Severe air pollution links to higher mortality in COVID-19 patients: The "double-hit" hypothesis.
Identifieur interne : 000620 ( Main/Exploration ); précédent : 000619; suivant : 000621Severe air pollution links to higher mortality in COVID-19 patients: The "double-hit" hypothesis.
Auteurs : Antonio Frontera [Italie] ; Lorenzo Cianfanelli [Italie] ; Konstantinos Vlachos [France] ; Giovanni Landoni [Italie] ; George Cremona [Italie]Source :
- The Journal of infection [ 1532-2742 ] ; 2020.
Descripteurs français
- KwdFr :
- Betacoronavirus (MeSH), Dioxyde d'azote (effets indésirables), Facteurs de risque (MeSH), Hospitalisation (statistiques et données numériques), Humains (MeSH), Indice de gravité de la maladie (MeSH), Infections à coronavirus (mortalité), Infections à coronavirus (épidémiologie), Infections à coronavirus (étiologie), Italie (épidémiologie), Matière particulaire (effets indésirables), Pandémies (MeSH), Pneumopathie virale (mortalité), Pneumopathie virale (épidémiologie), Pneumopathie virale (étiologie), Polluants atmosphériques (effets indésirables), Pollution de l'air (effets indésirables), Pollution de l'air (statistiques et données numériques), Unités de soins intensifs (statistiques et données numériques), Épidémies de maladies (statistiques et données numériques).
- MESH :
- effets indésirables : Dioxyde d'azote, Matière particulaire, Polluants atmosphériques, Pollution de l'air.
- mortalité : Infections à coronavirus, Pneumopathie virale.
- statistiques et données numériques : Hospitalisation, Pollution de l'air, Unités de soins intensifs, Épidémies de maladies.
- épidémiologie : Infections à coronavirus, Italie, Pneumopathie virale.
- étiologie : Infections à coronavirus, Pneumopathie virale.
- Betacoronavirus, Facteurs de risque, Humains, Indice de gravité de la maladie, Pandémies.
- Wicri :
- geographic : Italie.
English descriptors
- KwdEn :
- Air Pollutants (adverse effects), Air Pollution (adverse effects), Air Pollution (statistics & numerical data), Betacoronavirus (MeSH), Coronavirus Infections (epidemiology), Coronavirus Infections (etiology), Coronavirus Infections (mortality), Disease Outbreaks (statistics & numerical data), Hospitalization (statistics & numerical data), Humans (MeSH), Intensive Care Units (statistics & numerical data), Italy (epidemiology), Nitrogen Dioxide (adverse effects), Pandemics (MeSH), Particulate Matter (adverse effects), Pneumonia, Viral (epidemiology), Pneumonia, Viral (etiology), Pneumonia, Viral (mortality), Risk Factors (MeSH), Severity of Illness Index (MeSH).
- MESH :
- chemical , adverse effects : Air Pollutants, Nitrogen Dioxide, Particulate Matter.
- geographic , epidemiology : Italy.
- adverse effects : Air Pollution.
- epidemiology : Coronavirus Infections, Pneumonia, Viral.
- etiology : Coronavirus Infections, Pneumonia, Viral.
- mortality : Coronavirus Infections, Pneumonia, Viral.
- statistics & numerical data : Air Pollution, Disease Outbreaks, Hospitalization, Intensive Care Units.
- Betacoronavirus, Humans, Pandemics, Risk Factors, Severity of Illness Index.
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.
DOI: 10.1016/j.jinf.2020.05.031
PubMed: 32447007
PubMed Central: PMC7240268
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Betacoronavirus (MeSH)</term>
<term>Coronavirus Infections (epidemiology)</term>
<term>Coronavirus Infections (etiology)</term>
<term>Coronavirus Infections (mortality)</term>
<term>Disease Outbreaks (statistics & numerical data)</term>
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<front><div type="abstract" xml:lang="en"><p><b>OBJECTIVES</b>
</p>
<p>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.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS</b>
</p>
<p>COVID-19 cases, ICU admissions and mortality rate were correlated with severity of air pollution in the Italian regions.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>RESULTS</b>
</p>
<p>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.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>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.</p>
</div>
</front>
</TEI>
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<DateCompleted><Year>2020</Year>
<Month>08</Month>
<Day>06</Day>
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<DateRevised><Year>2020</Year>
<Month>08</Month>
<Day>10</Day>
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<Title>The Journal of infection</Title>
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<ArticleTitle>Severe air pollution links to higher mortality in COVID-19 patients: The "double-hit" hypothesis.</ArticleTitle>
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<Abstract><AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">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.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">COVID-19 cases, ICU admissions and mortality rate were correlated with severity of air pollution in the Italian regions.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="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.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="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.</AbstractText>
<CopyrightInformation>Copyright © 2020 Elsevier Ltd. All rights reserved.</CopyrightInformation>
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<ForeName>Antonio</ForeName>
<Initials>A</Initials>
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<ForeName>Lorenzo</ForeName>
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<AffiliationInfo><Affiliation>University of Bordeaux, France.</Affiliation>
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<ForeName>Giovanni</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>IRCCS San Raffaele Scientific Institute, Via Olgettina 60, Milan, Italy; Vita-Salute San Raffaele University of Milan, Italy. Electronic address: landoni.giovanni@hsr.it.</Affiliation>
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<ForeName>George</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>IRCCS San Raffaele Scientific Institute, Via Olgettina 60, Milan, Italy. Electronic address: cremona.george@hsr.it.</Affiliation>
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<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058873" MajorTopicYN="N">Pandemics</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D052638" MajorTopicYN="N">Particulate Matter</DescriptorName>
<QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011024" MajorTopicYN="N">Pneumonia, Viral</DescriptorName>
<QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName>
<QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="Y">mortality</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<CoiStatement>Declaration of Competing Interest The authors declare no conflict of interest and no financial support for this study.</CoiStatement>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year>
<Month>04</Month>
<Day>08</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2020</Year>
<Month>05</Month>
<Day>05</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2020</Year>
<Month>05</Month>
<Day>06</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2020</Year>
<Month>5</Month>
<Day>25</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2020</Year>
<Month>8</Month>
<Day>7</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2020</Year>
<Month>5</Month>
<Day>25</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">32447007</ArticleId>
<ArticleId IdType="pii">S0163-4453(20)30285-1</ArticleId>
<ArticleId IdType="doi">10.1016/j.jinf.2020.05.031</ArticleId>
<ArticleId IdType="pmc">PMC7240268</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>France</li>
<li>Italie</li>
</country>
<region><li>Lombardie</li>
</region>
<settlement><li>Milan</li>
</settlement>
</list>
<tree><country name="Italie"><region name="Lombardie"><name sortKey="Frontera, Antonio" sort="Frontera, Antonio" uniqKey="Frontera A" first="Antonio" last="Frontera">Antonio Frontera</name>
</region>
<name sortKey="Cianfanelli, Lorenzo" sort="Cianfanelli, Lorenzo" uniqKey="Cianfanelli L" first="Lorenzo" last="Cianfanelli">Lorenzo Cianfanelli</name>
<name sortKey="Cremona, George" sort="Cremona, George" uniqKey="Cremona G" first="George" last="Cremona">George Cremona</name>
<name sortKey="Landoni, Giovanni" sort="Landoni, Giovanni" uniqKey="Landoni G" first="Giovanni" last="Landoni">Giovanni Landoni</name>
</country>
<country name="France"><noRegion><name sortKey="Vlachos, Konstantinos" sort="Vlachos, Konstantinos" uniqKey="Vlachos K" first="Konstantinos" last="Vlachos">Konstantinos Vlachos</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>
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