Pulmonary function, diffusing capacity, and inflammation in healthy and asthmatic subjects exposed to ultrafine particles
Pulmonary function, diffusing capacity, and inflammation in healthy and asthmatic subjects exposed to ultrafine particles
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DOI：
10.1080/08958370490443079
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发表时间：
2004-01-01
影响因子：
2.1
通讯作者：
Utell, MJ
中科院分区：
文献类型：
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作者：
Pietropaoli, AP;Frampton, MW;Utell, MJ
空气颗粒物污染与哮喘恶化以及呼吸道疾病发病率和死亡率增加有关。超细颗粒（直径小于 0.1 微米的颗粒）可能会造成这些不良影响，因为与质量较大的颗粒相比，它们具有更高的预测肺部沉积、更大的诱发肺部炎症的潜力、更大的表面积和更强的氧化能力。我们假设超细颗粒暴露会诱发易感人群的气道炎症。这一假设在一系列随机、双盲研究中得到了检验，这些研究将健康受试者和轻度哮喘受试者暴露在碳超细颗粒与过滤空气中。两种暴露都是在休息和适度运动期间通过咬嘴系统进行的。健康受试者暴露于浓度为 10、25 和 50 微克/米 (3) 的颗粒物，而哮喘患者则暴露于 10 微克/米 (3) 的颗粒物浓度。通过症状评分、肺功能测试和气道一氧化氮参数评估肺功能和气道炎症。在几个方案中通过诱导痰分析来测量气道炎症细胞。当正常受试者或哮喘受试者暴露于浓度为 10 或 25 微克/米 (3) 的超细颗粒时，这些测量值均没有差异。然而，将 16 名正常受试者暴露于较高浓度 50 mug/m(3) 会导致最大呼气中期流速（-4.34 +/- 1.78% [超细颗粒] vs. +1.08 +/- 1.86% [空气]，p = 0.042）和一氧化碳扩散能力（-1.76 +/- 0.66 ml/min/mm Hg [超细颗粒]）降低暴露后 21 小时对比 -0.18 +/- 0.41 ml/min/mm Hg [空气], p =.040)。在这些研究中，症状、诱导痰或呼出一氧化氮参数均没有一致的差异。这些结果表明，接触碳超细颗粒会导致正常受试者轻度小气道功能障碍以及肺泡气体交换受损。这些影响似乎与气道炎症无关。需要更多的研究来证实正常受试者的这些发现，将其与其他易感患者群体进行比较，并确定其病理生理机制。
Particulate air pollution is associated with asthma exacerbations and increased morbidity and mortality from respiratory causes. Ultrafine particles (particles less than 0.1 mum in diameter) may contribute to these adverse effects because they have a higher predicted pulmonary deposition, greater potential to induce pulmonary inflammation, larger surface area, and enhanced oxidant capacity when compared with larger particles on a mass basis. We hypothesized that ultrafine particle exposure Would induce airway inflammation in susceptible humans. This hypothesis was tested in a series of randomized, double-blind studies by exposing healthy subjects and mild asthmatic subjects to carbon ultrafine particles versus filtered air. Both exposures were delivered via a mouthpiece system during rest and moderate exercise. Healthy subjects were exposed to particle concentrations of 10, 25, and 50 mug/m(3), while asthmatics were exposed to 10 mug/m(3). Lung function and airway inflammation were assessed by symptom scores, pulmonary function tests, and airway nitric oxide parameters. Airway inflammatory cells were measured via induced sputum analysis in several of the protocols. There were no differences in any of these measurements in normal or asthmatic subjects when exposed to ultrafine particles at concentrations of 10 or 25 mug/m(3). However, exposing 16 normal subjects to the higher concentration of 50 mug/m(3) caused a reduction in maximal midexpiratory flow rate (-4.34 +/- 1.78% [ultrafine particles] vs. +1.08 +/- 1.86% [air], p =.042) and carbon monoxide diffusing capacity (-1.76 +/- 0.66 ml/min/mm Hg [ultrafine particles] vs. -0.18 +/- 0.41 ml/min/mm Hg [air], p =.040) at 21 h after exposure. There were no consistent differences in symptoms, induced sputum, or exhaled nitric oxide parameters in any of these studies. These results suggest that exposure to carbon ultrafine particles results in mild small-airways dysfunction together with impaired alveolar gas exchange in normal subjects. These effects do not appear related to airway inflammation. Additional studies are required to confirm these findings in normal subjects, compare them with additional susceptible patient populations, and determine their pathophysiologic mechanisms.