目的:气道炎症是对许多类型的环境暴露的常见生物学反应,可导致呼出气中一氧化氮(NO)浓度升高。近年来,多项研究使用呼出气一氧化氮(FeNO)作为暴露于一系列空气污染物的生物标志物来评估气道炎症.本系统综述旨在总结收集个人水平空气污染数据的研究,以评估空气污染引起的FeNO反应,并确定利用个人水平数据是否可以改善空气污染暴露与FeNO之间关系的表征。
结果:确定了36项符合条件的研究。总的来说,这篇综述中包含的研究表明,增加个人对颗粒物和气态空气污染物的暴露可以显着增加FeNO。12项研究中有9项报告说,随着个人PM2.5暴露的增加,FeNO增加具有统计学意义。和高达11.5%的增加在FeNO每IQR的暴露也已报告在FeNO和暴露于气相污染物之间,如臭氧,NO2和苯。此外,慢性呼吸系统疾病等因素,过敏,发现药物使用是空气污染引起的FeNO反应的作用调节剂。大约一半的研究比较了使用个人和环境空气污染暴露方法的效果估计,报告说只有个人暴露与FeNO反应产生了显着关联。来自审查的研究的证据证实FeNO是空气污染物引起的气道炎症的敏感生物标志物。建议进行个人空气污染暴露评估,以准确评估空气污染引起的FeNO反应。此外,对潜在混杂因素的全面调整,包括共污染物的个人暴露,呼吸系统疾病状态,过敏状态,建议在评估空气污染引起的FeNO反应时使用哮喘和过敏药物。
Airway inflammation is a common biological response to many types of environmental exposures and can lead to increased nitric oxide (NO) concentrations in exhaled breath. In recent years, several studies have evaluated airway inflammation using fractional exhaled nitric oxide (FeNO) as a biomarker of exposures to a range of air pollutants. This systematic
review aims to summarize the studies that collected personal-level air pollution data to assess the air pollution-induced FeNO responses and to determine if utilizing personal-level data resulted in an improved characterization of the relationship between air pollution exposures and FeNO compared to using only ambient air pollution exposure data.
Thirty-six eligible studies were identified. Overall, the studies included in this
review establish that an increase in personal exposure to particulate and gaseous air pollutants can significantly increase FeNO. Nine out of the 12 studies reported statistically significant FeNO increases with increasing personal PM2.5 exposures, and up to 11.5% increase in FeNO per IQR increase in exposure has also been reported between FeNO and exposure to gas-phase pollutants, such as ozone, NO2, and benzene. Furthermore, factors such as chronic respiratory diseases, allergies, and medication use were found to be effect modifiers for air pollution-induced FeNO responses. About half of the studies that compared the effect estimates using both personal and ambient air pollution exposure methods reported that only personal exposure yielded significant associations with FeNO response. The evidence from the reviewed studies confirms that FeNO is a sensitive biomarker for air pollutant-induced airway inflammation. Personal air pollution exposure assessment is recommended to accurately assess the air pollution-induced FeNO responses. Furthermore, comprehensive adjustments for the potential confounding factors including the personal exposures of the co-pollutants, respiratory disease status, allergy status, and usage of medications for asthma and allergies are recommended while assessing the air pollution-induced FeNO responses.