Background

Mitochondria are sensitive to air pollutants due to their lack of repair capacity. Changes in mitochondrial DNA copy number (mtDNAcn) or content is a proxy of mitochondrial damage and has been associated with recent exposure to traffic-derived air pollutants, nitrogen dioxide (NO₂) and black carbon (BC). Inhaled BC can be phagocytosed by airway macrophages (AMs), and its amount in AM reflects personal exposure to traffic-related air pollution.

Objectives

The present study investigated the relation between the internal marker AM BC and ambient NO₂ concentration and examined the associations of mtDNAcn with NO₂ and AM BC.

Methods

A panel of 20 healthy retired participants (10 couples) living in Belgium underwent repeated assessments of health and air pollution exposure at 11 time points over one year. We increased exposure contrast temporarily by moving participants for 10 days to Milan, Italy (high exposure) and to Vindeln, Sweden (low exposure). Personal exposure to NO₂ was measured during 5 consecutive days prior to each assessment time point. The amount of BC was assessed by image analysis in AMs retrieved from induced sputum collected at 7 time points. Blood mtDNAcn was determined by qPCR at each time point. Associations between AM BC and NO₂, and of mtDNAcn with NO₂ and AM BC were estimated using linear mixed effect models adjusted for covariates and potential confounders.

Results

Mean concentrations of 5-day average NO₂ were higher in Milan (64 μg/m³) and lower in Vindeln (4 μg/m³) than Belgium (26 μg/m³). Each 10 μg/m³ increment in NO₂ exposure during the last 5 days was associated with 0.07 μm² (95% CI: 0.001 to 0.012) increase in median area of AM BC. A 10 μg/m³ increase in NO₂ was associated with 3.9% (95% CI: 2.2 to 5.5%) decrease in mtDNAcn. Consistently, each 1 μm² increment in median area of AM BC was associated with 24.8% (95% CI: 6.8 to 39.3%) decrease in mtDNAcn.

Conclusion

In this quasi-experimental setting involving moving persons to places with high and low ambient air pollution, we found changes in AM BC according to ambient air pollution levels measured during the previous 5 days. Both higher ambient NO₂ and the internal lung BC load, paralleled mitochondrial compromises as exemplified by lower mtDNA content.

中文翻译：

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血液中的线粒体DNA含量和气道巨噬细胞的碳负荷。一项针对老年人的小组研究

背景

线粒体由于缺乏修复能力而对空气污染物敏感。线粒体DNA拷贝数（mtDNAcn）或含量的变化是线粒体损伤的代表，并且与最近暴露于交通源性空气污染物，二氧化氮（NO ₂）和黑碳（BC）有关。吸入的BC可以被气道巨噬细胞（AM）吞噬，其AM含量反映了个人暴露于交通相关的空气污染中。

目标

本研究调查了内部标志物AM BC与环境NO ₂浓度之间的关系，并研究了mtDNAcn与NO ₂和AM BC的关系。

方法

居住在比利时的20名健康退休参与者（10对夫妇）组成的小组在一年中的11个时间点对健康和空气污染暴露进行了反复评估。通过将参与者移至意大利米兰（高曝光）和瑞典维德恩（低曝光）连续10天，我们暂时提高了曝光对比度。在每个评估时间点之前的连续5天中测量个人对NO _2的暴露。通过图像分析评估从7个时间点收集的诱导痰中回收的AM中的BC量。在每个时间点通过qPCR测定血液mtDNAcn。使用针对协变量和潜在混杂因素进行调整的线性混合效应模型，可以估算AM BC与NO ₂之间的关系以及mtDNAcn与NO ₂和AM BC之间的关系。

结果

米兰（64μg / m ³）的5天平均NO ₂平均浓度高于比利时（26μg/ m ³）的Vindeln（4μg / m ³）。每10微克/米³增量中的NO ₂在最近5天内曝光用0.07μm的相关²（95％CI：0.001〜0.012）的AM BC的中值面积的增加。NO ₂增加10μg/ m ³会导致mtDNAcn降低3.9％（95％CI：2.2至5.5％）。一致的是，每1微米²增量在AM BC的中区与24.8％（95％CI：6.8至39.3％）的mtDNAcn降低。

结论

在这种涉及将人员转移到环境空气污染程度高和低的地方的准实验环境中，我们发现AM BC的变化是根据过去5天中测得的环境空气污染水平得出的。较高的环境NO ₂和内部肺部BC负荷均与线粒体损害并存，如较低的mtDNA含量所示。