Evidences that oxidative stress plays a role in the associations between outdoor air pollution and asthma are growing. We aimed to study the role of plasma fluorescent oxidation products levels (FlOPs; an oxidative stress-related biomarker), as potential mediators, in the associations between outdoor air pollution and persistent asthma. Analyses were conducted in 204 adult asthmatics followed up in the French case-control and family study on asthma (EGEA; the Epidemiological study of the Genetic and Environmental factors of Asthma). Persistent asthma was defined as having current asthma at EGEA2 (baseline, 2003–2007) and EGEA3 (follow-up, 2011–2013). Exposures to nitrogen dioxide, nitrogen oxides, road traffic, particulate matter with a diameter ≤ 10 μm (PM10) and ≤ 2.5 μm were estimated by ESCAPE models (2009–2010), and ozone (O3) by IFEN models (2004). We used a mediation analysis to assess the mediated effect by FlOPs levels and the interaction between FlOPs levels and air pollution. FlOPs levels increased with PM10 and O3 (adjusted β = 0.04 (95%CI 0.001–0.08), aβ = 0.04 (95%CI 0.009–0.07) per 10 μg/m3, respectively), and the risk of persistent asthma increased with FlOPs levels (aOR = 1.81 (95%CI 1.08–3.02)). The risk of persistent asthma decreased with exposures to NO2, NOx and PM2.5 (aOR ranging from 0.62 to 0.94), and increased with exposures to PM10, O3, O3-summer and road traffic, the greater effect being observed for O3 (aOR = 1.78, 95% CI 0.73–4.37, per 10 μg/m3). Using mediation analysis, we observed a positive total effect (aOR = 2.16, 95%CI 0.70–11.9), a positive direct effect of O3 on persistent asthma (OR = 1.68, 95%CI 0.57–7.25), and a positive indirect effect mediated by FIOPs levels (aOR = 1.28 (95%CI 1.01–2.29)) accounting for 41% of the total effect. Our results add insights on the role of oxidative stress in the association between air pollution and persistent asthma.

中文翻译：

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氧化应激是否在成年人的室外空气污染与持续哮喘之间的关联中起作用？EGEA研究的结果

氧化应激在室外空气污染与哮喘之间的关系中起作用的证据正在增加。我们旨在研究血浆荧光氧化产物水平（FlOPs；与氧化应激相关的生物标志物）在室外空气污染与持续性哮喘之间的潜在介导作用。在法国的病例对照和哮喘家族研究（EGEA；哮喘的遗传和环境因素的流行病学研究）中对204名成人哮喘患者进行了分析。持续性哮喘的定义为目前处于EGEA2（基线，2003-2007）和EGEA3（后续，2011-2013）的哮喘。通过ESCAPE模型（2009-2010年）估算了二氧化氮，氮氧化物，道路交通，直径≤10μm（PM10）和≤2.5μm的颗粒物的暴露，和IFEN模型（2004年）中的臭氧（O3）。我们使用中介分析来评估FlOPs水平以及FlOPs水平与空气污染之间的相互作用所产生的介导作用。FlOPs水平随着PM10和O3的升高而升高（分别每10μg/ m3调整β= 0.04（95％CI 0.001-0.08），aβ= 0.04（95％CI 0.009-0.07）），并且FlOPs增加了持续性哮喘的风险水平（aOR = 1.81（95％CI 1.08–3.02））。持续性哮喘的风险随着暴露于NO2，NOx和PM2.5（aOR为0.62至0.94）而降低，并且随着暴露于PM10，O3，O3夏季和道路交通而增加，对于O3（aOR）观察到更大的影响= 1.78，95％CI 0.73–4.37，每10μg/ m3）。使用中介分析，我们观察到总的积极效果（aOR = 2.16，95％CI 0.70–11.9），O3对持续性哮喘的正面直接效果（OR = 1.68，95％CI 0.57–7.25），FIOPs水平介导的积极间接影响（aOR = 1.28（95％CI 1.01–2.29））占总影响的41％。我们的研究结果增加了氧化应激在空气污染与持续性哮喘之间的关系中的作用的见解。