A Randomized Controlled Trial of Home Air Purification for Eosinophilic COPD

项目摘要/摘要 慢性阻塞性肺疾病(COPD)是一种无法治愈的致命疾病，15%的人会受到影响 美国40岁以上的成年人，暴露在空气污染中更是雪上加霜。高达40%的 慢性阻塞性肺疾病患者有更多的炎症性亚型伴有嗜酸性粒细胞增多(每微克L有150个嗜酸性粒细胞)，并且似乎 对抗炎药物更敏感，包括吸入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，而且有副作用。它 尚不清楚是否预防暴露在空气污染和过敏原中--这两种物质已被证明相互作用 共同引起呼吸道炎症--可能对嗜酸性COPD有治疗作用。高 高效微粒空气(HEPA)净化器有望改善COPD症状和肺功能， 因为它们有效地去除了室内空气中的颗粒物，包括与交通相关的颗粒物 与COPD患者的肺功能降低有关，以及可能引发呼吸道炎症的过敏原， 尤其是那些患有特应性疾病的人，这种特应性疾病在嗜酸性COPD中很常见。最近的研究发现，HEPA 过滤器改善过敏性哮喘的症状和肺功能，但这种干预措施从未得到评估 用于嗜酸性慢性阻塞性肺病。总体目标是评估为期一年的随机盲法的效果。 HEPA与假空气净化器干预对肺功能、呼吸道症状和 200例既往吸烟者的上呼吸道(作为吸入暴露和生物反应的场所) 嗜酸性慢性阻塞性肺病。中心假设是卧室和起居室中的颗粒物被一种 HEPA空气净化器将改善嗜酸性COPD患者的呼吸健康。 第一个目标是测试在卧室和起居室进行为期一年的HEPA过滤器干预是否会影响肺部 功能(主要结果)、呼吸道症状和健康状况与假过滤器进行比较。第二个目标 将测试干预是否会影响鼻腔上皮衬里液体中炎症介质的水平。第三 (探索性)AIM将评估干预措施是否会影响 鼻腔上皮衬里液。调查人员假设，由于高效空气过滤器改善空气质量将 通过圣乔治呼吸问卷调查改善肺功能、呼吸道症状和健康状况。它是 进一步假设空气净化将减少与过敏性和非过敏性相关的炎症介质 此外，还可以减少呼吸道中与粉尘和燃烧相关的金属。 该项目的发现可能会为医学界提供两个新工具--(1)高效空气过滤器 干预，以及(2)上呼吸道暴露和反应的分析--可用于促进 嗜酸性慢性阻塞性肺病患者的生活更健康。在没有这些知识的情况下，医学界可能会 错过了一个减少接触有毒颗粒物的机会，而不是依赖于 仅限于在这种炎症性更强的COPD亚型中用于疾病控制的昂贵药物。

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.