Evidence for a connection between coronavirus disease-19 and 5G; may have exacerbated the COVID-19 pandemic by weakening host immunity and increasing SARS-CoV-2 virulence

Dec 3, 2021


There is a substantial overlap in pathobiology between COVID-19 and WCR exposure. The evidence presented here indicates that mechanisms involved in the clinical progression of COVID-19 could also be generated, according to experimental data, by WCR exposure. Therefore, we propose a link between adverse bioeffects of WCR exposure from wireless devices and COVID-19.

Specifically, evidence presented here supports a premise that WCR and, in particular, 5G, which involves densification of 4G, may have exacerbated the COVID-19 pandemic by weakening host immunity and increasing SARS-CoV-2 virulence by (1) causing morphologic changes in erythrocytes including echinocyte and rouleaux formation that may be contributing to hypercoagulation; (2) impairing microcirculation and reducing erythrocyte and hemoglobin levels exacerbating hypoxia; (3) amplifying immune dysfunction, including immunosuppression, autoimmunity, and hyperinflammation; (4) increasing cellular oxidative stress and the production of free radicals exacerbating vascular injury and organ damage; (5) increasing intracellular Ca2+ essential for viral entry, replication, and release, in addition to promoting pro-inflammatory pathways; and (6) worsening heart arrhythmias and cardiac disorders.

WCR exposure is a widespread, yet often neglected, environmental stressor that can produce a wide range of adverse bioeffects. For decades, independent research scientists worldwide have emphasized the health risks and cumulative damage caused by WCR [,]. The evidence presented here is consistent with a large body of established research. Healthcare workers and policymakers should consider WCR a potentially toxic environmental stressor. Methods for reducing WCR exposure should be provided to all patients and the general population.


Coronavirus disease (COVID-19) public health policy has focused on the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus and its effects on human health while environmental factors have been largely ignored. In considering the epidemiological triad (agent-host-environment) applicable to all disease, we investigated a possible environmental factor in the COVID-19 pandemic: ambient radiofrequency radiation from wireless communication systems including microwaves and millimeter waves. SARS-CoV-2, the virus that caused the COVID-19 pandemic, surfaced in Wuhan, China shortly after the implementation of city-wide (fifth generation [5G] of wireless communications radiation [WCR]), and rapidly spread globally, initially demonstrating a statistical correlation to international communities with recently established 5G networks. In this study, we examined the peer-reviewed scientific literature on the detrimental bioeffects of WCR and identified several mechanisms by which WCR may have contributed to the COVID-19 pandemic as a toxic environmental cofactor. By crossing boundaries between the disciplines of biophysics and pathophysiology, we present evidence that WCR may: (1) cause morphologic changes in erythrocytes including echinocyte and rouleaux formation that can contribute to hypercoagulation; (2) impair microcirculation and reduce erythrocyte and hemoglobin levels exacerbating hypoxia; (3) amplify immune system dysfunction, including immunosuppression, autoimmunity, and hyperinflammation; (4) increase cellular oxidative stress and the production of free radicals resulting in vascular injury and organ damage; (5) increase intracellular Ca2+ essential for viral entry, replication, and release, in addition to promoting pro-inflammatory pathways; and (6) worsen heart arrhythmias and cardiac disorders.


3.1. Blood changes

WCR exposure can cause morphologic changes in blood readily seen through phase contrast or dark-field microscopy of live peripheral blood samples. In 2013, Havas observed erythrocyte aggregation including rouleaux (rolls of stacked red blood cells) in live peripheral blood samples following 10 min human exposure to a 2.4 GHz cordless phone []. Although not peer reviewed, one of us (Rubik) investigated the effect of 4G LTE mobile phone radiation on the peripheral blood of ten human subjects, each of whom had been exposed to cell phone radiation for two consecutive 45-min intervals []. Two types of effects were observed: increased stickiness and clumping of red blood cells with rouleaux formation, and subsequent formation of echinocytes (spiky red blood cells). Red blood cell clumping and aggregation are known to be actively involved in blood clotting []. The prevalence of this phenomenon on exposure to WCR in the human population has not yet been determined. Larger controlled studies should be performed to further investigate this phenomenon.

Similar red blood cell changes have been described in peripheral blood of COVID-19 patients []. Rouleaux formation has been observed in 1/3 of COVID-19 patients, whereas spherocytes and echinocyte formation is more variable. Spike protein engagement with ACE2 receptors on cells lining the blood vessels can lead to endothelial damage, even when isolated []. Rouleaux formation, particularly in the setting of underlying endothelial damage, can clog the microcirculation, impeding oxygen transport, contributing to hypoxia, and increasing the risk of thrombosis []. Thrombogenesis associated with SARS-CoV-2 infection may also be caused by direct viral binding to ACE2 receptors on platelets [].

Additional blood effects have been observed in both humans and animals exposed to WCR. In 1977, a Russian study reported that rodents irradiated with 5 – 8 mm waves (60 – 37 GHz) at 1 mW/cm2 for 15 min/day over 60 days developed hemodynamic disorders, suppressed red blood cell formation, reduced hemoglobin, and an inhibition of oxygen utilization (oxidative phosphorylation by the mitochondria) []. In 1978, a 3-year Russian study on 72 engineers exposed to millimeter wave generators emitting at 1 mW/cm2 or less showed a decrease in their hemoglobin levels and red blood cell counts, and a tendency toward hypercoagulation, whereas a control group showed no changes []. Such deleterious hematologic effects from WCR exposure may also contribute to the development of hypoxia and blood clotting observed in COVID-19 patients.

It has been proposed that the SARS-CoV-2 virus attacks erythrocytes and causes degradation of hemoglobin []. Viral proteins may attack the 1-beta chain of hemoglobin and capture the porphyrin, along with other proteins from the virus catalyzing the dissociation of iron from heme []. In principle this would reduce the number of functional erythrocytes and cause the release of free iron ions that could cause oxidative stress, tissue damage, and hypoxia. With hemoglobin partially destroyed and lung tissue damaged by inflammation, patients would be less able to exchange carbon dioxide (CO2) and oxygen (O2), and would become oxygen depleted. In fact, some COVID-19 patients show reduced hemoglobin levels, measuring 7.1 g/L and even as low as 5.9 g/L in severe cases []. Clinical studies of almost 100 patients from Wuhan revealed that the hemoglobin levels in the blood of most patients infected with SARS-CoV-2 are significantly lowered resulting in compromised delivery of oxygen to tissues and organs []. In a meta-analysis of four studies with a total of 1210 patients and 224 with severe disease, hemoglobin values were reduced in COVID-19 patients with severe disease compared to those with milder forms []. In another study on 601 COVID-19 patients, 14.7% of anemic COVID-19 ICU patients and 9% of non-ICU COVID-19 patients had autoimmune hemolytic anemia []. In patients with severe COVID-19 disease, decreased hemoglobin along with elevated erythrocyte sedimentation rate (ESR), C-reactive protein, lactate dehydrogenase, albumin [], serum ferritin [], and low oxygen saturation [] provide additional support for this hypothesis. In addition, packed red blood cell transfusion may promote recovery of COVID-19 patients with acute respiratory failure [].

In short, both WCR exposure and COVID-19 may cause deleterious effects on red blood cells and reduced hemoglobin levels contributing to hypoxia in COVID-19. Endothelial injury may further contribute to hypoxia and many of the vascular complications seen in COVID-19 [] that are discussed in the next section.

3.2. Oxidative stress

Oxidative stress is a non-specific pathological condition reflecting an imbalance between an increased production of ROS and an inability of the organism to detoxify the ROS or to repair the damage they cause to biomolecules and tissues []. Oxidative stress can disrupt cell signaling, cause the formation of stress proteins, and generate highly reactive free radicals, which can cause DNA and cell membrane damage.

SARS-CoV-2 inhibits intrinsic pathways designed to reduce ROS levels, thereby increasing morbidity. Immune dysregulation, that is, the upregulation of interleukin (IL)-6 and tumor necrosis factor α (TNF-α) [] and suppression of interferon (IFN) α and IFN β [] have been identified in the cytokine storm accompanying severe COVID-19 infections and generates oxidative stress []. Oxidative stress and mitochondrial dysfunction may further perpetuate the cytokine storm, worsening tissue damage, and increasing the risk of severe illness and death.

Similarly low-level WCR generates ROS in cells that cause oxidative damage. In fact, oxidative stress is considered to be one of the primary mechanisms in which WCR exposure causes cellular damage. Among 100 currently available peer-reviewed studies investigating oxidative effects of low-intensity WCR, 93 of these studies confirmed that WCR induces oxidative effects in biological systems []. WCR is an oxidative agent with a high pathogenic potential especially when exposure is continuous [].

Oxidative stress is also an accepted mechanism causing endothelial damage []. This may manifest in patients with severe COVID-19 in addition to increasing the risk for blood clot formation and worsening hypoxemia []. Low levels of glutathione, the master antioxidant, have been observed in a small group of COVID-19 patients, with the lowest level found in the most severe cases []. The finding of low glutathione levels in these patients further supports oxidative stress as a component of this disease []. In fact, glutathione, the major source of sulfhydryl-based antioxidant activity in the human body, may be pivotal in COVID-19 []. Glutathione deficiency has been proposed as the most likely cause of serious manifestations in COVID-19 []. The most common co-morbidities, hypertension []; obesity []; diabetes []; and chronic obstructive pulmonary disease [] support the concept that pre-existing conditions causing low levels of glutathione may work synergistically to create the “perfect storm” for both the respiratory and vascular complications of severe infection. Another paper citing two cases of COVID-19 pneumonia treated successfully with intravenous glutathione also supports this hypothesis [].

Many studies report oxidative stress in humans exposed to WCR. Peraica et al. [] found diminished blood levels of glutathione in workers exposed to WCR from radar equipment (0.01 mW/cm2 – 10 mW/cm2; 1.5 – 10.9 GHz). Garaj-Vrhovac et al. [] studied bioeffects following exposure to non-thermal pulsed microwaves from marine radar (3 GHz, 5.5 GHz, and 9.4 GHz) and reported reduced glutathione levels and increased malondialdehyde (marker for oxidative stress) in an occupationally exposed group []. Blood plasma of individuals residing near mobile phone base stations showed significantly reduced glutathione, catalase, and superoxide dismutase levels over unexposed controls []. In a study on human exposure to WCR from mobile phones, increased blood levels of lipid peroxide were reported, while enzymatic activities of superoxide dismutase and glutathione peroxidase in the red blood cells decreased, indicating oxidative stress [].

In a study on rats exposed to 2450 MHz (wireless router frequency), oxidative stress was implicated in causing red blood cell lysis (hemolysis) []. In another study, rats exposed to 945 MHz (base station frequency) at 0.367 mW/cm2 for 7 h/day, over 8 days, demonstrated low glutathione levels and increased malondialdehyde and superoxide dismutase enzyme activity, hallmarks for oxidative stress []. In a long-term controlled study on rats exposed to 900 MHz (mobile phone frequency) at 0.0782 mW/cm2 for 2 h/day for 10 months, there was a significant increase in malondialdehyde and total oxidant status over controls []. In another long-term controlled study on rats exposed to two mobile phone frequencies, 1800 MHz and 2100 MHz, at power densities 0.04 – 0.127 mW/cm2 for 2 h/day over 7 months, significant alterations in oxidant-antioxidant parameters, DNA strand breaks, and oxidative DNA damage were found [].

There is a correlation between oxidative stress and thrombogenesis []. ROS can cause endothelial dysfunction and cellular damage. The endothelial lining of the vascular system contains ACE2 receptors that are targeted by SARS-CoV-2. The resulting endotheliitis can cause luminal narrowing and result in diminished blood flow to downstream structures. Thrombi in arterial structures can further obstruct blood flow causing ischemia and/or infarcts in involved organs, including pulmonary emboli and strokes. Abnormal blood coagulation leading to micro-emboli was a recognized complication early in the history of COVID-19 []. Out of 184 ICU COVID-19 patients, 31% showed thrombotic complications []. Cardiovascular clotting events are a common cause of COVID-19 deaths []. Pulmonary embolism, disseminated intravascular coagulation (DIC), liver, cardiac, and renal failure have all been observed in COVID-19 patients [].

Patients with the highest cardiovascular risk factors in COVID-19 includ males, the elderly, diabetics, and obese and hypertensive patients. However, increased incidence of strokes in younger patients with COVID-19 has also been described [].

Oxidative stress is caused by WCR exposure and is known to be implicated in cardiovascular disease. Ubiquitous environmental exposure to WCR may contribute to cardiovascular disease by creating a chronic state of oxidative stress []. This would lead to oxidative damage to cellular constituents and alter signal transduction pathways. In addition, pulse-modulated WCR can cause oxidative injury in liver, lung, testis, and heart tissues mediated by lipid peroxidation, increased levels of nitric oxides, and suppression of the antioxidant defense mechanism [].

In summary, oxidative stress is a major component in the pathophysiology of COVID-19 as well as in cellular damage caused by WCR exposure.

3.3. Immune system disruption and activation

When SARS-CoV-2 first infects the human body, it attacks cells lining the nose, throat, and upper airway harboring ACE2 receptors. Once the virus gains access to a host cell through one of its spike proteins, which are the multiple protuberances projecting from the viral envelope that bind to ACE2 receptors, it converts the cell into a virus self-replicating entity.

In response to COVID-19 infection, both an immediate systemic innate immune response as well as a delayed adaptive response has been shown to occur []. The virus can also cause a dysregulation of the immune response, particularly in the decreased production of T-lymphocytes. []. Severe cases tend to have lower lymphocyte counts, higher leukocyte counts and neutrophil-lymphocyte ratios, as well as lower percentages of monocytes, eosinophils, and basophils []. Severe cases of COVID-19 show the greatest impairment in T-lymphocytes.

In comparison, low-level WCR studies on laboratory animals also show impaired immune function []. Findings include physical alterations in immune cells, a degradation of immunological responses, inflammation, and tissue damage. Baranski [] exposed guinea pigs and rabbits to continuous or pulse-modulated 3000 MHz microwaves at an average power density of 3.5 mW/cm2 for 3 h/day over 3 months and found nonthermal changes in lymphocyte counts, abnormalities in nuclear structure, and mitosis in the erythroblastic cell series in the bone marrow and in lymphoid cells in lymph nodes and spleen. Other investigators have shown diminished T-lymphocytes or suppressed immune function in animals exposed to WCR. Rabbits exposed to 2.1 GHz at 5mW/cm2 for 3 h/day, 6 days/week, for 3 months, showed suppression of T-lymphocytes []. Rats exposed to 2.45 GHz and 9.7 GHz for 2 h/day, 7 days/week, for 21 months showed a significant decrease in the levels of lymphocytes and an increase in mortality at 25 months in the irradiated group []. Lymphocytes harvested from rabbits irradiated with 2.45 GHz for 23 h/day for 6 months show a significant suppression in immune response to a mitogen [].

In 2009, Johansson conducted a literature review, which included the 2007 Bioinitiative Report. He concluded that electromagnetic fields (EMF) exposure, including WCR, can disturb the immune system and cause allergic and inflammatory responses at exposure levels significantly less than current national and international safety limits and raise the risk for systemic disease []. A review conducted by Szmigielski in 2013 concluded that weak RF/microwave fields, such as those emitted by mobile phones, can affect various immune functions both in vitro and in vivo []. Although the effects are historically somewhat inconsistent, most research studies document alterations in the number and activity of immune cells from RF exposure. In general, short-term exposure to weak microwave radiation may temporarily stimulate an innate or adaptive immune response, but prolonged irradiation inhibits those same functions.

In the acute phase of COVID-19 infection, blood tests demonstrate elevated ESR, C-reactive protein, and other elevated inflammatory markers [], typical of an innate immune response. Rapid viral replication can cause death of epithelial and endothelial cells and result in leaky blood vessels and pro-inflammatory cytokine release []. Cytokines, proteins, peptides, and proteoglycans that modulate the body’s immune response, are modestly elevated in patients with mild-to-moderate disease severity []. In those with severe disease, an uncontrolled release of pro-inflammatory cytokines–a cytokine storm–can occur. Cytokine storms originate from an imbalance in T-cell activation with dysregulated release of IL-6, IL-17, and other cytokines. Programmed cell death (apoptosis), ARDS, DIC, and multi-organ system failure can all result from a cytokine storm and increase the risk of mortality.

By comparison, Soviet researchers found in the 1970s that radiofrequency radiation can damage the immune system of animals. Shandala [] exposed rats to 0.5 mW/cm2 microwaves for 1 month, 7 h/day, and found impaired immune competence and induction of autoimmune disease. Rats irradiated with 2.45 GHz at 0.5 mW/cm2 for 7 h daily for 30 days produced autoimmune reactions, and 0.1 – 0.5 mW/cm2 produced persistent pathological immune reactions []. Exposure to microwave radiation, even at low levels (0.1 – 0.5 mW/cm2), can impair immune function, causing physical alterations in the essential cells of the immune system and a degradation of immunologic responses []. Szabo et al. [] examined the effects of 61.2 GHz exposure on epidermal keratinocytes and found an increase in IL-1b, a pro-inflammatory cytokine. Makar et al. [] found that immunosuppressed mice irradiated 30 min/day for 3 days by 42.2 GHz showed increased levels of TNF-α, a cytokine produced by macrophages.

In short, COVID-19 can lead to immune dysregulation as well as cytokine storms. By comparison, exposure to low-level WCR as observed in animal studies can also compromise the immune system, with chronic daily exposure producing immunosuppression or immune dysregulation including hyperactivation.

3.4. Increased intracellular calcium

In 1992, Walleczek first suggested that ELF electromagnetic fields (<3000 Hz) may be affecting membrane-mediated Ca2+ signaling and lead to increased intracellular Ca2+ []. The mechanism of irregular gating of voltage-gated ion channels in cell membranes by polarized and coherent, oscillating electric or magnetic fields was first presented in 2000 and 2002 [,]. Pall [] in his review of WCR-induced bioeffects combined with use of calcium channel blockers (CCB) noted that voltage-gated calcium channels play a major role in WCR bioeffects. Increased intracellular Ca+2 results from the activation of voltage-gated calcium channels, and this may be one of the primary mechanisms of action of WCR on organisms.

Intracellular Ca2+ is essential for virus entry, replication, and release. It has been reported that some viruses can manipulate voltage-gated calcium channels to increase intracellular Ca2+ thereby facilitating viral entry and replication []. Research has shown that the interaction between a virus and voltage-gated calcium channels promote virus entry at the virus-host cell fusion step []. Thus, after the virus binds to its receptor on a host cell and enters the cell through endocytosis, the virus takes over the host cell to manufacture its components. Certain viral proteins then manipulate calcium channels, thereby increasing intracellular Ca2+, which facilitates further viral replication.

Even though direct evidence has not been reported, there is indirect evidence that increased intracellular Ca2+ may be involved in COVID-19. In a recent study, elderly hospitalized COVID-19 patients treated with CCBs, amlodipine or nifedipine, were more likely to survive and less likely to require intubation or mechanical ventilation than controls []. Furthermore, CCBs strongly limit SARS-CoV-2 entry and infection in cultured epithelial lung cells []. CCBs also block the increase of intracellular Ca2+ caused by WCR exposure as well as exposure to other electromagnetic fields [].

Intracellular Ca2+ is a ubiquitous second messenger relaying signals received by cell surface receptors to effector proteins involved in numerous biochemical processes. Increased intracellular Ca2+ is a significant factor in upregulation of transcription nuclear factor KB (NF-κB) [], an important regulator of pro-inflammatory cytokine production as well as coagulation and thrombotic cascades. NF-κB is hypothesized to be a key factor underlying severe clinical manifestations of COVID-19 [].

In short, WCR exposure, therefore, may enhance the infectivity of the virus by increasing intracellular Ca2+ that may also indirectly contribute to inflammatory processes and thrombosis.

3.5. Cardiac effects

Cardiac arrhythmias are more commonly encountered in critically ill patients with COVID-19 []. The cause for arrhythmia in COVID-19 patients is multifactorial and includes cardiac and extra-cardiac processes []. Direct infection of the heart muscle by SARS-CoV-19 causing myocarditis, myocardial ischemia caused by a variety of etiologies, and heart strain secondary to pulmonary or systemic hypertension can result in cardiac arrhythmia. Hypoxemia caused by diffuse pneumonia, ARDS, or extensive pulmonary emboli represent extra-cardiac causes of arrhythmia. Electrolyte imbalances, intravascular fluid imbalance, and side effects from pharmacologic regimens can also result in arrhythmias in COVID-19 patients. Patients admitted to ICUs have been shown to have a higher increase in cardiac arrhythmias, 16.5% in one study []. Although no correlation between EMFs and arrhythmia in COVID-19 patients has been described in the literature, many ICUs are equipped with wireless patient monitoring equipment and communication devices producing a wide range of EMF pollution [].

COVID-19 patients commonly show increased levels of cardiac troponin, indicating damage to the heart muscle []. Cardiac damage has been associated with arrhythmias and increased mortality. Cardiac injury is thought to be more often secondary to pulmonary emboli and viral sepsis, but direct infection of the heart, that is, myocarditis, can occur through direct viral binding to ACE2 receptors on cardiac pericytes, affecting local, and regional cardiac blood flow [].

Immune system activation along with alterations in the immune system may result in atherosclerotic plaque instability and vulnerability, that is, presenting an increased risk for thrombus formation, and contributing to development of acute coronary events and cardiovascular disease in COVID-19.

Regarding WCR exposure bioeffects, in 1969 Christopher Dodge of the Biosciences Division, U.S. Naval Observatory in Washington DC, reviewed 54 papers and reported that radiofrequency radiation can adversely affect all major systems of the body, including impeding blood circulation; altering blood pressure and heart rate; affecting electrocardiograph readings; and causing chest pain and heart palpitations []. In the 1970s Glaser reviewed more than 2000 publications on radiofrequency radiation exposure bioeffects and concluded that microwave radiation can alter the electrocardiogram, cause chest pain, hypercoagulation, thrombosis, and hypertension in addition to myocardial infarction [,]. Seizures, convulsions, and alteration of the autonomic nervous system response (increased sympathetic stress response) have also been observed.

Since then, many other researchers have concluded that WCR exposure can affect the cardiovascular system. Although the nature of the primary response to millimeter waves and consequent events are poorly understood, a possible role for receptor structures and neural pathways in the development of continuous millimeter wave-induced arrhythmia has been proposed []. In 1997, a review reported that some investigators discovered cardiovascular changes including arrhythmias in humans from long-term low-level exposure to WCR including microwaves []. However, the literature also shows some unconfirmed findings as well as some contradictory findings []. Havas et al. [] reported that human subjects in a controlled, double-blinded study were hyper-reactive when exposed to 2.45 GHz, digitally pulsed (100 Hz) microwave radiation, developing either an arrhythmia or tachycardia and upregulation of the sympathetic nervous system, which is associated with the stress response. Saili et al. [] found that exposure to Wi-Fi (2.45 GHz pulsed at 10 Hz) affects heart rhythm, blood pressure, and the efficacy of catecholamines on the cardiovascular system, indicating that WCR can act directly and/or indirectly on the cardiovascular system. Most recently, Bandara and Weller [] present evidence that people who live near radar installations (millimeter waves: 5G frequencies) have a greater risk of developing cancer and experiencing heart attacks. Similarly, those occupationally exposed have a greater risk of coronary heart disease. Microwave radiation affects the heart, and some people are more vulnerable if they have an underlying heart abnormality []. More recent research suggests that millimeter waves may act directly on the pacemaker cells of the sinoatrial node of the heart to change the beat frequency, which may underlie arrhythmias and other cardiac issues [].

In short, both COVID-19 and WCR exposure can affect the heart and cardiovascular system, directly and/or indirectly.

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