张颖, 贺玲, 魏槐, 吴卫东, 李娟. PM2.5对变应性鼻炎影响研究进展[J]. 环境与职业医学, 2023, 40(7): 834-838, 847. DOI: 10.11836/JEOM22511
引用本文: 张颖, 贺玲, 魏槐, 吴卫东, 李娟. PM2.5对变应性鼻炎影响研究进展[J]. 环境与职业医学, 2023, 40(7): 834-838, 847. DOI: 10.11836/JEOM22511
ZHANG Ying, HE Ling, WEI Huai, WU Weidong, LI Juan. Research progress on influence of PM2.5 on allergic rhinitis[J]. Journal of Environmental and Occupational Medicine, 2023, 40(7): 834-838, 847. DOI: 10.11836/JEOM22511
Citation: ZHANG Ying, HE Ling, WEI Huai, WU Weidong, LI Juan. Research progress on influence of PM2.5 on allergic rhinitis[J]. Journal of Environmental and Occupational Medicine, 2023, 40(7): 834-838, 847. DOI: 10.11836/JEOM22511

PM2.5对变应性鼻炎影响研究进展

Research progress on influence of PM2.5 on allergic rhinitis

  • 摘要:

    变应性鼻炎(AR)是危害全球范围的主要慢性炎症疾病之一,其症状持续时间长,反复发作,严重影响人群身心健康。现有研究表明,AR发生发展与遗传和环境因素相关。近年来,空气污染对人体健康的危害日益受到关注,而细颗粒物(PM2.5)是大气污染物的主要有害效应成分,其粒径小,易吸附多种有害物质,可进入呼吸道,损害鼻黏膜,参与AR的发生发展过程。目前大量流行病学研究证实PM2.5与AR发病率及发病症状严重程度呈正相关,但其确切作用机制尚不清楚。因此,研究PM2.5暴露对AR损害作用机制有望为探究AR发病及恶化提供新的线索。本文回顾了近年来关于PM2.5暴露与AR的流行病学研究和毒理学机制研究;论述了PM2.5诱导AR发生发展的潜在生物学机制包括鼻黏膜炎性损伤、氧化应激和免疫损伤;进一步提出了研究PM2.5暴露致AR加重的新的研究方向,即神经免疫失调和菌群失衡可能参与AR的进展,其在PM2.5诱发的毒性效应中发挥一定作用。通过对PM2.5暴露与AR的现有研究进行综述,以期为制定有效防治AR措施提供思路及理论依据。

     

    Abstract:

    Allergic rhinitis (AR) is one of the main chronic inflammatory diseases that pose a global threat. Its symptoms persist for a long time, recur, and seriously affect the physical and mental health of the patients. Existing research has shown that the occurrence and development of AR are related to genetic and environmental factors. In recent years, the harm of air pollution to human health has received increasing attention, and fine particulate matter (PM2.5) is the main harmful component of air pollutants. Its small particle size makes it easy to absorb various harmful substances, enter the respiratory tract, damage the nasal mucosa, and participate in the occurrence and development process of AR. At present, a large number of epidemiological studies have confirmed that PM2.5 is positively related to the incidence rate and severity of symptoms of AR, but its exact mechanism is still unclear. Therefore, studying the mechanism of PM2.5 exposure on AR damage is expected to provide new clues for exploring the pathogenesis and deterioration of AR. This article reviewed the epidemiological studies and toxicological mechanisms of PM2.5 exposure and AR in recent years; discussed the potential biological mechanisms of PM2.5 induced AR occurrence and development, including nasal mucositis damage, oxidative stress, and immune damage. Furthermore, a new research direction was proposed, which suggested that neuroimmune disorders and bacterial imbalance may be involved in the progression of AR and play a certain role in the toxic effects induced by PM2.5. We aim to provide ideas and a theoretical basis for developing effective measures to prevent and treat AR.

     

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