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严重空气污染与 COVID-19 患者死亡率升高有关:“双重打击”假说。

Severe air pollution links to higher mortality in COVID-19 patients: The "double-hit" hypothesis.

机构信息

IRCCS San Raffaele Scientific Institute, Via Olgettina 60, Milan, Italy.

University of Bordeaux, France.

出版信息

J Infect. 2020 Aug;81(2):255-259. doi: 10.1016/j.jinf.2020.05.031. Epub 2020 May 21.

DOI:10.1016/j.jinf.2020.05.031
PMID:32447007
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7240268/
Abstract

OBJECTIVES

In areas of SARS-CoV-2 outbreak worldwide mean air pollutants concentrations vastly exceed the maximum limits. Chronic exposure to air pollutants have been associated with lung ACE-2 over-expression which is known to be the main receptor for SARS-CoV-2. The aim of this study was to analyse the relationship between air pollutants concentration (PM 2.5 and NO2) and COVID-19 outbreak, in terms of transmission, number of patients, severity of presentation and number of deaths.

METHODS

COVID-19 cases, ICU admissions and mortality rate were correlated with severity of air pollution in the Italian regions.

RESULTS

The highest number of COVID-19 cases were recorded in the most polluted regions with patients presenting with more severe forms of the disease requiring ICU admission. In these regions, mortality was two-fold higher than the other regions.

CONCLUSIONS

From the data available we propose a "double-hit hypothesis": chronic exposure to PM 2.5 causes alveolar ACE-2 receptor overexpression. This may increase viral load in patients exposed to pollutants in turn depleting ACE-2 receptors and impairing host defences. High atmospheric NO2 may provide a second hit causing a severe form of SARS-CoV-2 in ACE-2 depleted lungs resulting in a worse outcome.

摘要

目的

在全球 SARS-CoV-2 爆发地区,空气中的污染物浓度普遍大幅超过最高限值。慢性暴露于空气污染物与肺部 ACE-2 的过度表达有关,而 ACE-2 已知是 SARS-CoV-2 的主要受体。本研究旨在分析空气中污染物浓度(PM2.5 和 NO2)与 COVID-19 爆发之间的关系,包括传播、患者数量、发病严重程度和死亡人数。

方法

将意大利各地区的空气污染严重程度与 COVID-19 病例、重症监护病房(ICU)入院和死亡率相关联。

结果

COVID-19 病例最多的地区污染最严重,患者的疾病表现更为严重,需要 ICU 入院治疗。在这些地区,死亡率是其他地区的两倍。

结论

根据现有数据,我们提出了一个“双重打击假说”:慢性暴露于 PM2.5 会导致肺泡 ACE-2 受体过度表达。这可能会增加暴露于污染物的患者的病毒载量,进而耗尽 ACE-2 受体并损害宿主防御。大气中高浓度的 NO2 可能会造成第二次打击,导致 ACE-2 耗尽的肺部出现严重的 SARS-CoV-2 感染,从而导致更糟糕的结果。

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