Lee Kang-Yun, Chiang Ling-Ling, Ho Shu-Chuan, Liu Wen-Te, Chen Tzu-Tao, Feng Po-Hao, Su Chien-Ling, Chuang Kai-Jen, Chang Chih-Cheng, Chuang Hsiao-Chi
Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital; Department of Internal Medicine, School of Medicine.
Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital; School of Respiratory Therapy.
Int J Chron Obstruct Pulmon Dis. 2016 Jul 11;11:1569-78. doi: 10.2147/COPD.S108993. eCollection 2016.
Although traffic exposure has been associated with the development of COPD, the role of particulate matter <10 μm in aerodynamic diameter (PM10) in the pathogenesis of COPD is not yet fully understood. We assessed the 1-year effect of exposure to PM10 on the pathogenesis of COPD in a retrospective cohort study. We recruited 53 subjects with COPD stages III and IV and 15 healthy controls in a hospital in Taiwan. We estimated the 1-year annual mean levels of PM10 at all residential addresses of the cohort participants. Changes in PM10 for the 1-year averages in quintiles were related to diffusion capacity of the lung for carbon monoxide levels (r=-0.914, P=0.029), changes in the pulse oxygen saturation (ΔSaO2; r=-0.973, P=0.005), receptor for advanced glycation end-products (r=-0.881, P=0.048), interleukin-6 (r=0.986, P=0.002), ubiquitin (r=0.940, P=0.017), and beclin 1 (r=0.923, P=0.025) in COPD. Next, we observed that ubiquitin was correlated with ΔSaO2 (r=-0.374, P=0.019). Beclin 1 was associated with diffusion capacity of the lung for carbon monoxide (r=-0.362, P=0.028), ΔSaO2 (r=-0.354, P=0.032), and receptor for advanced glycation end-products (r=-0.471, P=0.004). Autophagy may be an important regulator of the PM10-related pathogenesis of COPD, which could cause deterioration in the lung diffusion capacity and oxygen saturation.
尽管交通暴露与慢性阻塞性肺疾病（COPD）的发生有关，但空气动力学直径小于10μm的颗粒物（PM10）在COPD发病机制中的作用尚未完全明确。我们在一项回顾性队列研究中评估了暴露于PM10一年对COPD发病机制的影响。我们在台湾的一家医院招募了53例III期和IV期COPD患者以及15名健康对照者。我们估算了队列参与者所有居住地址处PM10的1年年均水平。PM10五分位数的1年平均值变化与肺一氧化碳弥散量水平（r = -0.914，P = 0.029）、脉搏血氧饱和度变化（ΔSaO2；r = -0.973，P = 0.005）、晚期糖基化终末产物受体（r = -0.881，P = 0.048）、白细胞介素-6（r = 0.986，P = 0.002）、泛素（r = 0.940，P = 0.017）和自噬相关蛋白1（r = 0.923，P = 0.025）有关。接下来，我们观察到泛素与ΔSaO2相关（r = -0.374，P = 0.019）。自噬相关蛋白1与肺一氧化碳弥散量（r = -0.362，P = 0.028）、ΔSaO2（r = -0.354，P = 0.032）和晚期糖基化终末产物受体（r = -0.471，P = 0.004）有关。自噬可能是PM10相关COPD发病机制的重要调节因子，可导致肺弥散功能和血氧饱和度恶化。
