (PEF) and respiratory symptoms was examined. Forty-nine children with chronic respiratory symptoms aged 8-13 yrs were followed daily for six weeks in spring, 1995, in Kuopio, Finland. Daily concentrations of particulate material with a 50% cut-off aerodynamic diameter < or = 10 microm and < or = 2.5 microm (PM10 and PM2.5, respectively), black carbon, and the number concentrations of particles from 0.01-10 microm diameter were measured. During the study period, PM10 were mainly resuspended soil and street dust, and the concentration was estimated using aluminum content of PM10 samples. No consistent effect of particles was found as the associations varied by lag. Of the lags examined, only 1-day lagged PM2.5 was statistically significantly associated with morning PEF (beta=-1.06, SE=0.52 (per interquartile increase in pollutant)). Evening PEF was significantly associated with the 1-day lagged number of particles in the size range 0.1-1.0 microm (beta=-1.56, SE=0.72). One-day lagged PM10, PM2.5-10, PM2.5 and resuspended PM10, and 4-day average of PM2.5 were significantly associated with increased risk of cough. Given the short duration of the study, separating the effects of different types of particles was difficult. The present study demonstrates the highly variable size and number distribution and chemical composition of particles in Finland, and underlines the importance of measuring the size and chemical composition of particles to determine which types of particles are associated with health effects.