State Key Joint Laboratory for Environmental Simulation and Pollution Control, College of Environmental Sciences and Engineering, And Center for Environment and Health, Peking University, Beijing, 100871, PR China.
State Key Joint Laboratory for Environmental Simulation and Pollution Control, College of Environmental Sciences and Engineering, And Center for Environment and Health, Peking University, Beijing, 100871, PR China; Department of Epidemiology and Biostatistics, MRC Centre for Environment and Health, Imperial College London, London, UK.
Chemosphere. 2020 Aug;253:126748. doi: 10.1016/j.chemosphere.2020.126748. Epub 2020 Apr 11.
Polycyclic aromatic hydrocarbons (PAHs) are key air pollutants that may contribute to the risk of numerous diseases by inducing inflammation and oxidative stress. Individuals with metabolic disorders may be more susceptible to PAH-induced inflammation and oxidative stress. To test this hypothesis, we designed a panel study involving 60 patients with pre-type 2 diabetes (pre-T2D) and 60 reference participants, and conducted up to seven repeated clinical examinations. Urinary metabolites of PAHs (i.e., OH-PAHs), measured as indicators of total PAH exposure, showed significant associations with markers of respiratory and systemic inflammation, including exhaled nitric oxide, interleukin (IL)-6 in exhaled breath condensate, and blood IL-2 and IL-8 levels and leucocyte count. The most significant effect was on urinary malondiadehyde (MDA), a marker of lipid peroxidation; a onefold increase of OH-PAHs was associated with 9.2-46.0% elevation in MDA in pre-T2D participants and 9.8-31.2% increase in healthy references. Pre-T2D participants showed greater increase in MDA, suggesting that metabolic disorder enhanced the oxidative damage induced by PAH exposure. This study revealed the association between PAH exposure and markers of inflammation and oxidative stress, and the enhanced responses of pre-T2D patients suggested that individuals with metabolic disorders were more susceptible to the adverse health effects of PAH exposure.
多环芳烃(PAHs)是主要的空气污染物,通过诱导炎症和氧化应激,可能会增加罹患多种疾病的风险。患有代谢紊乱的个体可能更容易受到 PAH 诱导的炎症和氧化应激的影响。为了验证这一假设,我们设计了一项包含 60 名前驱 2 型糖尿病(pre-T2D)患者和 60 名参照参与者的面板研究,并进行了多达 7 次重复的临床检查。作为总 PAH 暴露的指标,尿液中多环芳烃(PAHs)的代谢物(即 OH-PAHs)与呼吸和全身炎症标志物(包括呼出气一氧化氮、呼出气冷凝液中的白细胞介素-6(IL-6)和血液中白细胞介素-2(IL-2)和白细胞介素-8(IL-8)水平及白细胞计数)呈显著相关。其影响最显著的是尿液丙二醛(MDA),这是一种脂质过氧化的标志物;PAHs 中 OH-PAHs 增加一倍,与 pre-T2D 参与者 MDA 升高 9.2-46.0%和健康参照者 MDA 升高 9.8-31.2%有关。pre-T2D 参与者的 MDA 升高幅度更大,这表明代谢紊乱增强了 PAH 暴露引起的氧化损伤。这项研究揭示了 PAH 暴露与炎症和氧化应激标志物之间的关联,以及 pre-T2D 患者反应增强的现象,这表明患有代谢紊乱的个体更容易受到 PAH 暴露对健康产生不良影响。