Zhang Y, Song X M, Zhao Q, Wang T, Li L J, Chen J, Xu H B, Liu B B, Sun X Y, He B, Huang W
Department of Occupational and Environmental Health, Peking University School of Public Health, Beijing 100191, China.
Institute of Earth Environment, Chinese Academy of Sciences, Xi'an 710061, China.
Beijing Da Xue Xue Bao Yi Xue Ban. 2017 Jun 18;49(3):394-402.
To investigate the effects of exposure to ambient particulate matter (PM) and polycyclic aromatic hydrocarbons (PAHs) on systemic oxidative stress biomarkers in chronic obstructive pulmonary disease (COPD) patients.
A panel of forty-five diagnosed and stable COPD patients, whose residences were within 5 kilometers from Peking University Health Science Center (PKUHSC), were recruited and followed up twice between November 2014 and May 2015. The lung function index percentage of forced expiratory volume in 1 second (FEV) to predicted value (FEV%pred), was measured to reflect the severity of COPD patients. The systemic oxidative stress biomarkers malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in their urine samples were measured using high performance liquid chromatography (HPLC) and enzyme-linked immunosorbent assay (ELISA), respectively. Concentrations of ambient air pollutants and levels of meteorological factors were measured continuously through the air pollution-monitoring station located in PKUHSC. PM samples, which were used for measuring the concentrations of PAHs, were collected by PM high volume air sampler. We constructed linear mixed-effects models, including single-pollutant model, 2-pollutant models and stratification analysis, to estimate the effects of air pollutants on urinary MDA and 8-OHdG after adjusting for confounding factors.
In our COPD-patient panel, the associations between ultrafine particles (UFP) and PAHs and urinary MDA were statistically significant at lag2 (P<0.05). For an interquartile range (IQR) increase in UFP and PAHs, respective increases of 28% (95%CI: 4%-57%) and 36% (95%CI: 4%-77%) in urinary MDA were observed, and the effects became stronger after adjusting for the concentration of black carbon (BC). The COPD patients were divided into 2 groups stratified by FEV%pred. Most air pollutants had stronger effects of systemic oxidative stress in the COPD patients of FEV%pred≥50%. In this group, we observed that an IQR increase in UFP was associated with a 98% (95%CI: 38%-186%) increase in urinary MDA, and an IQR increase in BC, UFP and PAHs were associated with respective increases of 87% (95%CI: 32%-166%), 69% (95%CI: 24%-130%) and 156% (95%CI: 66%-294%) in urinary 8-OHdG. We didn't find significant associations between fine particulate matter (PM) and urinary oxidative stress biomarkers.
Our results suggested that exposure to air pollutants, especially UFP and PAHs, was responsible for exacerbation of systemic oxidative stress in COPD patients. Most air pollutants had stronger effects of systemic oxidative stress in mild to moderate COPD patients.
探讨暴露于环境颗粒物（PM）和多环芳烃（PAHs）对慢性阻塞性肺疾病（COPD）患者全身氧化应激生物标志物的影响。
招募了45名确诊且病情稳定的COPD患者，其住所距离北京大学医学部（PKUHSC）在5公里以内，并于2014年11月至2015年5月期间进行了两次随访。测量了1秒用力呼气容积（FEV）占预测值的百分比（FEV%pred）这一肺功能指标，以反映COPD患者的病情严重程度。分别采用高效液相色谱法（HPLC）和酶联免疫吸附测定法（ELISA）测定其尿液样本中的全身氧化应激生物标志物丙二醛（MDA）和8-羟基-2'-脱氧鸟苷（8-OHdG）。通过位于PKUHSC的空气污染监测站连续测量环境空气污染物浓度和气象因素水平。用于测量PAHs浓度的PM样本通过PM大容量空气采样器收集。我们构建了线性混合效应模型，包括单污染物模型、双污染物模型和分层分析，以在调整混杂因素后估计空气污染物对尿MDA和8-OHdG的影响。
在我们的COPD患者组中，超细颗粒物（UFP）和PAHs与尿MDA之间的关联在滞后2时具有统计学意义（P<0.05）。UFP和PAHs每增加一个四分位数间距（IQR），尿MDA分别增加28%（95%CI：4%-57%）和36%（95%CI：4%-77%），在调整黑碳（BC）浓度后，这种影响变得更强。根据FEV%pred将COPD患者分为2组。大多数空气污染物在FEV%pred≥50%的COPD患者中对全身氧化应激的影响更强。在该组中，我们观察到UFP每增加一个IQR，尿MDA增加98%（95%CI：38%-186%），BC、UFP和PAHs每增加一个IQR，尿8-OHdG分别增加87%（95%CI：32%-166%）、69%（95%CI：24%-130%）和156%（95%CI：66%-294%）。我们未发现细颗粒物（PM）与尿氧化应激生物标志物之间存在显著关联。
我们的结果表明，暴露于空气污染物，尤其是UFP和PAHs，是导致COPD患者全身氧化应激加剧的原因。大多数空气污染物在轻度至中度COPD患者中对全身氧化应激的影响更强。
