Zhang Shaocheng, Hu Juan, Xiao Guangjun, Chen Shu, Wang Huanhuan
Department of Clinical Laboratory Medicine, Suining Central Hospital, Suining, 629000, Sichuan, China.
School of Laboratory Medicine, Chengdu Medical College, Chengdu, 610500, Sichuan, China.
Chemosphere. 2023 Apr;319:138040. doi: 10.1016/j.chemosphere.2023.138040. Epub 2023 Feb 3.
Air particulate matter (PM) is an essential risk factor for lipid metabolism disorders. However, the underlying mechanism remains unclear. In this cross-sectional study, 216 healthcare workers were recruited to estimate the associations among the daily exposure dose (DED) of air PM, innate immune cells, and plasma lipid levels. All participants were divided into two groups according to the air particulate combined DED (DED-PMC). The peripheral white blood cell counts, lymphocyte counts, and monocyte counts and percentages were higher in the higher-exposure group (HEG) than in the lower-exposure group (LEG), whereas the percentage of natural-killer cells was lower in the HEG than in the LEG. The plasma concentrations of the total cholesterol, triglycerides, LDL-C, and apolipoprotein B were higher in the HEG than in the LEG, whereas the HDL-C and apolipoprotein A1 were lower in the HEG than in the LEG. A dose-effect analysis indicated that when the DED of the air PM increased, there were increased peripheral monocyte counts and percentages, a decreased NK cell percentage, elevated plasma concentrations of total cholesterol, triglycerides, LDL-C, and apolipoprotein B, and reduced plasma levels of HDL-C and apolipoprotein A1. In addition, the modification of the innate immune cells was accompanied by alterations in the plasma lipid levels in a dose-dependent manner. Mediation effect analysis suggested innate immune cells were the potential mediators for the associations among air PM exposure on abnormal lipid metabolism. These results indicated that chronic exposure to air PM may disturb lipid metabolism by altering the distribution of innate immune cells in the peripheral blood, ultimately advancing cardiovascular disease risk.
空气颗粒物（PM）是脂质代谢紊乱的一个重要风险因素。然而，其潜在机制仍不清楚。在这项横断面研究中，招募了216名医护人员，以评估空气PM的每日暴露剂量（DED）、固有免疫细胞和血浆脂质水平之间的关联。所有参与者根据空气颗粒物综合DED（DED-PMC）分为两组。高暴露组（HEG）的外周白细胞计数、淋巴细胞计数、单核细胞计数及百分比均高于低暴露组（LEG），而高暴露组的自然杀伤细胞百分比低于低暴露组。高暴露组的总胆固醇、甘油三酯、低密度脂蛋白胆固醇和载脂蛋白B的血浆浓度高于低暴露组，而高暴露组的高密度脂蛋白胆固醇和载脂蛋白A1低于低暴露组。剂量效应分析表明，当空气PM的DED增加时，外周单核细胞计数及百分比增加，NK细胞百分比降低，总胆固醇、甘油三酯、低密度脂蛋白胆固醇和载脂蛋白B的血浆浓度升高，高密度脂蛋白胆固醇和载脂蛋白A1的血浆水平降低。此外，固有免疫细胞的改变与血浆脂质水平的改变呈剂量依赖性。中介效应分析表明，固有免疫细胞是空气PM暴露与脂质代谢异常之间关联的潜在中介。这些结果表明，长期暴露于空气PM可能通过改变外周血中固有免疫细胞的分布来扰乱脂质代谢，最终增加心血管疾病风险。
