Research and Development Service, VA Boston Healthcare System, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Environ Int. 2018 Jun;115:188-195. doi: 10.1016/j.envint.2018.02.040. Epub 2018 Mar 22.
We assessed relationships between indoor black carbon (BC) exposure and urinary oxidative stress biomarkers, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), in participants with chronic obstructive pulmonary disease (COPD).
Eighty-two participants completed in-home air sampling for one week prior to providing urine samples up to four times in a year. Weekly indoor and daily outdoor concentrations were used to estimate indoor daily lags and moving averages. There were no reported in-home BC sources, thus indoor levels closely represented outdoor BC infiltration. Mixed effects regression models with a random intercept for each participant were used to assess relationships between indoor BC and 8-OHdG and MDA, adjusting for age, race, BMI, diabetes, heart disease, season, time of urine collection, urine creatinine, and outdoor humidity and temperature.
There were positive effects of BC on 8-OHdG and MDA, with the greatest effect the day before urine collection (6.9% increase; 95% CI 0.9-13.3%, per interquartile range: 0.22 μg/m) for 8-OHdG and 1 to 4 days before collection (8.3% increase; 95% CI 0.03-17.3% per IQR) for MDA. Results were similar in models adjusting for PM not associated with BC and NO (10.4% increase, 95% CI: 3.5-17.9 for 8-OHdG; 8.1% increase, 95% CI: -1.1-18.1 for MDA). Effects on 8-OHdG were greater in obese participants.
We found positive associations between BC exposure and 8-OHdG and MDA, in which associations with 8-OHdG were stronger in obese participants. These results suggest that exposure to low levels of traffic-related pollution results in lipid peroxidation and oxidative DNA damage in individuals with COPD.
我们评估了室内黑碳（BC）暴露与慢性阻塞性肺疾病（COPD）患者尿液氧化应激生物标志物 8-羟基-2'-脱氧鸟苷（8-OHdG）和丙二醛（MDA）之间的关系。
82 名参与者在家中进行了为期一周的空气采样，然后在一年中最多四次提供尿液样本。每周室内和每日室外浓度用于估计室内每日滞后和移动平均值。没有报告家中有 BC 来源，因此室内水平密切反映了室外 BC 的渗透。使用具有每个参与者随机截距的混合效应回归模型，调整年龄、种族、BMI、糖尿病、心脏病、季节、尿液采集时间、尿肌酐以及室外湿度和温度，评估室内 BC 与 8-OHdG 和 MDA 之间的关系。
BC 对 8-OHdG 和 MDA 有正向影响，尿液采集前一天的影响最大（增加 6.9%；95%CI 0.9-13.3%，每四分位距增加 0.22μg/m）8-OHdG 和采集前 1 至 4 天（增加 8.3%；95%CI 0.03-17.3%，每 IQR 增加）MDA。在调整与 BC 不相关的 PM 和 NO 的模型中，结果相似（8-OHdG 增加 10.4%，95%CI：3.5-17.9；MDA 增加 8.1%，95%CI：-1.1-18.1）。肥胖参与者的 8-OHdG 影响更大。
我们发现 BC 暴露与 8-OHdG 和 MDA 之间存在正相关关系，其中与 8-OHdG 的相关性在肥胖参与者中更强。这些结果表明，暴露于低水平的交通相关污染会导致 COPD 患者的脂质过氧化和氧化 DNA 损伤。
