McCreanor James, Cullinan Paul, Nieuwenhuijsen Mark J, Stewart-Evans James, Malliarou Eleni, Jarup Lars, Harrington Robert, Svartengren Magnus, Han In-Kyu, Ohman-Strickland Pamela, Chung Kian Fan, Zhang Junfeng
National Heart and Lung Institute, Imperial College, and Royal Brompton Hospital, London, United Kingdom.
N Engl J Med. 2007 Dec 6;357(23):2348-58. doi: 10.1056/NEJMoa071535.
Air pollution from road traffic is a serious health hazard, and people with preexisting respiratory disease may be at increased risk. We investigated the effects of short-term exposure to diesel traffic in people with asthma in an urban, roadside environment.
We recruited 60 adults with either mild or moderate asthma to participate in a randomized, crossover study. Each participant walked for 2 hours along a London street (Oxford Street) and, on a separate occasion, through a nearby park (Hyde Park). We performed detailed real-time exposure, physiological, and immunologic measurements.
Participants had significantly higher exposures to fine particles (<2.5 microm in aerodynamic diameter), ultrafine particles, elemental carbon, and nitrogen dioxide on Oxford Street than in Hyde Park. Walking for 2 hours on Oxford Street induced asymptomatic but consistent reductions in the forced expiratory volume in 1 second (FEV1) (up to 6.1%) and forced vital capacity (FVC) (up to 5.4%) that were significantly larger than the reductions in FEV1 and FVC after exposure in Hyde Park (P=0.04 and P=0.01, respectively, for the overall effect of exposure, and P<0.005 at some time points). The effects were greater in subjects with moderate asthma than in those with mild asthma. These changes were accompanied by increases in biomarkers of neutrophilic inflammation (sputum myeloperoxidase, 4.24 ng per milliliter after exposure in Hyde Park vs. 24.5 ng per milliliter after exposure on Oxford Street; P=0.05) and airway acidification (maximum decrease in pH, 0.04% after exposure in Hyde Park and 1.9% after exposure on Oxford Street; P=0.003). The changes were associated most consistently with exposures to ultrafine particles and elemental carbon.
Our observations serve as a demonstration and explanation of the epidemiologic evidence that associates the degree of traffic exposure with lung function in asthma.
道路交通产生的空气污染对健康危害严重，已有呼吸道疾病的人群可能面临更高风险。我们在城市路边环境中研究了哮喘患者短期接触柴油车尾气的影响。
我们招募了60名轻度或中度哮喘成年患者参与一项随机交叉研究。每位参与者沿着伦敦的一条街道（牛津街）步行2小时，另一次则穿过附近的公园（海德公园）。我们进行了详细的实时暴露、生理和免疫测量。
与海德公园相比，参与者在牛津街接触到的细颗粒物（空气动力学直径<2.5微米）、超细颗粒物、元素碳和二氧化氮显著更多。在牛津街步行2小时导致1秒用力呼气量（FEV1）（最多降低6.1%）和用力肺活量（FVC）（最多降低5.4%）出现无症状但持续的下降，且下降幅度显著大于在海德公园暴露后的FEV1和FVC下降幅度（暴露的总体效应分别为P = 0.04和P = 0.01，在某些时间点P<0.005）。中度哮喘患者的影响大于轻度哮喘患者。这些变化伴随着中性粒细胞炎症生物标志物的增加（痰液髓过氧化物酶，海德公园暴露后为每毫升4.24纳克，牛津街暴露后为每毫升24.5纳克；P = 0.05）和气道酸化（pH值最大降幅，海德公园暴露后为0.04%，牛津街暴露后为1.9%；P = 0.003）。这些变化与超细颗粒物和元素碳的暴露最为一致相关。
我们的观察结果证实并解释了将交通暴露程度与哮喘患者肺功能相关联的流行病学证据。
