National Institute of Environmental Health Sciences, National Health Research Institutes, Zhunan, Taiwan.
Institute of Cellular and System Medicine, National Health Research Institutes, Zhunan, Taiwan.
Sci Total Environ. 2020 Jun 1;719:137243. doi: 10.1016/j.scitotenv.2020.137243. Epub 2020 Feb 10.
Exposure to ambient fine particulate matter (PM) has been associated with vascular diseases in epidemiological studies. We have demonstrated previously that exposure to ambient PM caused pulmonary vascular remodeling in mice and increased vascular smooth muscle cells (VSMCs) viability. Here, we further demonstrated that exposure of mice to ambient PM increased urinary 8‑hydroxy‑2'‑deoxyguanosine (8-OHdG) and cytokines concentrations in the broncheoalveolar lavage. The objective of the present study was to identify the PM components related to vascular dysfunction. Exposure to PM collected from various areas and seasons in Taiwan significantly increased viability, oxidative stress, and inflammatory cytokines secretion in VSMCs. The mass concentrations of benz[a]anthracene (BaA), benzo[e]pyrene (BeP), perylene, dibenzo[a,e]pyrene, molybdenum, zinc (Zn), vanadium (V), and nickel in the PM were significantly associated with increased viability of VSMCs. These components, except BaA and BeP, also were significantly associated with chemokine (CC motif) ligand 5 (CCL5) concentrations in the VSMCs. The effects of V and Zn on cell viability and CCL5 expression, respectively, were verified. In addition, the mass concentrations of sulfate and manganese (Mn) in PM were significantly correlated with increased oxidative stress; this correlation was also confirmed. After extraction, the inorganic fraction of PM increased cell viability and oxidative stress, but the organic fraction of PM increased only cell viability, which was inhibited by an aryl hydrocarbon receptor antagonist. These data suggest that controlling the emission of Zn, V, Mn, sulfate, and PAHs may prevent the occurrence of PM-induced vascular diseases.
暴露于环境细颗粒物（PM）已在流行病学研究中与血管疾病相关。我们之前已经证明，暴露于环境 PM 会导致小鼠肺部血管重构，并增加血管平滑肌细胞（VSMCs）的活力。在这里，我们进一步证明，暴露于环境 PM 会增加小鼠尿液中 8-羟基-2'-脱氧鸟苷（8-OHdG）和细胞因子的浓度。本研究的目的是确定与血管功能障碍相关的 PM 成分。暴露于从台湾不同地区和季节采集的 PM 显著增加了 VSMCs 的活力、氧化应激和炎性细胞因子的分泌。PM 中苯并[a]蒽（BaA）、苯并[e]芘（BeP）、苝、二苯并[a，e]芘、钼、锌（Zn）、钒（V）和镍的质量浓度与 VSMCs 活力的增加显著相关。除 BaA 和 BeP 外，这些成分也与 VSMCs 中的趋化因子（CC 基序）配体 5（CCL5）浓度显著相关。验证了 V 和 Zn 对细胞活力和 CCL5 表达的影响。此外，PM 中硫酸盐和锰（Mn）的质量浓度与氧化应激增加显著相关，这一相关性也得到了证实。提取后，PM 的无机部分增加了细胞活力和氧化应激，但 PM 的有机部分仅增加了细胞活力，这一作用被芳香烃受体拮抗剂所抑制。这些数据表明，控制 Zn、V、Mn、硫酸盐和多环芳烃的排放可能有助于预防 PM 引起的血管疾病的发生。
