Racial Disparities-Associated COVID-19 Mortality among Minority Populations in the US

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a betacoronavirus that causes the novel coronavirus disease 2019 (COVID-19), is highly transmissible and pathogenic for humans and may cause life-threatening disease and mortality, especially in individuals with underlying comorbidities. First identified in an outbreak in Wuhan, China, COVID-19 is affecting more than 185 countries and territories around the world, with more than 15,754,651 confirmed cases and more than 640,029 deaths. Since December 2019, SARS-CoV-2 transmission has become a global threat, which includes confirmed cases in all 50 states within the United States (US). As of 25 July 2020, the Johns Hopkins Whiting School of Engineering Center for Systems Science and Engineering reports more than 4,112,651 cases and 145,546 deaths. To date, health disparities are associated with COVID-19 mortality among underserved populations. Here, the author explores potential underlying reasons for reported disproportionate, increased risks of mortality among African Americans and Hispanics/Latinos with COVID-19 compared with non-Hispanic Whites. The author examines the underlying clinical implications that may predispose minority populations and the adverse clinical outcomes that may contribute to increased risk of mortality. Government and community-based strategies to safeguard minority populations at risk for increased morbidity and mortality are essential. Underserved populations living in poverty with limited access to social services across the US are more likely to have underlying medical conditions and are among the most vulnerable. Societal and cultural barriers for ethnic minorities to achieve health equity are systemic issues that may be addressed only through shifts in governmental policies, producing long-overdue, substantive changes to end health care inequities.

Keywords: African Americans; COVID-19; Hispanics/Latinos; coronavirus; health disparities; health inequities; infection; minorities; mortality; non-Hispanic Whites.

Figure 1

Diabetes and increased risk for severe coronavirus disease 2019 (COVID-19). Hypothetical model of uncontrolled glycemia in diabetic patients and increased risk for complications due to COVID-19. Patients who clinically present with normal or high blood pressure may be subject to undue complications related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. This is an illustration of the pancreas, responsible for insulin production and regulation and the immediate surrounding tissue and organs. Once infected with SARS-CoV-2 some patients will experience increased inflammation in the form of a cytokine storm. Corticosteroids often are prescribed to suppress inflammation but also are known to induce high glucose levels in the blood of both hypoglycemic and hyperglycemic patients. High blood glucose levels have been implicated in pulmonary injury and may affect the immune response, resulting in poor or delayed viral clearance. The degree of lung injury will include Angiotensin-converting enzyme 2 (ACE2)-mediated infection by SARS-CoV-2 that leads to hypoxia, vascular leakage, and potentially fatal pneumonia. TCR (T-cell receptor), CD4 (cluster designation 4), MHC (Major Histocompatibility). Adapted from Fraussen J et al. [40].

Figure 2

Hypertension and increased risk for severe COVID-19 disease. Hypothetical model of uncontrolled blood pressure in patients with hypertension and increased risk for complications due to COVID-19. The liver produces angiotensinogen, a peptide hormone that causes vasoconstriction that increases blood pressure. Angiotensinogen is converted to angiotensin I by renin from the kidneys then is converted to angiotensin II by the action of ACE (ACE-I). Normally angiotensin II (Ang. II) is converted to angiotensin-1–7 by the monocarboxypetidase ACEI homology ACE2. However, upon infection with SARS-CoV-2 the ACE2 protein serves as the entry receptor for the virus and is internalized in the endosome with SARS-CoV-2 during membrane fusion and uptake by infected cells. This leads to significant reduction in ACE2 surface expression and concomitant increase in angiotensin II, further leading to vasoconstriction that impacts blood pressure, inflammation, fibrosis, and oxidative stress in infected cells and tissues in multiple organs. Even more, the downregulation of ACE2 leads to the upregulation of aldosterone, a steroid hormone produced by the zona glomerulosa of the adrenal cortex, which increases the activity of ACE1. This action leads to higher levels of angiotensin II and an overall suppression of angiotensin-1–7, which is designed to mitigate the effects of angiotensin II via vasodilation, anti-inflammatory effects, and anti-oxidation. These levels of angiotensin II may result in MOD or failure. RAASA (renin-angiotensin-aldosterone system antagonist). ACE I (Angiotensin-converting enzyme 1).

Figure 3

Cardiovascular disease (CVD) and increased risk for severe COVID-19 disease. Hypothetical model of patients with CVD and increased risk for complications due to COVID-19. CVD patients with advanced age and elevated troponin I levels, and who have abnormal echocardiograms, are at high risk for developing more severe COVID-19 disease. These patients have been shown to have increased blood levels of IL-6, ferritin, LDH, and D-dimer, which are associated with the cytokine storm that likely would contribute to cardiac injury. High levels of ACE2 are known to be expressed on cardiomyocytes that could result in direct infection of heart tissue by SARS-CoV-2, which is thought to induce hypoxia leading to increase calcium levels resulting in apoptosis and death of cardiomyocytes; this likely would contribute to myocardial injury.

Figure 4

Lung disease and increased risk for severe COVID-19 disease. Hypothetical model of patients with pulmonary disease and increased risk for complications due to COVID-19. SARS-CoV-2 infection via ACE2 entry into alveolar epithelial cells in patients with COPD who smoke may lead to increased surface-expression ACE2 on lung epithelium that may increase the rate of infection in the lung and contribute to higher viral loads. Shown is the alveolar organization and resident cells that include pneumocytes Type I, pneumocytes Type II and alveolar macrophages. Elastic fibers are also shown and SARS-CoV-2 particles are shown as blue ovals. Alveolar cells pneumocytes type II are highly permissive for SARS-CoV-2 infection resulting in alveolar dysfunction, inflammation, vascular leakage, development of pulmonary emboli, and acute respiratory distress from poor gas exchange. Progressive viral infection and potential cytokine storm leads to pulmonary vascular leakage, alveolar edema, and monocyte infiltration at sites of infection, resulting in reduced lung function. Patients often require mechanical ventilation increasing the risk of delayed recovery, respiratory failure, septic shock, and MOD or failure. ARDS (Acute respiratory distress syndrome).