Sungkyunkwan University, Gyeonggi-do, Republic of Korea
Mutat Res. 2012 Dec 12;749(1-2):39-47. doi: 10.1016/j.mrgentox.2012.08.002.
Particulate matter (PM) has become an important health risk factor in our society. PM can easily deposit in the bronchi and lungs, causing diverse diseases such as respiratory infections, lung cancers and cardiovascular diseases. In recent days, more and more toxicological studies have been dealing with air particles in distinctive areas including industrial areas, transportation sites, or indoors. Studies on subway PM in particular, have been recognizing PM as an important health risk factor because many people use subways as a major mode of public transportation (4 million people a day in Korea). The main aim of the present study was to evaluate the genotoxic effects of organic extract (OE) of subway PM10 and potential attribution of PAHs to these effects. Particles were collected in the subway tunnel at Kil-eum station(Line 4) for one month and then extracted with Dichloromethane (DCM). Chinese Hamster Ovary cells(CHO-K1) and human normal bronchial cells (BEAS-2B) were exposed to OE, and MN and Comet assays were conducted to analyze the genotoxicity. The results showed that OE increased DNA or chromosome damages in both cell lines. In the modified Comet assay and MN assay with free radical scavengers, we confirmed that the genotoxic effect of OE was partially due to the oxidative damage on DNA. DCFHD Aassay also indicated that OE induced ROS generation in BEAS-2B cells. PAHs [benzo(a)anthracene,benzo(k)fluoranthrene, etc.], the most well-known carcinogens in polluted air, were detected in Kil-eum PM10. In conclusion, our findings confirmed that OE of subway PM10 has genotoxic effects on normal human lung cells, and oxidative stress could be one of the major mechanisms of these genotoxic effects.In addition, some genotoxic and carcinogenic PAHs were detected in OE by GC/MS/MS, even though PAHs level was not enough to increase CYP1A1 gene. Therefore, we suggest that additive or synergistic effects by unidentified chemicals as well as PAHs contained in OE of subway PM10 may induce genotoxic effects and further researches are needed to identify the genotoxic compounds in subway PM.
颗粒物（PM）已成为我们社会中的一个重要健康风险因素。PM 很容易沉积在支气管和肺部，导致多种疾病，如呼吸道感染、肺癌和心血管疾病。最近，越来越多的毒理学研究涉及到包括工业区、交通站点或室内等不同区域的空气颗粒。特别是对地铁 PM 的研究已经认识到 PM 是一个重要的健康风险因素，因为许多人将地铁作为主要的公共交通工具（韩国每天有 400 万人使用）。本研究的主要目的是评估地铁 PM10 有机提取物（OE）的遗传毒性作用，以及多环芳烃（PAHs）对这些作用的潜在归因。在基尔永站（4 号线）的地铁隧道中采集了一个月的颗粒物，然后用二氯甲烷（DCM）提取。将中国仓鼠卵巢细胞（CHO-K1）和人正常支气管细胞（BEAS-2B）暴露于 OE 中，并进行 MN 和彗星试验以分析遗传毒性。结果表明，OE 增加了两种细胞系的 DNA 或染色体损伤。在自由基清除剂存在的改良彗星试验和 MN 试验中，我们证实 OE 的遗传毒性作用部分是由于 DNA 的氧化损伤。DCFHD A 试验还表明，OE 诱导了 BEAS-2B 细胞中 ROS 的产生。多环芳烃（PAHs）[苯并（a）蒽、苯并（k）荧蒽等]是污染空气中最著名的致癌物质，在基尔永 PM10 中被检测到。总之，我们的研究结果证实，地铁 PM10 的 OE 对正常人类肺细胞具有遗传毒性作用，氧化应激可能是这些遗传毒性作用的主要机制之一。此外，通过 GC/MS/MS 检测到 OE 中存在一些遗传毒性和致癌性的 PAHs，尽管 PAHs 水平不足以增加 CYP1A1 基因。因此，我们建议，地铁 PM10 的 OE 中所含的未识别化学物质以及 PAHs 的附加或协同作用可能会引起遗传毒性作用，需要进一步研究以确定地铁 PM 中的遗传毒性化合物。
