Fine particulate matter (PM2.5) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies. To measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM2.5, in the form of concentrated ambient particles (mean: 37.8 μg/m3, SD 6.5), and filtered air (mean: 2.1 μg/m3, SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure. Low-level PM2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM2.5 concentration (37.8 μg/m3) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV1) and FEV1/ forced vital capacity (FEV1/FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure. This study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM2.5 particles at levels near the PM2.5 US NAAQS standard. clinicaltrials.gov ; Identifier: NCT03232086 . The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.

中文翻译：

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低水平的细颗粒物会增加健康年轻人的血管损伤并降低肺功能


在受控人体暴露研究中观察到细颗粒物 (PM2.5) 相关的轻度炎症、心血管功能自主控制的改变以及细胞功能的变化。为了测量低水平 PM 暴露对全身和心肺的影响，我们将 20 名健康的年轻志愿者暴露于浓缩环境颗粒形式的 PM2.5（平均值：37.8 μg/m3，SD 6.5）和过滤空气（平均值）中。 ：2.1 μg/m3，SD 2.6）。在这项双盲交叉研究中，暴露顺序是随机的。在 4 小时暴露期间，志愿者（7 名女性和 13 名男性）进行了光强度锻炼以调节通气率。我们在暴露前、暴露后 1 小时以及暴露后 20 小时再次测量了肺、心脏和血液学终点。低水平的 PM2.5 会导致肺部和肺外的变化，其特征是系统炎症标志物的改变、心脏复极和肺功能下降。 PM2.5 浓度平均增加 (37.8 μg/m3) 显着增加血清淀粉样蛋白 A (SAA)、C 反应蛋白 (CRP)、可溶性细胞间粘附分子-1 (sICAM-1) 和可溶性血管细胞粘附分子- 1 (sVCAM-1)，暴露 1 小时后，相对于过滤空气对照，分别增加 8.7%、9.1%、10.7% 和 6.6%。 PM2.5 暴露 20 小时后，SAA 仍显着升高 (34.6%)，同时中性粒细胞百分比下降 5.7%。暴露后 1 小时，观察到肺功能下降，1 秒用力呼气量 (FEV1) 和 FEV1/用力肺活量 (FEV1/FVC) 分别下降 0.8% 和 1.2%。此外，在 PM2.5 暴露后复极结果中观察到性别特异性变化。在男性中，P 波和 QRS 波群分别增加 15.4 和 5。暴露后 1 小时 4%。这项研究是第一项受控人体暴露研究，旨在证明暴露于接近 PM2.5 美国 NAAQS 标准的浓缩环境空气 PM2.5 颗粒的生物效应。临床试验.gov；标识符：NCT03232086。该研究于2017年7月25日进行回顾性登记，随后于2017年10月25日进行最终数据收集和数据分析。