Inhalable particulate matter and mitochondrial DNA copy number in highly exposed individuals in Beijing, China: a repeated-measure study.

Inhalable particulate matter and mitochondrial DNA copy number in highly exposed individuals in Beijing, China: a repeated-measure study.
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DOI:
10.1186/1743-8977-10-17
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发表时间:
2013-04-29
影响因子:
10
通讯作者:
Baccarelli AA
Baccarelli AA
中科院分区:
医学1区
文献类型:
--
作者:
Hou L;Zhang X;Dioni L;Barretta F;Dou C;Zheng Y;Hoxha M;Bertazzi PA;Schwartz J;Wu S;Wang S;Baccarelli AA

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线粒体是氧化应激的敏感靶点和主要来源,氧化应激是空气颗粒物(PM)相关疾病的关键途径。线粒体DNA拷贝数(MtDNAcn)是线粒体损伤和功能障碍的标志物。我们评估了环境PM暴露是否会影响中国北京高暴露人群中的MtDNAn。北京卡车司机空气污染研究是在2008年北京奥运会(2008年6月15日至7月27日)前不久进行的,包括60名卡车司机和60名办公室工作人员。个人PM2.5和元素碳(EC,交通颗粒物的示踪剂)在工作时间使用便携式监测器测量。在两个不同日期采集工作后血样。PM10是北京市27个监测站的平均值。通过实时PCR测定血液MtDNAn,并使用混合效应模型与颗粒水平相关联地进行检查。在所有参与者中,MtDNAcn与工作时间内测量的个人EC水平呈负相关(β=−0.059,95% CI:-0.011;-0.0006,p=0.03); 5天(β=−0.017,95% CI:-0.029;-0.005,p=0.01)和8天平均环境PM10(β=−0.008,95% CI:-0.043;-0.008,p=0.004),调整可能的混杂因素后,包括研究组。在办公室工作人员中,MtDNAn也与EC(β=-0.012,95% CI:-0.022;-0.002,p=0.02)和8天平均环境PM10(β=-0.030,95% CI:-0.051;-0.008,p=0.007)呈负相关。我们观察到降低血液MtDNAn与EC在工作时间和最近的环境PM10暴露增加。我们的研究结果表明,MtDNAcn可能会受到颗粒暴露的影响。需要进一步的研究来确定MtDNAn在颗粒相关疾病的病因学中的作用。
Mitochondria are both a sensitive target and a primary source of oxidative stress, a key pathway of air particulate matter (PM)-associated diseases. Mitochondrial DNA copy number (MtDNAcn) is a marker of mitochondrial damage and malfunctioning. We evaluated whether ambient PM exposure affects MtDNAcn in a highly-exposed population in Beijing, China. The Beijing Truck Driver Air Pollution Study was conducted shortly before the 2008 Beijing Olympic Games (June 15-July 27, 2008) and included 60 truck drivers and 60 office workers. Personal PM2.5 and elemental carbon (EC, a tracer of traffic particles) were measured during work hours using portable monitors. Post-work blood samples were obtained on two different days. Ambient PM10 was averaged from 27 monitoring stations in Beijing. Blood MtDNAcn was determined by real-time PCR and examined in association with particle levels using mixed-effect models. In all participants combined, MtDNAcn was negatively associated with personal EC level measured during work hours (β=−0.059, 95% CI: -0.011; -0.0006, p=0.03); and 5-day (β=−0.017, 95% CI: -0.029;-0.005, p=0.01) and 8-day average ambient PM10 (β=−0.008, 95% CI: -0.043; -0.008, p=0.004) after adjusting for possible confounding factors, including study groups. MtDNAcn was also negatively associated among office workers with EC (β=−0.012, 95% CI: -0.022;-0.002, p=0.02) and 8-day average ambient PM10 (β=−0.030, 95% CI: -0.051;-0.008, p=0.007). We observed decreased blood MtDNAcn in association with increased exposure to EC during work hours and recent ambient PM10 exposure. Our results suggest that MtDNAcn may be influenced by particle exposures. Further studies are required to determine the roles of MtDNAcn in the etiology of particle-related diseases.
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