A Randomized Controlled Trial of Home Air Purification for Eosinophilic COPD

项目总结/摘要 慢性阻塞性肺疾病（COPD）是一种无法治愈的致命疾病， 美国40岁以上的成年人，并因暴露于空气污染而加剧。高达40%的 COPD患者具有更多的嗜酸性粒细胞增多的炎性亚型（>150个嗜酸性粒细胞/μL）， 对抗炎药物更敏感，包括吸入性类固醇和新型靶向抗体 阻止嗜酸性粒细胞的形成然而，这些药物价格昂贵，并且有不良副作用。它 目前尚不清楚，如果预防暴露于空气污染和过敏原-这已被证明是相互作用的 可能对嗜酸性粒细胞性COPD有治疗益处。高 高效微粒空气（HEPA）净化器在改善COPD症状和肺功能方面有很大的希望， 因为它们可以有效地去除室内空气中的颗粒，包括与交通有关的颗粒， 与COPD中肺功能降低相关，以及可引起气道炎症的过敏原， 特别是在嗜酸性粒细胞性COPD中常见的特应性患者中。最近的研究发现，HEPA 过滤器可以改善过敏性哮喘的症状和肺功能，但这种干预从未被评估过。 嗜酸性粒细胞性COPD总体目标是评价为期一年的盲法随机 HEPA与假空气净化器干预对肺功能、呼吸道症状和 上呼吸道（作为吸入暴露和生物反应的部位）， 嗜酸性COPD。中心假设是，通过一种方法去除卧室和起居室中的颗粒物， HEPA空气净化器将改善嗜酸性COPD患者的呼吸健康。 第一个目标将测试在卧室和客厅进行为期一年的HEPA过滤器干预是否会影响肺部 功能（主要结局）、呼吸道症状和健康状况与假滤器相比。第二个目的 将测试干预是否影响鼻上皮衬里液中炎症介质的水平。第三 （探索性）目的将评估干预措施是否会影响某些与粉尘和燃烧有关的金属的水平， 鼻上皮衬液。研究人员假设，由于HEPA过滤器改善空气质量将 改善肺功能、呼吸道症状和圣乔治呼吸问卷健康状况。是 进一步假设空气净化将减少与过敏和非过敏相关的炎症介质， 呼吸道病理生理学，并减少粉尘和燃烧相关的金属在上呼吸道。 本项目的研究结果可能为医学界提供两种新工具-（1）HEPA过滤器 干预，以及（2）上呼吸道暴露和反应的测定-可用于促进 嗜酸性粒细胞性COPD患者更健康的生活。如果没有这些知识，医学界可能 错过了减少暴露于推动疾病进展的有害颗粒的机会，而是依赖于 只依赖昂贵的药物来控制这种炎症性更强的COPD亚型。

PROJECT SUMMARY/ABSTRACT Chronic obstructive pulmonary disease (COPD) is an incurable and deadly disease that affects 15% of adults over 40 years of age in the United States, and is exacerbated by exposure to air pollution. Up to 40% of COPD patients have a more inflammatory subtype with eosinophilia (>150 eosinophils per µL) and appear to be more responsive to anti-inflammatory medications, including inhaled steroids and novel targeted antibodies that block eosinophil formation. However, these medications are expensive and have adverse side effects. It is unknown if prevention of exposure to air pollution and allergens—which have been demonstrated to interact with each other to cause airway inflammation—may be of therapeutic benefit in eosinophilic COPD. High efficiency particulate air (HEPA) purifiers hold great promise to improve COPD symptoms and lung function, because they effectively remove particles from the indoor air, including traffic-related particles that are associated with reduced lung function in COPD, and allergens that can provoke airway inflammation, especially in those with atopy which is common in eosinophilic COPD. Recent studies have found that HEPA filters improve symptoms and lung function for allergic asthma, but this intervention has never been evaluated for eosinophilic COPD. The overall objective is to evaluate the effect of a one-year blinded randomized controlled trial of a HEPA vs sham air purifier intervention on lung function, respiratory symptoms, and the upper respiratory tract (as a site of inhaled exposure and biologic response) among 200 former smokers with eosinophilic COPD. The central hypothesis is that removal of particles in the bedroom and living room by a HEPA air purifier will improve the respiratory health of patients with eosinophilic COPD. The first aim will test if a one-year HEPA filter intervention in the bedroom and living room affects lung function (primary outcome), respiratory symptoms, and health status compared to sham filter. The second aim will test if the intervention affects levels of inflammatory mediators in the nasal epithelial lining fluid. The third (exploratory) aim will evaluate if the intervention affects levels of certain dust- and combustion-related metals in the nasal epithelial lining fluid. The investigators hypothesize that improved air quality due to HEPA filters will improve lung function, respiratory symptoms, and health status by St. George Respiratory Questionnaire. It is further hypothesized that air purification will reduce inflammatory mediators relevant to allergic and non-allergic airway pathophysiology, and also reduce dust- and combustion-related metals in the upper respiratory tract. The findings of this project may provide the medical community with two new tools—(1) a HEPA filter intervention, and (2) an assay of upper respiratory exposure and response—that can be used to promote healthier lives among people with eosinophilic COPD. Without such knowledge, the medical community may miss an opportunity to reduce exposure to noxious particles that drive disease progression, and instead rely only on costly medications for disease control in this more inflammatory subtype of COPD.