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PM、NO、野火和其他环境暴露与更高的新冠发病率、严重程度和死亡率有关。

PM, NO, wildfires, and other environmental exposures are linked to higher Covid 19 incidence, severity, and death rates.

机构信息

East Carolina University, Greenville, NC, 5371 Knollwood Parkway Court #F, Hazelwood, MO, 63042, USA.

出版信息

Environ Sci Pollut Res Int. 2021 Oct;28(39):54429-54447. doi: 10.1007/s11356-021-15556-0. Epub 2021 Aug 19.

DOI:10.1007/s11356-021-15556-0
PMID:34410599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8374108/
Abstract

Numerous studies have linked outdoor levels of PM, PM, NO, O, SO, and other air pollutants to significantly higher rates of Covid 19 morbidity and mortality, although the rate in which specific concentrations of pollutants increase Covid 19 morbidity and mortality varies widely by specific country and study. As little as a 1-μg/m increase in outdoor PM is estimated to increase rates of Covid 19 by as much as 0.22 to 8%. Two California studies have strongly linked heavy wildfire burning periods with significantly higher outdoor levels of PM and CO as well as significantly higher rates of Covid 19 cases and deaths. Active smoking has also been strongly linked significantly increased risk of Covid 19 severity and death. Other exposures possibly related to greater risk of Covid 19 morbidity and mortality include incense, pesticides, heavy metals, dust/sand, toxic waste sites, and volcanic emissions. The exact mechanisms in which air pollutants increase Covid 19 infections are not fully understood, but are probably related to pollutant-related oxidation and inflammation of the lungs and other tissues and to the pollutant-driven alternation of the angiotensin-converting enzyme 2 in respiratory and other cells.

摘要

许多研究表明,室外的 PM、PM、NO、O、SO 等空气污染物水平与 COVID-19 的发病率和死亡率显著相关,尽管特定浓度的污染物增加 COVID-19 的发病率和死亡率的速度因特定国家和研究而异。据估计,室外 PM 每增加 1μg/m,COVID-19 的发病率就会增加 0.22 到 8%。两项加利福尼亚州的研究强烈表明,野火集中燃烧期与室外 PM 和 CO 水平显著升高以及 COVID-19 病例和死亡人数显著增加有关。主动吸烟也与 COVID-19 严重程度和死亡风险显著增加密切相关。其他可能与 COVID-19 发病率和死亡率增加相关的暴露包括香薰、农药、重金属、灰尘/沙子、有毒废物场和火山喷发。空气污染物增加 COVID-19 感染的具体机制尚未完全了解,但可能与污染物引起的肺部和其他组织的氧化和炎症有关,以及污染物驱动的呼吸和其他细胞中血管紧张素转化酶 2 的改变有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce2a/8374108/e50c4db94da3/11356_2021_15556_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce2a/8374108/9e38ea015a6b/11356_2021_15556_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce2a/8374108/6fda41f115fe/11356_2021_15556_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce2a/8374108/e50c4db94da3/11356_2021_15556_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce2a/8374108/9e38ea015a6b/11356_2021_15556_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce2a/8374108/6fda41f115fe/11356_2021_15556_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce2a/8374108/e50c4db94da3/11356_2021_15556_Fig3_HTML.jpg

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