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Association of COVID-19 transmission with high levels of ambient pollutants: Initiation and impact of the inflammatory response on cardiopulmonary disease.
Lai, Angela; Chang, Megan L; O'Donnell, Ryan P; Zhou, Changcheng; Sumner, Jennifer A; Hsiai, Tzung K.
  • Lai A; Division of Cardiology, Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, CA, United States of America.
  • Chang ML; Division of Cardiology, Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, CA, United States of America.
  • O'Donnell RP; Division of Cardiology, Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, CA, United States of America.
  • Zhou C; Division of Biomedical Sciences, School of Medicine, University of California, Riverside, CA, United States of America.
  • Sumner JA; Department of Psychology, College of Life Sciences, University of California, Los Angeles, United States of America.
  • Hsiai TK; Division of Cardiology, Department of Medicine, David Geffen School of Medicine at University of California, Los Angeles, CA, United States of America; Department of Medicine, Greater Los Angeles VA Healthcare System, Los Angeles, CA, United States of America; Department of Bioengineering, Henry Sam
Sci Total Environ ; 779: 146464, 2021 Jul 20.
Article in English | MEDLINE | ID: covidwho-1135565
ABSTRACT
Ambient air pollution contributes to 7 million premature deaths annually. Concurrently, the ongoing coronavirus disease 2019 (COVID-19) pandemic, complicated with S-protein mutations and other variants, caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in over 2.5 million deaths globally. Chronic air pollution-mediated cardiopulmonary diseases have been associated with an increased incidence of hospitalization and mechanical ventilation following COVID-19 transmission. While the underlying mechanisms responsible for this association remain elusive, air pollutant-induced vascular oxidative stress and inflammatory responses have been implicated in amplifying COVID-19-mediated cytokine release and vascular thrombosis. In addition, prolonged exposure to certain types of particulate matter (PM2.5, d < 2.5 µm) has also been correlated with increased lung epithelial and vascular endothelial expression of the angiotensin-converting enzyme-2 (ACE2) receptors to which the SARS-CoV-2 spike glycoproteins (S) bind for fusion and internalization into host cells. Emerging literature has linked high rates of SARS-CoV-2 infection to regions with elevated levels of PM2.5, suggesting that COVID-19 lockdowns have been implicated in regional reductions in air pollutant-mediated cardiopulmonary effects. Taken together, an increased incidence of SARS-CoV-2-mediated cardiopulmonary diseases seems to overlap with highly polluted regions. To this end, we will review the redox-active components of air pollutants, the pathophysiology of SARS-CoV-2 transmission, and the key oxidative mechanisms and ACE2 overexpression underlying air pollution-exacerbated SARS-CoV-2 transmission.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Environmental Pollutants / COVID-19 Type of study: Experimental Studies / Observational study Topics: Variants Limits: Humans Language: English Journal: Sci Total Environ Year: 2021 Document Type: Article Affiliation country: J.scitotenv.2021.146464

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Environmental Pollutants / COVID-19 Type of study: Experimental Studies / Observational study Topics: Variants Limits: Humans Language: English Journal: Sci Total Environ Year: 2021 Document Type: Article Affiliation country: J.scitotenv.2021.146464