短期柴油废气暴露对慢性阻塞性肺部疾病中的原血栓标记物的影响:一个随机,双盲,交叉研究
Min Hyung Ryu1, Seo Am Hur1, Tina Afshar1
1Air Pollution Exposure Laboratory, Division of Respiratory Medicine, Department of Medicine, Vancouver Coastal Health Research Institute, University of British Columbia, Vancouver, British Columbia, Canada.
在患有慢性阻塞性肺病 (COPD) 的个体中,柴油排气暴露会增加前血栓标记物,如纤维素和血栓素B2代谢物. 这表明,与健康人相比,COPD患者更容易受到污染引起的凝血风险.
科学领域:
- 环境健康 环境健康
- 肺部医学 肺部医学
- 心血管研究研究心血管研究
背景情况:
- 空气污染是慢性阻塞性肺部疾病 (COPD) 的重要风险因素,与增加的血栓状况和心血管问题有关.
- 现有的研究往往依赖于观察数据或与年轻参与者的研究,使COPD患者污染诱导的原血栓反应的生物学因果关系和机制未被探索.
研究的目的:
- 为了研究短期柴油废气 (DE) 暴露对循环前列血栓标记物 (纤维素原,等离子素激活剂抑制剂-1) 和COPD患者尿液eicosanoids的影响.
- 为了比较患有COPD的个体,没有COPD的前吸烟者和健康的从未吸烟者的DE暴露的影响.
主要方法:
- 一项随机,双盲,交叉研究,涉及29名参与者:有/没有COPD的前吸烟者和健康的从未吸烟者.
- 参与者暴露在DE (300μg/m3 PM2.5) 和过空气中2小时,在暴露前和后收集血液和尿液样本.
- 血纤维素素,血清PAI-1和尿液eicosanoids使用ELISA和LC-MS/MS量化;使用线性混合效应模型进行统计分析.
主要成果:
- 与过空气相比,COPD患者在DE暴露后表现出血纤维素的增加 (1.27 [1.06-1.53],P=0.01).
- 在COPD患者中没有观察到与DE相关的PAI-1的显著变化,在没有COPD的从不吸烟者和前吸烟者中也没有观察到纤维素/PAI-1.
- 慢性肺炎患者的尿中血栓素B2 (TXB2) 代谢物:11-dehydro-TXB2 (1.45 [1.02-2.08],P=0.04) 和2,3-dinor-TXB2 (1.45 [1.05-2.00],P=0.03) 的增加是由于DE引起的.
结论:
- 在COPD患者中,短期暴露于柴油废气会增加血纤维素和尿液TXB2代谢物.
- 这些发现表明,与没有COPD的健康对照组或前吸烟者相比,COPD患者可能更容易受到空气污染引发的前血栓反应.
- 该研究强调了COPD患者与空气污染相关的潜在心血管风险,并要求进一步调查潜在机制.
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