Air Pollution Exposure Laboratory, Division of Respiratory Medicine, Department of Medicine, and.
Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada.
Am J Respir Crit Care Med. 2019 Sep 1;200(5):565-574. doi: 10.1164/rccm.201809-1657OC.
Diesel exhaust (DE), an established model of traffic-related air pollution, contributes significantly to the global burden of asthma and may augment the effects of allergen inhalation. Newer diesel particulate-filtering technologies may increase NO emissions, raising questions regarding their effectiveness in reducing harm from associated engine output. To assess the effects of DE and allergen coexposure on lung function, airway responsiveness, and circulating leukocytes, and determine whether DE particle depletion remediates these effects. In this randomized, double-blind crossover study, 14 allergen-sensitized participants (9 with airway hyperresponsiveness) underwent inhaled allergen challenge after 2-hour exposures to DE, particle-depleted DE (PDDE), or filtered air. The control condition was inhaled saline after filtered air. Blood sampling and spirometry were performed before and up to 48 hours after exposures. Airway responsiveness was evaluated at 24 hours. PDDE plus allergen coexposure impaired lung function more than DE plus allergen, particularly in those genetically at risk. DE plus allergen and PDDE plus allergen each increased airway responsiveness in normally responsive participants. DE plus allergen increased blood neutrophils and was associated with persistent eosinophilia at 48 hours. DE and PDDE each increased total peripheral leukocyte counts in a manner affected by participant genotypes. Changes in peripheral leukocytes correlated with lung function decline. Coexposure to DE and allergen impaired lung function, which was worse after particle depletion (which increased NO). Thus, particulates are not necessarily the sole or main culprit responsible for all harmful effects of DE. Policies and technologies aimed at protecting public health should be scrutinized in that regard.Clinical trial registered with www.clinicaltrials.gov (NCT02017431).
柴油机尾气（DE）是一种已确立的交通相关空气污染模型，它对哮喘的全球负担有重大影响，并且可能增强过敏原吸入的作用。新型的柴油机微粒过滤技术可能会增加氮氧化物（NO）的排放，这引发了对其在降低相关发动机排放物危害方面的有效性的质疑。为了评估 DE 和过敏原共同暴露对肺功能、气道反应性和循环白细胞的影响，并确定 DE 颗粒耗尽是否能缓解这些影响。在这项随机、双盲交叉研究中，14 名过敏原致敏参与者（9 名具有气道高反应性）在暴露于柴油机尾气、颗粒耗尽的柴油机尾气（PDDE）或过滤空气 2 小时后接受吸入性过敏原挑战。对照条件是在过滤空气后吸入生理盐水。在暴露前和暴露后最多 48 小时进行血液采样和肺活量测定。在 24 小时时评估气道反应性。与柴油机尾气加过敏原共同暴露相比，PDDE 加过敏原共同暴露对肺功能的损害更大，特别是在那些遗传易感性的参与者中。DE 加过敏原和 PDDE 加过敏原都增加了正常反应参与者的气道反应性。DE 加过敏原增加了血液中性粒细胞，并与 48 小时时的持续性嗜酸性粒细胞增多有关。DE 和 PDDE 都以受参与者基因型影响的方式增加了外周白细胞总数。外周白细胞的变化与肺功能下降相关。DE 和过敏原的共同暴露损害了肺功能，颗粒耗尽后情况更糟（增加了 NO）。因此，颗粒不一定是柴油机尾气所有有害影响的唯一或主要罪魁祸首。在这方面，旨在保护公众健康的政策和技术应该受到仔细审查。临床试验在 www.clinicaltrials.gov（NCT02017431）注册。
