Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, The State University of New York, Buffalo, NY, USA.
Department of Biotechnical and Clinical Laboratory Sciences, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, USA.
Environ Res. 2021 Sep;200:111401. doi: 10.1016/j.envres.2021.111401. Epub 2021 Jun 2.
Untargeted metabolomics analyses have indicated that fatty acids and their hydroxy derivatives may be important metabolites in the mechanism through which air pollution potentiates diseases. This study aimed to use targeted analysis to investigate how metabolites in arachidonic acid (AA) and linoleic acid (LA) pathways respond to short-term changes in air pollution exposure. We further explored how they might interact with markers of antioxidant enzymes and systemic inflammation.
This study included a subset of participants (n = 53) from the Beijing Olympics Air Pollution (BoaP) study in which blood samples were collected before, during, and after the Beijing Olympics. Hydroxy fatty acids were measured by liquid chromatography/mass spectrometry (LC/MS). Native total fatty acids were measured as fatty acid methyl esters (FAMEs) using gas chromatography. A set of chemokines were measured by ELISA-based chemiluminescent assay and antioxidant enzyme activities were analyzed by kinetic enzyme assays. Changes in levels of metabolites over the three time points were examined using linear mixed-effects models, adjusting for age, sex, body mass index (BMI), and smoking status. Pearson correlation and repeated measures correlation coefficients were calculated to explore the relationships of metabolites with levels of serum chemokines and antioxidant enzymes.
12-hydroxyeicosatetraenoic acid (12-HETE) decreased by 50.5% (95% CI: -66.5, -34.5; p < 0.0001) when air pollution dropped during the Olympics and increased by 119.4% (95% CI: 36.4, 202.3; p < 0.0001) when air pollution returned to high levels after the Olympics. In contrast, 13-hydroxyoctadecadienoic acid (13-HODE) elevated significantly (p = 0.023) during the Olympics and decreased nonsignificantly after the games (p = 0.104). Interleukin 8 (IL-8) correlated with 12-HETE (r = 0.399, BH-adjusted p = 0.004) and 13-HODE (r = 0.342, BH-adjusted p = 0.014) over the three points; it presented a positive and moderate correlation with 12-HETE during the Olympics (r = 0.583, BH-adjusted p = 0.002) and with 13-HODE before the Olympics (r = 0.543, BH-adjusted p = 0.008).
AA- and LA-derived hydroxy metabolites are associated with air pollution and might interact with systemic inflammation in response to air pollution exposure.
非靶向代谢组学分析表明，脂肪酸及其羟基衍生物可能是空气污染增强疾病机制中的重要代谢物。本研究旨在使用靶向分析来研究花生四烯酸（AA）和亚油酸（LA）途径中的代谢物如何响应短期空气污染暴露的变化。我们进一步探讨了它们可能与抗氧化酶和全身炎症的标志物相互作用的方式。
本研究包括北京奥运会空气污染（BoaP）研究中的一部分参与者（n=53），其中在奥运会前、期间和之后采集了血液样本。使用液相色谱/质谱（LC/MS）测量羟基脂肪酸。使用气相色谱以脂肪酸甲酯（FAME）的形式测量天然总脂肪酸。通过基于 ELISA 的化学发光测定法测量一组趋化因子，并通过动力学酶测定法分析抗氧化酶活性。使用线性混合效应模型检查三个时间点的代谢物水平变化，调整年龄、性别、体重指数（BMI）和吸烟状况。计算 Pearson 相关和重复测量相关系数，以探讨代谢物与血清趋化因子和抗氧化酶水平的关系。
当奥运会期间空气污染下降时，12-羟基二十碳四烯酸（12-HETE）下降 50.5%（95%CI：-66.5，-34.5；p<0.0001），当奥运会后空气污染恢复到高水平时增加 119.4%（95%CI：36.4，202.3；p<0.0001）。相比之下，13-羟基十八碳二烯酸（13-HODE）在奥运会期间显著升高（p=0.023），赛后略有下降（p=0.104）。白细胞介素 8（IL-8）与 12-HETE（r=0.399，BH 调整后 p=0.004）和 13-HODE（r=0.342，BH 调整后 p=0.014）在三个时间点相关；它在奥运会期间与 12-HETE 呈正相关且中等相关（r=0.583，BH 调整后 p=0.002），在奥运会前与 13-HODE 呈正相关且中等相关（r=0.543，BH 调整后 p=0.008）。
AA 和 LA 衍生的羟基代谢物与空气污染有关，并且可能与空气污染暴露引起的全身炎症相互作用。
