细颗粒物对呼吸系统疾病的影响

大城市阴霾天气的频频出现,引起社会对其罪魁祸首——细颗粒物(即PM2.5)的广泛关注。PM2.5对健康的影响成为人们普遍担忧的问题。本文综述了PM2.5与呼吸系统疾病关系的流行病学研究进展。结果显示,短期暴露于较高浓度的PM2.5与哮喘急诊就诊率、慢性阻塞性肺病(COPD)患者急性加重住院率、肺炎急诊住院率的上升及COPD日死亡风险的增加均有关;长期暴露于较高浓度的PM2.5与肺癌及肺炎死亡风险增加、肺腺癌和哮喘发病风险增加有关。上述研究结果大部分来自西方发达国家,提示了我国有效控制PM2.5浓度及开展更多关于PM2.5流行病学研究的必要性和紧迫性。     

长沙市PM10与脑卒中急诊关系的病例交叉研究

目的:探讨长沙市大气可吸入颗粒物(PM10)与脑卒中急诊的相关性。方法:收集2008-2009年间长沙市每日脑出血和脑梗死急诊数据,同期收集长沙市大气可吸入颗粒物(PM10)及相关气象数据,利用季节分层的单向回顾性1:1配对病例交叉研究设计,建立单污染物模型和多污染物模型进行分析。结果:在调整气温和相对湿度的单污染物滞后模型中,秋季滞后0、1、2天的PM10日均浓度每增加10μg/m3,与脑出血和脑梗死的的OR(95%CI)值分别为0.953(0.871-1.042)和0.970(0.910-1.034)、0.984(0.913-1.061)和0.965(0.902-1.031)、0.996(0.928-1.069)和0.964(0.904-1.029),关联具有统计学意义(P0.05)。结论:长沙市PM10浓度变化对脑卒中发病有影响。     

室内生物燃料烟雾颗粒物污染与呼吸系统疾病的关系

本文综述了国内外室内生物燃料烟雾颗粒物污染源的种类,烟雾中有害物质的种类及其与呼吸系统疾病的关系,并以慢性阻塞性肺病作为案例阐述了其发病的病因,为制定该类由生物燃料烟雾颗粒诱发的疾病的预防策略提供参考.     

虫草对肺部疾病治疗的研究进展

肺纤维化、慢性阻塞性肺病和哮喘是人类主要的呼吸系统疾病,它们均以肺部或呼吸道的慢性炎症为特征,当前的治疗方法尚不理想并伴随着很多的副作用,人们迫切需要一种更安全的替代疗法。冬虫夏草是我国传统的名贵药用真菌,被广泛用来治疗多种肺部疾病。近年来,冬虫夏草对肺部疾病治疗作用的研究取得了较大进展,本文综述了冬虫夏草、其无性型中国被毛孢(Hirsutella sinensis或Ophicordyceps sinensis)和其他相关虫草及其提取物对肺纤维化、慢性阻塞性肺病、哮喘等肺部疾病治疗作用的研究进展,并介绍了其作用机制的研究成果。     

大气细颗粒污染物 PM2.5 浓度及对肺上皮细胞炎性因子的影响

目的:研究大气细颗粒污染物(PM2.5)浓度及对肺上皮细胞(A549细胞)炎性因子的影响。方法:测定2013年1月至2013年12月北京市某城区PM2.5浓度,比较不同PM2.5浓度对A549细胞炎性因子IL-6、TNF-α表达水平的影响。结果:北京市细颗粒污染物PM2.5日均值春季、夏季、秋季、冬季分别为174.3μg/m3、143.5μg/m3、166.7μg/m3、189.6μg/m3,四季超标率差异无统计学意义(P>0.05);大气细颗粒污染物PM2.5对肺上皮细胞IL-6、TNF-α的影响,春季、夏季、秋季、冬季四季之间差异无统计学意义(P>0.05);随着PM2.5浓度升高IL-6、TNF-α表达水平升高,差异有统计学意义(P<0.05);随着染毒时间延长IL-6、TNF-α表达水平升高,差异有统计学意义(P<0.05)。结论:大气细颗粒污染物浓度升高会使肺上皮细胞炎性因子表达增强。     

兰州市西固区大气污染对呼吸系统的健康效应

大气污染极易诱发各类呼吸系统疾病,对人体健康造成严重损害。运用Poisson回归的时间序列广义相加模型(GAM)和人群分层的分析方法,探究了2014—2018年兰州市西固区大气污染对呼吸系统的健康效应。结果表明：(1)PM_2.5、PM₁₀、SO₂、NO₂、O₃8h和CO对呼吸系统疾病的发生存在滞后效应,其浓度每升高10μg/m~3(CO升高1 mg/m~3),在最佳滞后天数,疾病住院量分别增加1.06%、1.04%、1.10%、1.07%、0.97%和3.83%,气态污染物(SO₂和NO₂)暴露是诱发呼吸系统疾病的重要风险因素;(2)PM_2.5、PM₁₀、SO₂和NO₂对肺炎的影响最大,且对女性健康的危害稍高于男性,O₃8h对慢性阻塞性肺病的影响最大,且对男性患病的影响稍高于女性;(3)0—14岁儿童是呼吸系统疾病的易感人群,...     

PM2.5对呼吸系统的影响及其作用机制的研究

现如今PM_2.5已成为我国主要的大气污染物,它会导致各种呼吸系统疾病的发生。PM_2.5是粒径小于2.5 μm的细颗粒物,可以携带多种有毒物质。PM_2.5与其他颗粒物相比,体积较小,表面积较大,更容易进入人体,对人体健康造成危害,其中呼吸系统首当其冲。许多流行病学证据表明PM_2.5与呼吸系统疾病密切相关,在体内和体外均证实了细颗粒物对呼吸系统的损伤。而PM_2.5对呼吸系统的毒性机制是国内外专家和学者研究的重点,主要包括氧化应激、炎性损伤、细胞内钙稳态失衡、免疫细胞功能不全和功能障碍、致突变性、微生态学改变、气道上皮防御功能缺陷等。本文综述了PM_2.5的定义、特征和对呼吸系统的影响及毒性机制。     

探究老年慢性喘息性支气管炎的预后因素

近年来,患有慢性阻塞性肺病的人数逐渐增加。然而医务人员在临床这段治疗的过程中发现,老年慢性喘息性支气管炎患者,并没有引发呼吸系统衰竭的现象,但是其但预后的状况却极为不佳,所以仅仅依靠分析患者的血气指标还不能预后。针对这一问题,重点研究老年慢性喘息性支气管炎的预后因素,以期为相关治疗提供借鉴。     

慢性阻塞性肺病动物模型的研究进展

慢性阻塞性肺病(COPD)是一种严重的呼吸系统疾病,该病主要包括慢性肺气肿及慢性支气管炎,其发病率、死亡率高,医疗负担重。由于其发病机制、临床发展过程较为复杂,对COPD诊断、治疗的研究工作进展仍然相当缓慢。目前,国内外研究人员通过建立COPD动物模型对该病进行了大量研究工作。旨在对COPD动物模型的建立及评价方法进行总结,并对模型动物选择,评价方法的选择提出一点新的思路。     

职业性肺部疾病

职业性肺部疾病种类繁多,涉及学科较广,是职业医学和肺病学研究的重要课题。常见的职业性肺部疾病可分为5类:尘肺;非特异性气道疾病与过敏性肺炎;吸入有毒气体所引起的急、慢性呼吸系统损伤;棉尘病及职业性哮喘。现分述如下:     

How air pollution influences clinical management of respiratory diseases. A case-crossover study in Milan

Background

Environmental pollution is a known risk factor for multiple diseases and furthermore increases rate of hospitalisations. We investigated the correlation between emergency room admissions (ERAs) of the general population for respiratory diseases and the environmental pollutant levels in Milan, a metropolis in northern Italy.

Methods

We collected data from 45770 ERAs for respiratory diseases. A time-stratified case-crossover design was used to investigate the association between air pollution levels and ERAs for acute respiratory conditions. The effects of air pollutants were investigated at lag 0 to lag 5, lag 0–2 and lag 3–5 in both single and multi-pollutant models, adjusted for daily weather variables.

Results

An increase in ozone (O₃) levels at lag 3–5 was associated with a 78% increase in the number of ERAs for asthma, especially during the warm season. Exposure to carbon monoxide (CO) proved to be a risk factor for pneumonia at lag 0–2 and in the warm season increased the risk of ERA by 66%. A significant association was found between ERAs for COPD exacerbation and levels of sulphur dioxide (SO₂), CO, nitrate dioxide (NO₂), and particulate matter (PM₁₀ and PM_2.5). The multipollutant model that includes all pollutants showed a significant association between CO (26%) and ERA for upper respiratory tract diseases at lag 0–2. For chronic obstructive pulmonary disease (COPD) exacerbations, only CO (OR 1.19) showed a significant association.

Conclusions

Exposure to environmental pollution, even at typical low levels, can increase the risk of ERA for acute respiratory diseases and exacerbation of obstructive lung diseases in the general population.     

Fine Particulate Air Pollution and Hospital Emergency Room Visits for Respiratory Disease in Urban Areas in Beijing,China, in 2013

BackgroundHeavy fine particulate matter (PM_2.5) air pollution occurs frequently in China. However, epidemiological research on the association between short-term exposure to PM_2.5 pollution and respiratory disease morbidity is still limited. This study aimed to explore the association between PM_2.5 pollution and hospital emergency room visits (ERV) for total and cause-specific respiratory diseases in urban areas in Beijing.MethodsDaily counts of respiratory ERV from Jan 1 to Dec 31, 2013, were obtained from ten general hospitals located in urban areas in Beijing. Concurrently, data on PM_2.5 were collected from the Beijing Environmental Protection Bureau, including 17 ambient air quality monitoring stations. A generalized-additive model was used to explore the respiratory effects of PM_2.5, after controlling for confounding variables. Subgroup analyses were also conducted by age and gender.ResultsA total of 92,464 respiratory emergency visits were recorded during the study period. The mean daily PM_2.5 concentration was 102.1±73.6 μg/m³. Every 10 μg/m³ increase in PM_2.5 concentration at lag₀ was associated with an increase in ERV, as follows: 0.23% for total respiratory disease (95% confidence interval [CI]: 0.11%-0.34%), 0.19% for upper respiratory tract infection (URTI) (95%CI: 0.04%-0.35%), 0.34% for lower respiratory tract infection (LRTI) (95%CI: 0.14%-0.53%) and 1.46% for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) (95%CI: 0.13%-2.79%). The strongest association was identified between AECOPD and PM_2.5 concentration at lag_0-3 (3.15%, 95%CI: 1.39%-4.91%). The estimated effects were robust after adjusting for SO₂, O₃, CO and NO₂. Females and people 60 years of age and older demonstrated a higher risk of respiratory disease after PM_2.5 exposure.ConclusionPM_2.5 was significantly associated with respiratory ERV, particularly for URTI, LRTI and AECOPD in Beijing. The susceptibility to PM_2.5 pollution varied by gender and age.     

Long-range ozone transport and its impact on respiratory and cardiovascular health in the north of Portugal

Ozone dynamics depend on meteorological characteristics such as wind, radiation, sunshine, air temperature and precipitation. The aim of this study was to determine ozone trajectories along the northern coast of Portugal during the summer months of 2005, when there was a spate of forest fires in the region, evaluating their impact on respiratory and cardiovascular health in the greater metropolitan area of Porto. We investigated the following diseases, as coded in the ninth revision of the International Classification of Diseases: hypertensive disease (codes 401–405); ischemic heart disease (codes 410–414); other cardiac diseases, including heart failure (codes 426–428); chronic obstructive pulmonary disease and allied conditions, including bronchitis and asthma (codes 490–496); and pneumoconiosis and other lung diseases due to external agents (codes 500–507). We evaluated ozone data from air quality monitoring stations in the study area, together with data collected through HYbrid Single-Particle Lagrangian Integrated Trajectory (HYSPLIT) model analysis of air mass circulation and synoptic-scale zonal wind from National Centers for Environmental Prediction data. High ozone levels in rural areas were attributed to the dispersion of pollutants induced by local circulation, as well as by mesoscale and synoptic scale processes. The fires of 2005 increased the levels of pollutants resulting from the direct emission of gases and particles into the atmosphere, especially when there were incoming frontal systems. For the meteorological case studies analyzed, peaks in ozone concentration were positively associated with higher rates of hospital admissions for cardiovascular diseases, although there were no significant associations between ozone peaks and admissions for respiratory diseases.     

Serum angiotensin converting enzyme values in chronic obstructive pulmonary disease

Angiotensin converting enzyme (ACE) is stored in the endothelium. Its activity depends--among others--on the O2-concentration of the blood. Aim of the study was to examine the serum ACE values in chronic obstructive lung diseases (bronchial asthma, chronic bronchitis, lung fibrosis etc.). At the time of blood sampling, blood-gas tensions and respiratory function parameters of the patients were also determined. On the basis of the blood-gas parameters and SACE x + SD and x--SD values, obtained from the normoxic-normocapnic group, the patients could be divided into sub-groups. In contrast to data in the literature increased enzyme levels in response to hypoxia could be found only in patients suffering from a pulmonary disease associated with severe tissue damage.     

Diesel Exhaust Particle Exposure In Vitro Alters Monocyte Differentiation and Function

Air pollution by diesel exhaust particles is associated with elevated mortality and increased hospital admissions in individuals with respiratory diseases such as asthma and chronic obstructive pulmonary disease. During active inflammation monocytes are recruited to the airways and can replace resident alveolar macrophages. We therefore investigated whether chronic fourteen day exposure to low concentrations of diesel exhaust particles can alter the phenotype and function of monocytes from healthy individuals and those with chronic obstructive pulmonary disease. Monocytes were purified from the blood of healthy individuals and people with a diagnosis of chronic obstructive pulmonary disease. Monocyte-derived macrophages were generated in the presence or absence of diesel exhaust particles and their phenotypes studied through investigation of their lifespan, cytokine generation in response to Toll like receptor agonists and heat killed bacteria, and expression of surface markers. Chronic fourteen day exposure of monocyte-derived macrophages to concentrations of diesel exhaust particles >10 µg/ml caused mitochondrial and lysosomal dysfunction, and a gradual loss of cells over time both in healthy and chronic obstructive pulmonary disease individuals. Chronic exposure to lower concentrations of diesel exhaust particles impaired CXCL8 cytokine responses to lipopolysaccharide and heat killed E. coli, and this phenotype was associated with a reduction in CD14 and CD11b expression. Chronic diesel exhaust particle exposure may therefore alter both numbers and function of lung macrophages differentiating from locally recruited monocytes in the lungs of healthy people and patients with chronic obstructive pulmonary disease.     

A Modeling-Derived Hypothesis on Chronicity in Respiratory Diseases: Desensitized Pathogen Recognition Secondary to Hyperactive IRAK/TRAF6 Signaling

Several chronic respiratory diseases exhibit hyperactive immune responses in the lung: abundant inflammatory mediators; infiltrating neutrophils, macrophages, lymphocytes and other immune cells; and increased level of proteases. Such diseases include cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD) and severe/neutrophilic asthma. Paradoxically, patients with these diseases are also susceptible to detrimental bacterial infection and colonization. In this paper, we seek to explain how a positive feedback mechanism via IL-8 could lead to desensitization of epithelial cells to pathogen recognition thus perpetuating bacterial colonization and chronic disease states in the lung. Such insight was obtained from mathematical modeling of the IRAK/TRAF6 signaling module, and is consistent with existing clinical evidence. The potential implications for targeted treatment regimes for these persistent respiratory diseases are explored.     

Pulmonary function and incident bronchitis and asthma in children: a community-based prospective cohort study

Background

Previous studies revealed that reduction of airway caliber in infancy might increase the risks for wheezing and asthma. However, the evidence for the predictive effects of pulmonary function on respiratory health in children was still inconsistent.

Methods

We conducted a population-based prospective cohort study among children in 14 Taiwanese communities. There were 3,160 children completed pulmonary function tests in 2007 and follow-up questionnaire in 2009. Poisson regression models were performed to estimate the effect of pulmonary function on the development of bronchitis and asthma.

Results

After adjustment for potential confounders, pulmonary function indices consistently showed protective effects on respiratory diseases in children. The incidence rate ratios of bronchitis and asthma were 0.86 (95% CI 0.79–0.95) and 0.91 (95% CI 0.82–0.99) for forced expiratory volume in 1 second (FEV₁). Similar adverse effects of maximal mid-expiratory flow (MMEF) were also observed on bronchitis (RR = 0.73, 95% CI 0.67–0.81) and asthma (RR = 0.85, 95% CI 0.77–0.93). We found significant decreasing trends in categorized FEV₁ (p for trend = 0.02) and categories of MMEF (p for trend = 0.01) for incident bronchitis. Significant modification effects of traffic-related air pollution were noted for FEV₁ and MMEF on bronchitis and also for MMEF on asthma.

Conclusions

Children with high pulmonary function would have lower risks on the development of bronchitis and asthma. The protective effect of high pulmonary function would be modified by traffic-related air pollution exposure.     

Vanadium pentoxide (V(2)O(5)) induced mucin production by airway epithelium

Exposure to environmental pollutants has been linked to various airway diseases and disease exacerbations. Almost all chronic airway diseases such as chronic obstructive pulmonary disease and asthma are caused by complicated interactions between gene and environment. One of the major hallmarks of those diseases is airway mucus overproduction (MO). Excessive mucus causes airway obstruction and significantly increases morbidity and mortality. Metals are major components of environmental particulate matters (PM). Among them, vanadium has been suggested to play an important role in PM-induced mucin production. Vanadium pentoxide (V(2)O(5)) is the most common commercial source of vanadium, and it has been associated with occupational chronic bronchitis and asthma, both of which are MO diseases. However, the underlying mechanism is not entirely clear. In this study, we used both in vitro and in vivo models to demonstrate the robust inductions of mucin production by V(2)O(5). Furthermore, the follow-up mechanistic study revealed a novel v-raf-1 murine leukemia viral oncogene homolog 1-IKK-NF-κB pathway that mediated V(2)O(5)-induced mucin production. Most interestingly, the reactive oxygen species and the classical mucin-inducing epidermal growth factor receptor (EGFR)-MAPK pathway appeared not to be involved in this process. Thus the V(2)O(5)-induced mucin production may represent a novel EGFR-MAPK-independent and environmental toxicant-associated MO model. Complete elucidation of the signaling pathway in this model will not only facilitate the development of the treatment for V(2)O(5)-associated occupational diseases but also advance our understanding on the EGFR-independent mucin production in other chronic airway diseases.     

Microbiota: A Missing Link in The Pathogenesis of Chronic Lung Inflammatory Diseases

Chronic respiratory diseases account for high morbidity and mortality, with asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) being the most prevalent globally. Even though the diseases increase in prevalence, the exact underlying mechanisms have still not been fully understood. Despite their differences in nature, pathophysiologies, and clinical phenotypes, a growing body of evidence indicates that the presence of lung microbiota can shape the pathogenic processes underlying chronic inflammation, typically observed in the course of the diseases. Therefore, the characterization of the lung microbiota may shed new light on the pathogenesis of these diseases. Specifically, in chronic respiratory tract diseases, the human microbiota may contribute to the disease’s development and severity. The present review explores the role of the microbiota in the area of chronic pulmonary diseases, especially COPD, asthma, and CF.     

Air pollution and the lung: epidemiological approach

Epidemiological evidence has concurred with clinical and experimental evidence to correlate current levels of ambient air pollution, both indoors and outdoors, with respiratory effects. In this respect, the use of specific epidemiological methods has been crucial. Common outdoor pollutants are particulate matter, nitrogen dioxide, carbon monoxide, volatile organic compounds and ozone. Short-term effects of outdoor air pollution include changes in lung function, respiratory symptoms and mortality due to respiratory causes. Increase in the use of health care resources has also been associated with short-term effects of air pollution. Long-term effects of cumulated exposure to urban air pollution include lung growth impairment, chronic obstructive pulmonary disease (COPD), lung cancer, and probably the development of asthma and allergies. Lung cancer and COPD have been related to a shorter life expectancy. Common indoor pollutants are environmental tobacco smoke, particulate matter, nitrogen dioxide, carbon monoxide, volatile organic compounds and biological allergens. Concentrations of these pollutants can be many times higher indoors than outdoors. Indoor air pollution may increase the risk of irritation phenomena, allergic sensitisation, acute and chronic respiratory disorders and lung function impairment. Recent conservative estimates have shown that 1.5-2 million deaths per year worldwide could be attributed to indoor air pollution. Further epidemiological research is necessary to better evaluate the respiratory health effects of air pollution and to implement protective programmes for public health.