柴油交通废气对支气管哮喘患者呼吸道的影响

2008/04/30

    道路交通空气污染是严重的卫生公害,而对原有呼吸疾病的人来说,危害可能会增加。以往关于柴油交通废气对哮喘患者的影响的研究大多是在实验室条件下模拟完成的。英国伦敦牛津街的交通工具规定只限柴油机公交车和出租车。James McCreanor等则选择英国伦敦的牛津街作为实际暴露环境,以确切观察哮喘患者短期接触柴油交通废气后呼吸道的反应。
    作者收集60个轻-中度成年支气管哮喘患者,随机分为牛津街步行组和海德公园步行组。牛津街步行组沿伦敦街(牛津街)交通道路旁步行2小时(上午10:30 a.m. 到中午12:30 p.m.),海德公园步行组则同一时间在附近公园(伦敦海德公园)步行2小时。
    研究结果显示牛津街空气中的微小颗粒(<空气动力学直径<2.5μm)、超微颗粒、碳元素和二氧化氮密度明显高于伦敦海德公园的空气。牛津街步行组步行后1小时内虽然没有出现哮喘症状,但肺功能复查显示第1秒用力肺活量(FEV1)下降6.1%,用力肺活量(FVC)下降5.4%,均明显大于海德公园步行组(P=0.04、P=0.01;在某些时间点上P=0.005)。中度哮喘患者的肺功能变化大于轻度哮喘患者。这些改变伴随嗜中性粒细胞炎症生物标记的增高[痰髓过氧化酶(sputum myeloperoxidase);牛津街步行组为24.5ng/ml,海德公园步行组为4.24ng/ml, P=0.05]及呼吸道的酸化(牛津街步行组呼吸道的pH值降低最大值为1.9%,而海德公园步行组为0.04%, P=0.003)。上述改变与接触超微颗粒及碳元素密切相关。
    作者认为他们的研究对哮喘患者肺功能改变与接触交通废气程度密切相关的流行病学调查提供了很好的证据。
 
                  (张清玲 广州呼吸疾病研究所 510120  摘译)
                        (N Engl J Med ,2007 ;357:2348-2358)
 
 
James McCreanor, Paul Cullinan, Mark J. Nieuwenhuijsen, et al. Respiratory Effects of Exposure to Diesel Traffic in Persons with Asthma. N Engl J Med, 2007; 357: 2348-58.
 
Background: 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.
Methods: 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.
Results: Participants had significantly higher exposures to fine particles (<2.5 μm in aerodynamicdiameter), ultrafine particles, elemental carbon, and nitrogen dioxide on
Oxford Street than in Hyde Park. Walking for 2 hours on Oxford Street induced asymptomaticbut 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.
Conclusions: Our observations serve as a demonstration and explanation of the epidemiologic evidence that associates the degree of traffic exposure with lung function in asthma.
 


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