Kim Hyun-Jin, Hwang Juyeon, Park Jin-Ho
National Cancer Control Institute, National Cancer Center, Goyang, Korea.
Department of Family Medicine, Seoul National University Hospital, Seoul, Korea.
J Obes Metab Syndr. 2025 Apr 30;34(2):91-104. doi: 10.7570/jomes24036. Epub 2025 Mar 17.
Ambient air pollution is a serious public health issue worldwide. A growing number of studies has highlighted the negative effects of air pollution on metabolic syndrome (MetS) and its components, including abdominal obesity, disorders of lipid metabolism, elevated blood pressure, and impaired fasting blood glucose. This review provides a brief overview of epidemiological and genetic interaction studies of the links between chronic exposure to ambient air pollution and MetS and its components, as well as plausible mechanisms underlying these relationships. The cumulative evidence suggests that long-term exposure to air pollution, especially particulate matter, increases the risk of MetS and its components. These associations can be partly modified by baseline characteristics, lifestyle, and health conditions. Gene-by-air-pollution interaction studies, limited to candidate genes in the past, have recently been conducted at an expanded genome-wide level. However, more such studies are needed to comprehensively understand the genetics involved in the association between air pollution and MetS. Mechanistic evidence suggests potential biological pathways, including inflammation, oxidative stress, and endothelial dysfunction.
环境空气污染是全球一个严重的公共卫生问题。越来越多的研究强调了空气污染对代谢综合征(MetS)及其组成部分的负面影响,包括腹型肥胖、脂质代谢紊乱、血压升高和空腹血糖受损。本综述简要概述了长期暴露于环境空气污染与MetS及其组成部分之间联系的流行病学和基因相互作用研究,以及这些关系背后可能的机制。累积证据表明,长期暴露于空气污染,尤其是颗粒物,会增加患MetS及其组成部分的风险。这些关联可部分通过基线特征、生活方式和健康状况来改变。过去仅限于候选基因的基因与空气污染相互作用研究,最近已在全基因组水平上展开。然而,需要更多此类研究来全面了解空气污染与MetS关联中涉及的遗传学。机制证据表明了潜在的生物学途径,包括炎症、氧化应激和内皮功能障碍。