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二氧化氮污染通过改变免疫功能增加 COVID-19 的易感性。

Nitrogen dioxide pollution increases vulnerability to COVID-19 through altered immune function.

机构信息

Department of Biomedical Sciences and Human Oncology, Clinica Medica "A. Murri", University of Bari "Aldo Moro" Medical School, Bari, Italy.

International Society of Doctors for Environment (ISDE), Arezzo, Italy.

出版信息

Environ Sci Pollut Res Int. 2022 Jun;29(29):44404-44412. doi: 10.1007/s11356-022-19025-0. Epub 2022 Feb 8.

DOI:10.1007/s11356-022-19025-0
PMID:35133597
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9200946/
Abstract

Previous ecological studies suggest the existence of possible interplays between the exposure to air pollutants and SARS-CoV-2 infection. Confirmations at individual level, however, are lacking. To explore the relationships between previous exposure to particulate matter < 10 μm (PM) and nitrogen dioxide (NO), the clinical outcome following hospital admittance, and lymphocyte subsets in COVID-19 patients with pneumonia. In 147 geocoded patients, we assessed the individual exposure to PM and NO in the 2 weeks before hospital admittance. We divided subjects according to the clinical outcome (i.e., discharge at home vs in-hospital death), and explored the lymphocyte-related immune function as an index possibly affecting individual vulnerability to the infection. As compared with discharged subjects, patients who underwent in-hospital death presented neutrophilia, lymphopenia, lower number of T CD45, CD3, CD4, CD16/56 + CD3 + , and B CD19 + cells, and higher previous exposure to NO, but not PM. Age and previous NO exposure were independent predictors for mortality. NO concentrations were also negatively related with the number of CD45, CD3, and CD4 cells. Previous NO exposure is a co-factor independently affecting the mortality risk in infected individuals, through negative immune effects. Lymphopenia and altered lymphocyte subsets might precede viral infection due to nonmodifiable (i.e., age) and external (i.e., air pollution) factors. Thus, decreasing the burden of air pollutants should be a valuable primary prevention measure to reduce individual susceptibility to SARS-CoV-2 infection and mortality.

摘要

先前的生态学研究表明,暴露于空气污染物和 SARS-CoV-2 感染之间可能存在相互作用。然而,个体水平上的证实仍然缺乏。为了探索 COVID-19 肺炎患者先前暴露于颗粒物<10μm(PM)和二氧化氮(NO)与住院后临床结局以及淋巴细胞亚群之间的关系。在 147 名经地理编码的患者中,我们评估了住院前 2 周内个体暴露于 PM 和 NO 的情况。我们根据临床结局(即在家中出院与住院死亡)对受试者进行分组,并探讨了可能影响个体对感染易感性的淋巴细胞相关免疫功能作为指标。与出院患者相比,住院死亡患者表现为中性粒细胞增多、淋巴细胞减少、T CD45、CD3、CD4、CD16/56+CD3+和 B CD19+细胞数量减少,以及更高的先前 NO 暴露,但 PM 暴露则不然。年龄和先前的 NO 暴露是死亡的独立预测因子。NO 浓度与 CD45、CD3 和 CD4 细胞数量呈负相关。先前的 NO 暴露是通过负性免疫作用影响感染个体死亡风险的独立影响因素。淋巴细胞减少和改变的淋巴细胞亚群可能由于不可改变的(即年龄)和外部的(即空气污染)因素而先于病毒感染。因此,减少空气污染物的负担应该是一项有价值的初级预防措施,以降低个体对 SARS-CoV-2 感染和死亡率的易感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1864/9200946/48ace50f7e99/11356_2022_19025_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1864/9200946/dff323112946/11356_2022_19025_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1864/9200946/48ace50f7e99/11356_2022_19025_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1864/9200946/dff323112946/11356_2022_19025_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1864/9200946/48ace50f7e99/11356_2022_19025_Fig2_HTML.jpg

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