哮喘联盟

   摘要
   流行病学研究表明：相对于非哮喘患儿，哮喘患儿更易受与交通有关的空气污染影响。局部和全身的炎症合并氧化应激被认为是一个可能的敏感因素。我们研究了哮喘状态对空气污染暴露与全身炎症反应（以全血中细胞因子反应作为炎症的标志）的相关性的效应修饰。本研究基于两个德国出生队列研究GINIplus和 LISAplus，且最初设计为哮喘患儿的随机亚样本研究。我们对6岁哮喘患儿（n=27）和非哮喘患儿（n=59）进行研究，检测他们经城市可吸入颗粒物（EHC-93）离体刺激后血中白介素-6（IL）-6、IL-8、IL-10、单核细胞趋化蛋白-1（MCP-1）、肿瘤坏死因子-α（TNF-α）及干扰素γ(IFN-γ)的含量。采用土地利用回归，对儿童家庭住址的空气污染暴露（二氧化氮（NO2）、氮氧化物(NOx)、气体动力学直径＜10μm (PM10)的颗粒物、气体动力学直径＜2.5μm (PM2.5)的颗粒物、粗颗粒物(PMcoarse)和PM2.5吸收率 (PM2.5abs)）造模。采用乘法交互项线性回归模型评估哮喘状态的效应修饰。在哮喘患者中，NO2暴露与高促炎细胞因子产生相关（对于IL-6/2.68µg/m³ NO2，校正后平均比值（MR）为2.22（95%可信区间1.22-4.04））。哮喘状态与NO2暴露之间存在明显的交互作用。NOx、PM10、PM2.5mass 和PM2.5abs暴露与哮喘状态之间也存在相同的趋势。在非哮喘患儿和整个群体中，空气污染和细胞因子反应无相关性。与交通有关的空气污染暴露和哮喘患儿血中高促炎性细胞因子反应相关。
 

（杨冬 审校）
Environ Res. 2015 Mar 10;138:381-390. doi: 10.1016/j.envres.2015.02.034. [Epub ahead of print]

 

Air pollution and cytokine responsiveness in asthmatic and non-asthmatic children.
 

Klümper C1, Krämer U2, Lehmann I3, von Berg A4, Berdel D4, Herberth G3, Beckmann C4, Link E2, Heinrich J5, Hoffmann B6, Schins RP2; GINIplus and LISAplus study groups.
 

ABSTRACt
Epidemiological studies indicate that asthmatic children are more susceptible to traffic-related air pollution exposure than non-asthmatic children. Local and systemic inflammation in combination with oxidative stress have been suggested as a possible susceptibility factor. We investigated effect modification by asthma status for the association between air pollution exposure and systemic effects using whole blood cytokine responsiveness as an inflammatory marker. The study was nested within the two German birth cohort studies GINIplus and LISAplus and initially designed as a random sub-sample enriched with asthmatic children. Using data from 27 asthmatic and 59 non-asthmatic six-year-old children we measured the production of Interleukin-6 (IL)-6, IL-8, IL-10, monocyte chemotactic protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in whole blood after ex-vivo stimulation with urban particulate matter (EHC-93). Air pollution exposure (nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter with an aerodynamic diameter <10μm (PM10), particulate matter with an aerodynamic diameter <2.5μm (PM2.5mass), coarse particulate matter (PMcoarse) and PM2.5absorbance (PM2.5abs)) was modelled for children´s home addresses applying land-use regression. To assess effect modification by asthma status linear regression models with multiplicative interaction terms were used. In asthmatics exposure to NO2 was associated with higher production of pro-inflammatory cytokines: adjusted means ratio (MR) 2.22 (95% confidence interval 1.22-4.04) for IL-6 per 2.68µg/m³ NO2. The interaction term between asthma status and NO2exposure was significant. Results for NOx, PM10, PM2.5mass and PM2.5abs were in the same direction. No association between air pollution and cytokine responsiveness was found in the group of non-asthmatic children and in the overall group. Traffic-related air pollution exposure is associated with higher pro-inflammatory cytokine responsiveness in whole blood of asthmatic children.
 

Environ Res. 2015 Mar 10;138:381-390. doi: 10.1016/j.envres.2015.02.034. [Epub ahead of print]